Genetic association between intronic variants in AS3MT and arsenic methylation efficiency is focused on a large linkage disequilibrium cluster in chromosome 10

Differences in arsenic metabolism are known to play a role in individual variability in arsenic‐induced disease susceptibility. Genetic variants in genes relevant to arsenic metabolism are considered to be partially responsible for the variation in arsenic metabolism. Specifically, variants in arsen...

Full description

Saved in:
Bibliographic Details
Published inJournal of applied toxicology Vol. 30; no. 3; pp. 260 - 270
Main Authors Gomez-Rubio, Paulina, Meza-Montenegro, Maria M., Cantu-Soto, Ernesto, Klimecki, Walter T.
Format Journal Article
LanguageEnglish
Published Chichester, UK John Wiley & Sons, Ltd 01.04.2010
Subjects
5'-Nucleotidase - genetics
Arsenic
Arsenic - metabolism
Arsenic - urine
Arsenic Poisoning - genetics
Arsenic Poisoning - urine
Arsenicals - urine
AS3MT
Chromosomes
Chromosomes, Human, Pair 10 - genetics
Clusters
Female
Genes
Genetic Association Studies
Genetics
Humans
Introns - genetics
Linkage Disequilibrium
Male
Metabolism
Methylation
Methyltransferases - genetics
Mexico
Mouth Mucosa - metabolism
Multigene Family
Polymorphism
Polymorphism, Single Nucleotide
SNP
Steroid 17-alpha-Hydroxylase - genetics
Mexico
AS3MT
polymorphism
Arsenic
SNP
Linkage Disequilibrium
Online AccessGet full text
ISSN0260-437X
1099-1263
1099-1263
DOI10.1002/jat.1492

Cover

Abstract Differences in arsenic metabolism are known to play a role in individual variability in arsenic‐induced disease susceptibility. Genetic variants in genes relevant to arsenic metabolism are considered to be partially responsible for the variation in arsenic metabolism. Specifically, variants in arsenic (3+ oxidation state) methyltransferase (AS3MT), the key gene in the metabolism of arsenic, have been associated with increased arsenic methylation efficiency. Of particular interest is the fact that different studies have reported that several of the AS3MT single nucleotide polymorphisms (SNPs) are in strong linkage‐disequilibrium (LD), which also extends to a nearby gene, CYP17A1. In an effort to characterize the extent of the region in LD, we genotyped 46 SNPs in a 347000 base region of chromosome 10 that included AS3MT in arsenic‐exposed subjects from Mexico. Pairwise LD analysis showed strong LD for these polymorphisms, represented by a mean r2 of 0.82, spanning a region that includes five genes. Genetic association analysis with arsenic metabolism confirmed the previously observed association between AS3MT variants, including this large cluster of linked polymorphisms, and arsenic methylation efficiency. The existence of a large genomic region sharing strong LD with polymorphisms associated with arsenic metabolism presents a predicament because the observed phenotype cannot be unequivocally assigned to a single SNP or even a single gene. The results reported here should be carefully considered for future genomic association studies involving AS3MT and arsenic metabolism. Copyright © 2009 John Wiley & Sons, Ltd. Several AS3MT single nucleotide polymorphisms (SNPs) that previously were associated with arsenic methylation efficiency have also shown strong linkage‐disequilibrium (LD) in the genomic region including AS3MT. To characterize the extent of LD in this region, 46 SNPs were genotyped in chromosome 10. Strong LD was observed spanning a region that includes AS3MT and four other genes. Genetic association analysis confirmed the association between this large cluster of linked polymorphisms and arsenic methylation efficiency.
AbstractList Differences in arsenic metabolism are known to play a role in individual variability in arsenic-induced disease susceptibility. Genetic variants in genes relevant to arsenic metabolism are considered to be partially responsible for the variation in arsenic metabolism. Specifically, variants in arsenic (3+ oxidation state) methyltransferase (AS3MT), the key gene in the metabolism of arsenic, have been associated with increased arsenic methylation efficiency. Of particular interest is the fact that different studies have reported that several of the AS3MT single nucleotide polymorphisms (SNPs) are in strong linkage-disequilibrium (LD), which also extends to a nearby gene, CYP17A1. In an effort to characterize the extent of the region in LD, we genotyped 46 SNPs in a 347,000 base region of chromosome 10 that included AS3MT in arsenic-exposed subjects from Mexico. Pairwise LD analysis showed strong LD for these polymorphisms, represented by a mean r(2) of 0.82, spanning a region that includes five genes. Genetic association analysis with arsenic metabolism confirmed the previously observed association between AS3MT variants, including this large cluster of linked polymorphisms, and arsenic methylation efficiency. The existence of a large genomic region sharing strong LD with polymorphisms associated with arsenic metabolism presents a predicament because the observed phenotype cannot be unequivocally assigned to a single SNP or even a single gene. The results reported here should be carefully considered for future genomic association studies involving AS3MT and arsenic metabolism.
Differences in arsenic metabolism are known to play a role in individual variability in arsenic-induced disease susceptibility. Genetic variants in genes relevant to arsenic metabolism are considered to be partially responsible for the variation in arsenic metabolism. Specifically, variants in arsenic (3+ oxidation state) methyltransferase (AS3MT), the key gene in the metabolism of arsenic, have been associated with increased arsenic methylation efficiency. Of particular interest is the fact that different studies have reported that several of the AS3MT single nucleotide polymorphisms (SNPs) are in strong linkage-disequilibrium (LD), which also extends to a nearby gene, CYP17A1. In an effort to characterize the extent of the region in LD, we genotyped 46 SNPs in a 347,000 base region of chromosome 10 that included AS3MT in arsenic-exposed subjects from Mexico. Pairwise LD analysis showed strong LD for these polymorphisms, represented by a mean r(2) of 0.82, spanning a region that includes five genes. Genetic association analysis with arsenic metabolism confirmed the previously observed association between AS3MT variants, including this large cluster of linked polymorphisms, and arsenic methylation efficiency. The existence of a large genomic region sharing strong LD with polymorphisms associated with arsenic metabolism presents a predicament because the observed phenotype cannot be unequivocally assigned to a single SNP or even a single gene. The results reported here should be carefully considered for future genomic association studies involving AS3MT and arsenic metabolism.Differences in arsenic metabolism are known to play a role in individual variability in arsenic-induced disease susceptibility. Genetic variants in genes relevant to arsenic metabolism are considered to be partially responsible for the variation in arsenic metabolism. Specifically, variants in arsenic (3+ oxidation state) methyltransferase (AS3MT), the key gene in the metabolism of arsenic, have been associated with increased arsenic methylation efficiency. Of particular interest is the fact that different studies have reported that several of the AS3MT single nucleotide polymorphisms (SNPs) are in strong linkage-disequilibrium (LD), which also extends to a nearby gene, CYP17A1. In an effort to characterize the extent of the region in LD, we genotyped 46 SNPs in a 347,000 base region of chromosome 10 that included AS3MT in arsenic-exposed subjects from Mexico. Pairwise LD analysis showed strong LD for these polymorphisms, represented by a mean r(2) of 0.82, spanning a region that includes five genes. Genetic association analysis with arsenic metabolism confirmed the previously observed association between AS3MT variants, including this large cluster of linked polymorphisms, and arsenic methylation efficiency. The existence of a large genomic region sharing strong LD with polymorphisms associated with arsenic metabolism presents a predicament because the observed phenotype cannot be unequivocally assigned to a single SNP or even a single gene. The results reported here should be carefully considered for future genomic association studies involving AS3MT and arsenic metabolism.
Differences in arsenic metabolism are known to play a role in individual variability in arsenic-induced disease susceptibility. Genetic variants in genes relevant to arsenic metabolism are considered to be partially responsible for the variation in arsenic metabolism. Specifically, variants in arsenic (3+ oxidation state) methyltransferase (AS3MT), the key gene in the metabolism of arsenic, have been associated with increased arsenic methylation efficiency. Of particular interest is the fact that different studies have reported that several of the AS3MT single nucleotide polymorphisms (SNPs) are in strong linkage-disequilibrium (LD), which also extends to a nearby gene, CYP17A1. In an effort to characterize the extent of the region in LD, we genotyped 46 SNPs in a 347000 base region of chromosome 10 that included AS3MT in arsenic-exposed subjects from Mexico. Pairwise LD analysis showed strong LD for these polymorphisms, represented by a mean r2 of 0.82, spanning a region that includes five genes. Genetic association analysis with arsenic metabolism confirmed the previously observed association between AS3MT variants, including this large cluster of linked polymorphisms, and arsenic methylation efficiency. The existence of a large genomic region sharing strong LD with polymorphisms associated with arsenic metabolism presents a predicament because the observed phenotype cannot be unequivocally assigned to a single SNP or even a single gene. The results reported here should be carefully considered for future genomic association studies involving AS3MT and arsenic metabolism.
Differences in arsenic metabolism are known to play a role in individual variability in arsenic‐induced disease susceptibility. Genetic variants in genes relevant to arsenic metabolism are considered to be partially responsible for the variation in arsenic metabolism. Specifically, variants in arsenic (3+ oxidation state) methyltransferase (AS3MT), the key gene in the metabolism of arsenic, have been associated with increased arsenic methylation efficiency. Of particular interest is the fact that different studies have reported that several of the AS3MT single nucleotide polymorphisms (SNPs) are in strong linkage‐disequilibrium (LD), which also extends to a nearby gene, CYP17A1. In an effort to characterize the extent of the region in LD, we genotyped 46 SNPs in a 347000 base region of chromosome 10 that included AS3MT in arsenic‐exposed subjects from Mexico. Pairwise LD analysis showed strong LD for these polymorphisms, represented by a mean r2 of 0.82, spanning a region that includes five genes. Genetic association analysis with arsenic metabolism confirmed the previously observed association between AS3MT variants, including this large cluster of linked polymorphisms, and arsenic methylation efficiency. The existence of a large genomic region sharing strong LD with polymorphisms associated with arsenic metabolism presents a predicament because the observed phenotype cannot be unequivocally assigned to a single SNP or even a single gene. The results reported here should be carefully considered for future genomic association studies involving AS3MT and arsenic metabolism. Copyright © 2009 John Wiley & Sons, Ltd. Several AS3MT single nucleotide polymorphisms (SNPs) that previously were associated with arsenic methylation efficiency have also shown strong linkage‐disequilibrium (LD) in the genomic region including AS3MT. To characterize the extent of LD in this region, 46 SNPs were genotyped in chromosome 10. Strong LD was observed spanning a region that includes AS3MT and four other genes. Genetic association analysis confirmed the association between this large cluster of linked polymorphisms and arsenic methylation efficiency.
Differences in arsenic metabolism are known to play a role in individual variability in arsenic-induced disease susceptibility. Genetic variants in genes relevant to arsenic metabolism are considered to be partially responsible for the variation in arsenic metabolism. Specifically, variants in arsenic (3+ oxidation state) methyltransferase (AS3MT), the key gene in the metabolism of arsenic, have been associated with increased arsenic methylation efficiency. Of particular interest is the fact that different studies have reported that several of the AS3MT single nucleotide polymorphisms (SNPs) are in strong linkage-disequilibrium (LD), which also extends to a nearby gene, CYP17A1. In an effort to characterize the extent of the region in LD, we genotyped 46 SNPs in a 347,000 base region of chromosome 10 that included AS3MT in arsenic-exposed subjects from Mexico. Pairwise LD analysis showed strong LD for these polymorphisms, represented by a mean r 2 of 0.82, spanning a region that includes 5 genes. Genetic association analysis with arsenic metabolism confirmed the previously observed association between AS3MT variants, including this large cluster of linked polymorphisms, and arsenic methylation efficiency. The existence of a large genomic region sharing strong LD with polymorphisms associated with arsenic metabolism presents a predicament because the observed phenotype cannot be unequivocally assigned to a single SNP or even a single gene. The results reported here should be carefully considered for future genomic association studies involving AS3MT and arsenic metabolism.
Differences in arsenic metabolism are known to play a role in individual variability in arsenic‐induced disease susceptibility. Genetic variants in genes relevant to arsenic metabolism are considered to be partially responsible for the variation in arsenic metabolism. Specifically, variants in arsenic (3+ oxidation state) methyltransferase (AS3MT), the key gene in the metabolism of arsenic, have been associated with increased arsenic methylation efficiency. Of particular interest is the fact that different studies have reported that several of the AS3MT single nucleotide polymorphisms (SNPs) are in strong linkage‐disequilibrium (LD), which also extends to a nearby gene, CYP17A1. In an effort to characterize the extent of the region in LD, we genotyped 46 SNPs in a 347000 base region of chromosome 10 that included AS3MT in arsenic‐exposed subjects from Mexico. Pairwise LD analysis showed strong LD for these polymorphisms, represented by a mean r 2 of 0.82, spanning a region that includes five genes. Genetic association analysis with arsenic metabolism confirmed the previously observed association between AS3MT variants, including this large cluster of linked polymorphisms, and arsenic methylation efficiency. The existence of a large genomic region sharing strong LD with polymorphisms associated with arsenic metabolism presents a predicament because the observed phenotype cannot be unequivocally assigned to a single SNP or even a single gene. The results reported here should be carefully considered for future genomic association studies involving AS3MT and arsenic metabolism. Copyright © 2009 John Wiley & Sons, Ltd. Several AS3MT single nucleotide polymorphisms (SNPs) that previously were associated with arsenic methylation efficiency have also shown strong linkage‐disequilibrium (LD) in the genomic region including AS3MT. To characterize the extent of LD in this region, 46 SNPs were genotyped in chromosome 10. Strong LD was observed spanning a region that includes AS3MT and four other genes. Genetic association analysis confirmed the association between this large cluster of linked polymorphisms and arsenic methylation efficiency.
Differences in arsenic metabolism are known to play a role in individual variability in arsenic-induced disease susceptibility. Genetic variants in genes relevant to arsenic metabolism are considered to be partially responsible for the variation in arsenic metabolism. Specifically, variants in arsenic (3+ oxidation state) methyltransferase (AS3MT), the key gene in the metabolism of arsenic, have been associated with increased arsenic methylation efficiency. Of particular interest is the fact that different studies have reported that several of the AS3MT single nucleotide polymorphisms (SNPs) are in strong linkage-disequilibrium (LD), which also extends to a nearby gene, CYP17A1. In an effort to characterize the extent of the region in LD, we genotyped 46 SNPs in a 347000 base region of chromosome 10 that included AS3MT in arsenic-exposed subjects from Mexico. Pairwise LD analysis showed strong LD for these polymorphisms, represented by a mean r super(2) of 0.82, spanning a region that includes five genes. Genetic association analysis with arsenic metabolism confirmed the previously observed association between AS3MT variants, including this large cluster of linked polymorphisms, and arsenic methylation efficiency. The existence of a large genomic region sharing strong LD with polymorphisms associated with arsenic metabolism presents a predicament because the observed phenotype cannot be unequivocally assigned to a single SNP or even a single gene. The results reported here should be carefully considered for future genomic association studies involving AS3MT and arsenic metabolism.
Author Meza-Montenegro, Maria M.
Gomez-Rubio, Paulina
Cantu-Soto, Ernesto
Klimecki, Walter T.
AuthorAffiliation 1 Department of Pharmacology and Toxicology, University of Arizona
2 Department of Environmental Sciences, Instituto Tecnologico de Sonora
AuthorAffiliation_xml – name: 2 Department of Environmental Sciences, Instituto Tecnologico de Sonora
– name: 1 Department of Pharmacology and Toxicology, University of Arizona
Author_xml – sequence: 1
  givenname: Paulina
  surname: Gomez-Rubio
  fullname: Gomez-Rubio, Paulina
  organization: Department of Pharmacology and Toxicology, University of Arizona, Tucson, Arizona, USA
– sequence: 2
  givenname: Maria M.
  surname: Meza-Montenegro
  fullname: Meza-Montenegro, Maria M.
  organization: Department of Environmental Science, Instituto Technologico de Sonora, Ciudad Obregon, Sonora, Mexico
– sequence: 3
  givenname: Ernesto
  surname: Cantu-Soto
  fullname: Cantu-Soto, Ernesto
  organization: Department of Environmental Science, Instituto Technologico de Sonora, Ciudad Obregon, Sonora, Mexico
– sequence: 4
  givenname: Walter T.
  surname: Klimecki
  fullname: Klimecki, Walter T.
  email: klimecki@pharmacy.arizona.edu
  organization: Department of Pharmacology and Toxicology, University of Arizona, Tucson, Arizona, USA
BackLink https://www.ncbi.nlm.nih.gov/pubmed/20014157$$D View this record in MEDLINE/PubMed
BookMark eNqFkt1u1DAQhSNURLcFiSdAvoObLP6LndwgVVW7ULZwwfJzZznOpOs2sVs7admn4VXxsmWhCOjVSD7fHGtmzl6247yDLHtK8JRgTF-e62FKeEUfZBOCqyonVLCdbIKpwDln8stuthfjOcZJo-WjbJdiTDgp5CT7NgMHgzVIx-iN1YP1DtUw3AA4ZN0QvEvitQ5WuyGmF3TwgZ0ukHYN0iHCWu1hWK66TSu0rTUWnFkhG1HrzRihQUnQqNPhDFBn3YVOtbERrkbb2TrYsUemG-MAYf2BWQbf--h7QAQ_zh62uovw5LbuZx-PjxaHr_P5-9mbw4N5bgopaN5qXgnDMS15AZwLKQjjdd3gupGNKWhbV5XGQvJWYMmoblkjCG0LUeu2ZhSz_ezVxvdyrHtoDKTRdacug-11WCmvrbqrOLtUZ_5a0VJQwlkyeH5rEPzVCHFQvY0Guk478GNUZcnSOSgX95OiKmRVEnovKRmrGBUlSeSL_5JEFqxIeymLhD77fdLtiD8z8cvLBB9jgHaLEKzWcVMpbmodt4RO_0CNHX4EIe3Idn9ryDcNN7aD1T-N1cnB4i5vUzq-bnkdLpSQTBbq87uZOq7m5O0J-6RO2Xd9tPb9
CitedBy_id crossref_primary_10_1289_EHP251
crossref_primary_10_1161_HYPERTENSIONAHA_115_06925
crossref_primary_10_1371_journal_pgen_1002522
crossref_primary_10_1016_j_scitotenv_2017_07_019
crossref_primary_10_1093_trstmh_try047
crossref_primary_10_1177_0960327120925891
crossref_primary_10_1093_toxsci_kfw181
crossref_primary_10_1093_toxsci_kfaa075
crossref_primary_10_1186_1476_069X_11_43
crossref_primary_10_1093_molbev_msv046
crossref_primary_10_1136_bmjopen_2020_038507
crossref_primary_10_3390_ijms12042351
crossref_primary_10_1016_j_tox_2021_152803
crossref_primary_10_1371_journal_pgen_1010588
crossref_primary_10_3390_ijerph10041527
crossref_primary_10_1289_ehp_1205504
crossref_primary_10_1289_ehp_1205305
crossref_primary_10_1038_jes_2012_103
crossref_primary_10_1177_0748233720918680
crossref_primary_10_1016_j_reprotox_2016_02_017
crossref_primary_10_1265_jjh_70_186
crossref_primary_10_1016_j_scitotenv_2011_10_023
crossref_primary_10_1093_toxsci_kfr184
crossref_primary_10_1371_journal_pone_0053732
crossref_primary_10_3390_ijms232012629
crossref_primary_10_1002_em_22026
crossref_primary_10_1093_toxsci_kfv164
crossref_primary_10_1007_s00204_010_0554_4
crossref_primary_10_1007_s40471_019_00186_5
crossref_primary_10_1016_j_scitotenv_2011_08_051
crossref_primary_10_1093_toxsci_kft181
crossref_primary_10_3389_fnins_2021_705297
crossref_primary_10_1016_j_chemosphere_2022_134764
crossref_primary_10_1080_15287394_2011_615107
crossref_primary_10_1186_1476_069X_13_15
crossref_primary_10_1248_bpb_b212015
crossref_primary_10_1016_j_taap_2011_02_007
crossref_primary_10_1097_YPG_0000000000000064
crossref_primary_10_1093_ije_dyz046
crossref_primary_10_1289_ehp_1103441
crossref_primary_10_7554_eLife_40260
crossref_primary_10_1002_bdra_23399
crossref_primary_10_1016_j_cell_2019_01_052
crossref_primary_10_3390_ijms25063349
Cites_doi 10.1016/j.mrfmmm.2008.07.003
10.1093/toxsci/kfn236
10.1289/ehp.96104620
10.1007/s00204-004-0620-x
10.1093/ajcn/85.5.1367
10.1101/gr.1982804
10.1016/S0960-9822(01)00348-7
10.1289/ehp.6254
10.1086/519795
10.1016/S0378-4274(02)00085-1
10.1016/j.mrfmmm.2007.07.004
10.1016/j.taap.2006.09.021
10.1038/nrg1123
10.1016/j.taap.2009.06.007
10.1016/S0960-0760(01)00105-4
10.1016/j.taap.2004.11.022
10.1097/01.jom.0000058336.05741.e8
10.1007/BF00223635
10.1006/taap.1999.8872
10.1016/j.mrrev.2008.06.003
10.1289/ehp.7780
10.1289/ehp.10026
10.1007/s10653-008-9235-0
10.1007/s10552-008-9146-5
10.1093/bioinformatics/bth457
10.1097/01.jom.0000169089.54549.db
10.1007/s002040000134
10.1289/ehp.00108655
10.1016/j.taap.2003.10.020
10.1289/ehp.9734
10.1086/429864
10.1289/ehp.7907
10.1093/toxsci/44.2.185
10.1093/toxsci/kfl160
10.1002/jat.1166
10.1016/j.taap.2003.10.028
10.1021/tx060076u
10.1016/j.taap.2006.10.022
10.1097/01.jom.0000200982.28276.70
ContentType Journal Article
Copyright Copyright © 2009 John Wiley & Sons, Ltd.
(c) 2009 John Wiley & Sons, Ltd.
Copyright_xml – notice: Copyright © 2009 John Wiley & Sons, Ltd.
– notice: (c) 2009 John Wiley & Sons, Ltd.
DBID BSCLL
AAYXX
CITATION
CGR
CUY
CVF
ECM
EIF
NPM
8FD
FR3
KR7
7X8
7ST
7TM
7TV
7U7
C1K
SOI
P64
RC3
5PM
DOI 10.1002/jat.1492
DatabaseName Istex
CrossRef
Medline
MEDLINE
MEDLINE (Ovid)
MEDLINE
MEDLINE
PubMed
Technology Research Database
Engineering Research Database
Civil Engineering Abstracts
MEDLINE - Academic
Environment Abstracts
Nucleic Acids Abstracts
Pollution Abstracts
Toxicology Abstracts
Environmental Sciences and Pollution Management
Environment Abstracts
Biotechnology and BioEngineering Abstracts
Genetics Abstracts
PubMed Central (Full Participant titles)
DatabaseTitle CrossRef
MEDLINE
Medline Complete
MEDLINE with Full Text
PubMed
MEDLINE (Ovid)
Technology Research Database
Civil Engineering Abstracts
Engineering Research Database
MEDLINE - Academic
Pollution Abstracts
Toxicology Abstracts
Environment Abstracts
Nucleic Acids Abstracts
Environmental Sciences and Pollution Management
Genetics Abstracts
Biotechnology and BioEngineering Abstracts
DatabaseTitleList MEDLINE
MEDLINE - Academic
Technology Research Database


Genetics Abstracts
CrossRef
Pollution Abstracts
Database_xml – sequence: 1
  dbid: NPM
  name: PubMed
  url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed
  sourceTypes: Index Database
– sequence: 2
  dbid: EIF
  name: MEDLINE
  url: https://proxy.k.utb.cz/login?url=https://www.webofscience.com/wos/medline/basic-search
  sourceTypes: Index Database
DeliveryMethod fulltext_linktorsrc
Discipline Public Health
Pharmacy, Therapeutics, & Pharmacology
EISSN 1099-1263
EndPage 270
ExternalDocumentID PMC2862143
20014157
10_1002_jat_1492
JAT1492
ark_67375_WNG_F9L1KJ3V_M
Genre article
Journal Article
Research Support, N.I.H., Extramural
GeographicLocations Mexico
GeographicLocations_xml – name: Mexico
GrantInformation_xml – fundername: NIEHS NIH HHS
  grantid: ES 006694
– fundername: NIEHS NIH HHS
  grantid: ES 04940
– fundername: NIEHS NIH HHS
  grantid: P30 ES006694
– fundername: NIEHS NIH HHS
  grantid: P42 ES004940
GroupedDBID ---
.3N
.GA
.GJ
.Y3
05W
0R~
10A
1L6
1OB
1OC
1ZS
31~
33P
3SF
3WU
4.4
4ZD
50Y
50Z
51W
51X
52M
52N
52O
52P
52S
52T
52U
52W
52X
53G
5GY
5VS
66C
702
7PT
8-0
8-1
8-3
8-4
8-5
8UM
930
A03
AAESR
AAEVG
AAHQN
AAMMB
AAMNL
AANHP
AANLZ
AAONW
AASGY
AAXRX
AAYCA
AAZKR
ABCQN
ABCUV
ABEFU
ABEML
ABIJN
ABJNI
ABPVW
ACAHQ
ACBWZ
ACCZN
ACGFO
ACGFS
ACPOU
ACPRK
ACRPL
ACSCC
ACXBN
ACXQS
ACYXJ
ADBBV
ADEOM
ADIZJ
ADKYN
ADMGS
ADNMO
ADOZA
ADXAS
ADZMN
AEFGJ
AEGXH
AEIGN
AEIMD
AENEX
AEUYR
AEYWJ
AFBPY
AFFNX
AFFPM
AFGKR
AFRAH
AFWVQ
AFZJQ
AGHNM
AGQPQ
AGXDD
AGYGG
AHBTC
AHMBA
AI.
AIAGR
AIDQK
AIDYY
AIQQE
AITYG
AIURR
AJXKR
ALAGY
ALMA_UNASSIGNED_HOLDINGS
ALUQN
ALVPJ
AMBMR
AMYDB
ASPBG
ATUGU
AUFTA
AVWKF
AZBYB
AZFZN
AZVAB
BAFTC
BDRZF
BFHJK
BHBCM
BMNLL
BMXJE
BNHUX
BROTX
BRXPI
BSCLL
BY8
CS3
D-E
D-F
DCZOG
DPXWK
DR2
DRFUL
DRSTM
EBD
EBS
EDH
EJD
F00
F01
F04
F5P
FEDTE
G-S
G.N
GNP
GODZA
GWYGA
H.T
H.X
HF~
HGLYW
HHZ
HVGLF
HZ~
IX1
J0M
JPC
KQQ
LATKE
LAW
LC2
LC3
LEEKS
LH4
LITHE
LOXES
LP6
LP7
LUTES
LW6
LYRES
M6Q
MEWTI
MK4
MRFUL
MRSTM
MSFUL
MSSTM
MXFUL
MXSTM
N04
N05
N9A
NF~
NNB
O66
O9-
OIG
P2P
P2W
P2X
P4D
PALCI
PQQKQ
Q.N
Q11
QB0
QRW
R.K
RIWAO
RJQFR
ROL
RX1
RYL
SAMSI
SUPJJ
UB1
V8K
VH1
W8V
W99
WBFHL
WBKPD
WH7
WIB
WIH
WIK
WJL
WOHZO
WQJ
WXSBR
WYISQ
XG1
XPP
XV2
YHZ
ZXP
ZZTAW
~02
~IA
~KM
~WT
AAHHS
AAYXX
ACCFJ
ADZOD
AEEZP
AEQDE
AIWBW
AJBDE
CITATION
CGR
CUY
CVF
ECM
EIF
NPM
8FD
FR3
KR7
7X8
7ST
7TM
7TV
7U7
C1K
SOI
P64
RC3
5PM
ID FETCH-LOGICAL-c5762-fa496c402845e44676134bbd0bd7dc52fb99a0674f60732af3d612f56bafb3203
IEDL.DBID DR2
ISSN 0260-437X
1099-1263
IngestDate Thu Aug 21 17:38:39 EDT 2025
Fri Sep 05 06:00:12 EDT 2025
Fri Sep 05 10:49:06 EDT 2025
Thu Sep 04 19:16:57 EDT 2025
Fri Sep 05 11:13:13 EDT 2025
Mon Jul 21 06:01:19 EDT 2025
Thu Apr 24 23:08:29 EDT 2025
Tue Jul 01 00:49:53 EDT 2025
Thu Sep 25 07:37:16 EDT 2025
Sun Sep 21 06:19:41 EDT 2025
IsPeerReviewed true
IsScholarly true
Issue 3
Keywords AS3MT
polymorphism
Arsenic
SNP
Linkage Disequilibrium
Language English
License http://onlinelibrary.wiley.com/termsAndConditions#vor
(c) 2009 John Wiley & Sons, Ltd.
LinkModel DirectLink
MergedId FETCHMERGED-LOGICAL-c5762-fa496c402845e44676134bbd0bd7dc52fb99a0674f60732af3d612f56bafb3203
Notes istex:BD66F6F866062E515925932BAA6548BE4D80DC02
ArticleID:JAT1492
ark:/67375/WNG-F9L1KJ3V-M
ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
PMID 20014157
PQID 1753544685
PQPubID 23462
PageCount 11
ParticipantIDs pubmedcentral_primary_oai_pubmedcentral_nih_gov_2862143
proquest_miscellaneous_883026246
proquest_miscellaneous_869579812
proquest_miscellaneous_733932681
proquest_miscellaneous_1753544685
pubmed_primary_20014157
crossref_primary_10_1002_jat_1492
crossref_citationtrail_10_1002_jat_1492
wiley_primary_10_1002_jat_1492_JAT1492
istex_primary_ark_67375_WNG_F9L1KJ3V_M
ProviderPackageCode CITATION
AAYXX
PublicationCentury 2000
PublicationDate April 2010
PublicationDateYYYYMMDD 2010-04-01
PublicationDate_xml – month: 04
  year: 2010
  text: April 2010
PublicationDecade 2010
PublicationPlace Chichester, UK
PublicationPlace_xml – name: Chichester, UK
– name: England
PublicationTitle Journal of applied toxicology
PublicationTitleAlternate J. Appl. Toxicol
PublicationYear 2010
Publisher John Wiley & Sons, Ltd
Publisher_xml – name: John Wiley & Sons, Ltd
References Wigginton JE, Cutler DJ, Abecasis GR. 2005. A note on exact tests of Hardy-Weinberg equilibrium. Am. J. Hum. Genet. 76: 887-893.
Concha G, Vogler G, Lezcano D, Nermell B, Vahter M. 1998. Exposure to inorganic arsenic metabolites during early human development. Toxicol. Sci. 44: 185-190.
Rahman MM, Ng JC, Naidu R. 2009. Chronic exposure of arsenic via drinking water and its adverse health impacts on humans. Environ. Geochem. Health 31: 189-200.
Hopenhayn-Rich C, Biggs ML, Smith AH, Kalman DA, Moore LE. 1996. Methylation study of a population environmentally exposed to arsenic in drinking water. Environ. Health Perspect. 104: 620-628.
Steinmaus C, Bates MN, Yuan Y, Kalman D, Atallah R, Rey OA, Biggs ML, Hopenhayn C, Moore LE, Hoang BK, Smith AH. 2006. Arsenic methylation and bladder cancer risk in case-control studies in Argentina and the United States. J. Occup. Environ. Med. 48: 478-488.
Eblin KE, Bredfeldt TG, Buffington S, Gandolfi AJ. 2007. Mitogenic signal transduction caused by monomethylarsonous acid in human bladder cells: role in arsenic-induced carcinogenesis. Toxicol. Sci. 95: 321-330.
Goldstein DB, Weale ME. 2001. Population genomics: linkage disequilibrium holds the key. Curr. Biol. 11: 576-579.
Huang YK, Huang YL, Hsueh YM, Yang MH, Wu MM, Chen SY, Hsu LI, Chen CJ. 2008. Arsenic exposure, urinary arsenic speciation, and the incidence of urothelial carcinoma: a twelve-year follow-up study. Cancer Causes Control 19: 829-839.
States JC, Srivastava S, Chen Y, Barchowsky A. 2009. Arsenic and cardiovascular disease. Toxicol. Sci. 107: 312-323.
Singh N, Kumar D, Sahu AP. 2007. Arsenic in the environment: effects on human health and possible prevention. J. Environ. Biol. 28: 359-365.
Hafeman DM, Ahsan H, Louis ED, Siddique AB, Slavkovich V, Cheng Z, van Geen A, Graziano JH. 2005 . Association between arsenic exposure and a measure of subclinical sensory neuropathy in Bangladesh. J. Occup. Environ. Med. 47: 778-784.
Lindberg AL, Kumar R, Goessler W, Thirumaran R, Gurzau E, Koppova K, Rudnai P, Leonardi G, Fletcher T, Vahter M. 2007. Metabolism of low-dose inorganic arsenic in a central European population: influence of sex and genetic polymorphisms. Environ. Health Perspect. 115: 1081-1086.
Petrick JS, Ayala-Fierro F, Cullen WR, Carter DE, Vasken Aposhian H. 2000. Monomethylarsonous acid (MMA(III)) is more toxic than arsenite in Chang human hepatocytes. Toxicol. Appl. Pharmacol. 163: 203-207.
Schläwicke Engström K, Broberg K, Concha G, Nermell B, Warholm M, Vahter M. 2007. Genetic polymorphisms influencing arsenic metabolism: evidence from Argentina. Environ. Health Perspect. 115: 599-605.
Morales KH, Ryan L, Kuo TL, Wu MM, Chen CJ. 2000. Risk of internal cancers from arsenic in drinking water. Environ. Health Perspect. 108: 655-661.
Schläwicke Engström K, Nermell B, Concha G, Strömberg U, Vahter M, Broberg K. 2009. Arsenic metabolism is influenced by polymorphisms in genes involved in one-carbon metabolism and reduction reactions. Mutat. Res. 667: 4-14.
Gerber S, Rodolphe F. 1994. Estimation and test for linkage between markers: a comparison of lod score and χ2 test in a linkage study of maritime pine (Pinus pinaster Ait.). Theor. Appl. Genet. 88: 293-297.
Jurinke C, van den Boom D, Cantor CR, Köster H. 2002. The use of MassARRAY technology for high throughput genotyping. Adv. Biochem. Eng. Biotechnol. 77: 57-74.
Chen YC, Guo YL, Su HJ, Hsueh YM, Smith TJ, Ryan LM, Lee MS, Chao SC, Lee JY, Christiani DC. 2003. Arsenic methylation and skin cancer risk in southwestern Taiwan. J. Occup. Environ. Med. 45: 241-248.
Chiou HY, Hsueh YM, Liaw KF, Horng SF, Chiang MH, Pu YS, Lin JS, Huang CH, Chen CJ. 1995. Incidence of internal cancers and ingested inorganic arsenic: a seven-year follow-up study in Taiwan. Cancer Res. 55: 1296-1300.
Meza MM, Yu L, Rodriguez YY, Guild M, Thompson D, Gandolfi AJ, Klimecki WT. 2005. Developmentally restricted genetic determinants of human arsenic metabolism: association between urinary methylated arsenic and CYT19 polymorphisms in children. Environ. Health Perspect. 113: 775-781.
Heck JE, Gamble MV, Chen Y, Graziano JH, Slavkovich V, Parvez F, Baron JA, Howe GR, Ahsan H. 2007. Consumption of folate-related nutrients and metabolism of arsenic in Bangladesh. Am. J. Clin. Nutr. 85: 1367-1374.
Trinklein ND, Aldred SF, Hartman SJ, Schroeder DI, Otillar RP, Myers RM. 2004. An abundance of bidirectional promoters in the human genome. Genome Res. 14: 62-66.
Tseng CH, Tseng CP, Chiou HY, Hsueh YM, Chong CK, Chen CJ. 2002. Epidemiologic evidence of diabetogenic effect of arsenic. Toxicol. Lett. 133: 69-76.
Hopenhayn C, Huang B, Christian J, Peralta C, Ferreccio C, Atallah R, Kalman D. 2003. Profile of urinary arsenic metabolites during pregnancy. Environ. Health Perspect. 111: 1888-1891.
Styblo M, Del Razo LM, Vega L, Germolec DR, LeCluyse EL, Hamilton GA, Reed W, Wang C, Cullen WR, Thomas DJ. 2000. Comparative toxicity of trivalent and pentavalent inorganic and methylated arsenicals in rat and human cells. Arch. Toxicol. 74: 289-299.
Lieberman S, Warne PA. 2001. 17-Hydroxylase: an evaluation of the present view of its catalytic role in steroidogenesis. J. Steroid Biochem. Mol. Biol. 78: 299-312.
Barrett JC, Fry B, Maller J, Daly MJ. 2005. Haploview: analysis and visualization of LD and haplotype maps. Bioinformatics. 21: 263-265.
Pu YS, Yang SM, Huang YK, Chung CJ, Huang SK, Chiu AW, Yang MH, Chen CJ, Hsueh YM. 2007. Urinary arsenic profile affects the risk of urothelial carcinoma even at low arsenic exposure. Toxicol. Appl. Pharmacol. 218: 99-106.
Ghosh P, Banerjee M, Giri AK, Ray K. 2008. Toxicogenomics of arsenic: classical ideas and recent advances. Mutat. Res. 659: 293-301.
Hayakawa T, Kobayashi Y, Cui X, Hirano S. 2005. A new metabolic pathway of arsenite: arsenic-glutathione complexes are substrates for human arsenic methyltransferase Cyt19. Arch. Toxicol. 79: 183-191.
Steinmaus C, Carrigan K, Kalman D, Atallah R, Yuan Y, Smith AH. 2005. Dietary intake and arsenic methylation in a U.S. population. Environ. Health Perspect. 113: 1153-1159.
Valenzuela OL, Drobna Z, Hernandez-Castellanos E, Sanchez-Pena LC, Garcia-Vargas GG, Borja-Aburto VH, Styblo M, Del Razo LM. 2009. Association of AS3MT polymorphisms and the risk of premalignant arsenic skin lesions. Toxicol. Appl. Pharmacol. 239: 200-207.
Oskarsson A, Ullerås E, Plant KE, Hinson JP, Goldfarb PS. 2006. Steroidogenic gene expression in H295R cells and the human adrenal gland: adrenotoxic effects of lindane in vitro. J. Appl. Toxicol. 26: 484-492.
Thomas DJ, Li J, Waters SB, Xing W, Adair BM, Drobna Z, Devesa V, Styblo M. 2007. Arsenic (+3 oxidation state) methyltransferase and the methylation of arsenicals. Exp. Biol. Med. (Maywood) 232: 3-13.
Purcell S, Neale B, Todd-Brown K, Thomas L, Ferreira MA, Bender D, Maller J, Sklar P, De Bakker PI, Daly MJ, Sham PC. 2007. PLINK: a tool set for whole-genome association and population-based linkage analyses. Am. J. Hum. Genet. 81: 559-575.
Tseng CH, Huang YK, Huang YL, Chung CJ, Yang MH, Chen CJ, Hsueh YM. 2005. Arsenic exposure, urinary arsenic speciation, and peripheral vascular disease in blackfoot disease-hyperendemic villages in Taiwan. Toxicol. Appl. Pharmacol. 206: 299-308.
Hernández A, Xamena N, Surrallés J, Sekaran C, Tokunaga H, Quinteros D, Creus A, Marcos R. 2008. Role of the Met(287)Thr polymorphism in the AS3MT gene on the metabolic arsenic profile. Mutat. Res. 637: 80-92.
Wall JD, Pritchard JK. 2003. Haplotype blocks and linkage disequilibrium in the human genome. Nat. Rev. Genet. 4: 587-597.
Waalkes MP, Liu J, Ward JM, Diwan BA. 2004. Animal models for arsenic carcinogenesis: inorganic arsenic is a transplacental carcinogen in mice. Toxicol. Appl. Pharmacol. 198: 377-384.
Drobna Z, Xing W, Thomas DJ, Stýblo M. 2006. shRNA Silencing of AS3MT expression minimizes arsenic methylation capacity of HepG2 cells. Chem. Res. Toxicol. 19: 894-898.
Huang YK, Tseng CH, Huang YL, Yang MH, Chen CJ, Hsueh YM. 2007. Arsenic methylation capability and hypertension risk in subjects living in arseniasis-hyperendemic areas in southwestern Taiwan. Toxicol. Appl. Pharmacol. 218: 135-142.
Thomas DJ, Waters SB, Styblo M. 2004. Elucidating the pathway for arsenic methylation. Toxicol. Appl. Pharmacol. 198: 319-326.
Nahar N, Hossain F, Hossain MD. 2008. Health and socioeconomic effects of groundwater arsenic contamination in rural Bangladesh: new evidence from field surveys. J. Environ. Health 70: 42-47.
2005; 113
2008; 19
1995; 55
2002; 133
2002; 77
1994; 88
2005; 21
2006; 19
2005
2007; 95
1996; 104
2009; 239
2008; 70
2003; 111
1998; 44
2005; 47
2007; 28
2007; 115
2004; 198
2007; 218
2009; 31
2004; 14
2007; 232
2000; 108
2000; 74
2006; 26
2006; 48
2008; 659
2008; 637
2005; 206
2003; 4
2000; 163
2007; 81
2005; 76
2007; 85
2001; 11
2009; 107
2001; 78
2005; 79
2003; 45
2009; 667
Chiou HY (e_1_2_1_4_1) 1995; 55
e_1_2_1_42_1
e_1_2_1_20_1
e_1_2_1_41_1
e_1_2_1_40_1
e_1_2_1_23_1
Nahar N (e_1_2_1_24_1) 2008; 70
e_1_2_1_46_1
e_1_2_1_45_1
e_1_2_1_21_1
e_1_2_1_44_1
e_1_2_1_22_1
e_1_2_1_43_1
e_1_2_1_27_1
e_1_2_1_28_1
e_1_2_1_25_1
e_1_2_1_26_1
e_1_2_1_29_1
Thomas DJ (e_1_2_1_39_1) 2007; 232
e_1_2_1_7_1
Jurinke C (e_1_2_1_19_1) 2002; 77
e_1_2_1_31_1
e_1_2_1_8_1
e_1_2_1_30_1
e_1_2_1_5_1
e_1_2_1_6_1
e_1_2_1_3_1
e_1_2_1_12_1
e_1_2_1_35_1
e_1_2_1_13_1
e_1_2_1_34_1
e_1_2_1_10_1
e_1_2_1_2_1
e_1_2_1_11_1
e_1_2_1_32_1
e_1_2_1_16_1
Singh N (e_1_2_1_33_1) 2007; 28
e_1_2_1_17_1
e_1_2_1_38_1
e_1_2_1_14_1
e_1_2_1_37_1
e_1_2_1_15_1
e_1_2_1_36_1
e_1_2_1_9_1
e_1_2_1_18_1
References_xml – reference: Pu YS, Yang SM, Huang YK, Chung CJ, Huang SK, Chiu AW, Yang MH, Chen CJ, Hsueh YM. 2007. Urinary arsenic profile affects the risk of urothelial carcinoma even at low arsenic exposure. Toxicol. Appl. Pharmacol. 218: 99-106.
– reference: Goldstein DB, Weale ME. 2001. Population genomics: linkage disequilibrium holds the key. Curr. Biol. 11: 576-579.
– reference: Schläwicke Engström K, Nermell B, Concha G, Strömberg U, Vahter M, Broberg K. 2009. Arsenic metabolism is influenced by polymorphisms in genes involved in one-carbon metabolism and reduction reactions. Mutat. Res. 667: 4-14.
– reference: Wigginton JE, Cutler DJ, Abecasis GR. 2005. A note on exact tests of Hardy-Weinberg equilibrium. Am. J. Hum. Genet. 76: 887-893.
– reference: Barrett JC, Fry B, Maller J, Daly MJ. 2005. Haploview: analysis and visualization of LD and haplotype maps. Bioinformatics. 21: 263-265.
– reference: Trinklein ND, Aldred SF, Hartman SJ, Schroeder DI, Otillar RP, Myers RM. 2004. An abundance of bidirectional promoters in the human genome. Genome Res. 14: 62-66.
– reference: Chen YC, Guo YL, Su HJ, Hsueh YM, Smith TJ, Ryan LM, Lee MS, Chao SC, Lee JY, Christiani DC. 2003. Arsenic methylation and skin cancer risk in southwestern Taiwan. J. Occup. Environ. Med. 45: 241-248.
– reference: Petrick JS, Ayala-Fierro F, Cullen WR, Carter DE, Vasken Aposhian H. 2000. Monomethylarsonous acid (MMA(III)) is more toxic than arsenite in Chang human hepatocytes. Toxicol. Appl. Pharmacol. 163: 203-207.
– reference: Wall JD, Pritchard JK. 2003. Haplotype blocks and linkage disequilibrium in the human genome. Nat. Rev. Genet. 4: 587-597.
– reference: Lieberman S, Warne PA. 2001. 17-Hydroxylase: an evaluation of the present view of its catalytic role in steroidogenesis. J. Steroid Biochem. Mol. Biol. 78: 299-312.
– reference: Hopenhayn C, Huang B, Christian J, Peralta C, Ferreccio C, Atallah R, Kalman D. 2003. Profile of urinary arsenic metabolites during pregnancy. Environ. Health Perspect. 111: 1888-1891.
– reference: Hafeman DM, Ahsan H, Louis ED, Siddique AB, Slavkovich V, Cheng Z, van Geen A, Graziano JH. 2005 . Association between arsenic exposure and a measure of subclinical sensory neuropathy in Bangladesh. J. Occup. Environ. Med. 47: 778-784.
– reference: Gerber S, Rodolphe F. 1994. Estimation and test for linkage between markers: a comparison of lod score and χ2 test in a linkage study of maritime pine (Pinus pinaster Ait.). Theor. Appl. Genet. 88: 293-297.
– reference: Concha G, Vogler G, Lezcano D, Nermell B, Vahter M. 1998. Exposure to inorganic arsenic metabolites during early human development. Toxicol. Sci. 44: 185-190.
– reference: Styblo M, Del Razo LM, Vega L, Germolec DR, LeCluyse EL, Hamilton GA, Reed W, Wang C, Cullen WR, Thomas DJ. 2000. Comparative toxicity of trivalent and pentavalent inorganic and methylated arsenicals in rat and human cells. Arch. Toxicol. 74: 289-299.
– reference: Hopenhayn-Rich C, Biggs ML, Smith AH, Kalman DA, Moore LE. 1996. Methylation study of a population environmentally exposed to arsenic in drinking water. Environ. Health Perspect. 104: 620-628.
– reference: Waalkes MP, Liu J, Ward JM, Diwan BA. 2004. Animal models for arsenic carcinogenesis: inorganic arsenic is a transplacental carcinogen in mice. Toxicol. Appl. Pharmacol. 198: 377-384.
– reference: Hayakawa T, Kobayashi Y, Cui X, Hirano S. 2005. A new metabolic pathway of arsenite: arsenic-glutathione complexes are substrates for human arsenic methyltransferase Cyt19. Arch. Toxicol. 79: 183-191.
– reference: States JC, Srivastava S, Chen Y, Barchowsky A. 2009. Arsenic and cardiovascular disease. Toxicol. Sci. 107: 312-323.
– reference: Tseng CH, Huang YK, Huang YL, Chung CJ, Yang MH, Chen CJ, Hsueh YM. 2005. Arsenic exposure, urinary arsenic speciation, and peripheral vascular disease in blackfoot disease-hyperendemic villages in Taiwan. Toxicol. Appl. Pharmacol. 206: 299-308.
– reference: Huang YK, Tseng CH, Huang YL, Yang MH, Chen CJ, Hsueh YM. 2007. Arsenic methylation capability and hypertension risk in subjects living in arseniasis-hyperendemic areas in southwestern Taiwan. Toxicol. Appl. Pharmacol. 218: 135-142.
– reference: Valenzuela OL, Drobna Z, Hernandez-Castellanos E, Sanchez-Pena LC, Garcia-Vargas GG, Borja-Aburto VH, Styblo M, Del Razo LM. 2009. Association of AS3MT polymorphisms and the risk of premalignant arsenic skin lesions. Toxicol. Appl. Pharmacol. 239: 200-207.
– reference: Rahman MM, Ng JC, Naidu R. 2009. Chronic exposure of arsenic via drinking water and its adverse health impacts on humans. Environ. Geochem. Health 31: 189-200.
– reference: Schläwicke Engström K, Broberg K, Concha G, Nermell B, Warholm M, Vahter M. 2007. Genetic polymorphisms influencing arsenic metabolism: evidence from Argentina. Environ. Health Perspect. 115: 599-605.
– reference: Tseng CH, Tseng CP, Chiou HY, Hsueh YM, Chong CK, Chen CJ. 2002. Epidemiologic evidence of diabetogenic effect of arsenic. Toxicol. Lett. 133: 69-76.
– reference: Jurinke C, van den Boom D, Cantor CR, Köster H. 2002. The use of MassARRAY technology for high throughput genotyping. Adv. Biochem. Eng. Biotechnol. 77: 57-74.
– reference: Singh N, Kumar D, Sahu AP. 2007. Arsenic in the environment: effects on human health and possible prevention. J. Environ. Biol. 28: 359-365.
– reference: Morales KH, Ryan L, Kuo TL, Wu MM, Chen CJ. 2000. Risk of internal cancers from arsenic in drinking water. Environ. Health Perspect. 108: 655-661.
– reference: Drobna Z, Xing W, Thomas DJ, Stýblo M. 2006. shRNA Silencing of AS3MT expression minimizes arsenic methylation capacity of HepG2 cells. Chem. Res. Toxicol. 19: 894-898.
– reference: Nahar N, Hossain F, Hossain MD. 2008. Health and socioeconomic effects of groundwater arsenic contamination in rural Bangladesh: new evidence from field surveys. J. Environ. Health 70: 42-47.
– reference: Steinmaus C, Carrigan K, Kalman D, Atallah R, Yuan Y, Smith AH. 2005. Dietary intake and arsenic methylation in a U.S. population. Environ. Health Perspect. 113: 1153-1159.
– reference: Hernández A, Xamena N, Surrallés J, Sekaran C, Tokunaga H, Quinteros D, Creus A, Marcos R. 2008. Role of the Met(287)Thr polymorphism in the AS3MT gene on the metabolic arsenic profile. Mutat. Res. 637: 80-92.
– reference: Chiou HY, Hsueh YM, Liaw KF, Horng SF, Chiang MH, Pu YS, Lin JS, Huang CH, Chen CJ. 1995. Incidence of internal cancers and ingested inorganic arsenic: a seven-year follow-up study in Taiwan. Cancer Res. 55: 1296-1300.
– reference: Purcell S, Neale B, Todd-Brown K, Thomas L, Ferreira MA, Bender D, Maller J, Sklar P, De Bakker PI, Daly MJ, Sham PC. 2007. PLINK: a tool set for whole-genome association and population-based linkage analyses. Am. J. Hum. Genet. 81: 559-575.
– reference: Ghosh P, Banerjee M, Giri AK, Ray K. 2008. Toxicogenomics of arsenic: classical ideas and recent advances. Mutat. Res. 659: 293-301.
– reference: Lindberg AL, Kumar R, Goessler W, Thirumaran R, Gurzau E, Koppova K, Rudnai P, Leonardi G, Fletcher T, Vahter M. 2007. Metabolism of low-dose inorganic arsenic in a central European population: influence of sex and genetic polymorphisms. Environ. Health Perspect. 115: 1081-1086.
– reference: Oskarsson A, Ullerås E, Plant KE, Hinson JP, Goldfarb PS. 2006. Steroidogenic gene expression in H295R cells and the human adrenal gland: adrenotoxic effects of lindane in vitro. J. Appl. Toxicol. 26: 484-492.
– reference: Thomas DJ, Waters SB, Styblo M. 2004. Elucidating the pathway for arsenic methylation. Toxicol. Appl. Pharmacol. 198: 319-326.
– reference: Steinmaus C, Bates MN, Yuan Y, Kalman D, Atallah R, Rey OA, Biggs ML, Hopenhayn C, Moore LE, Hoang BK, Smith AH. 2006. Arsenic methylation and bladder cancer risk in case-control studies in Argentina and the United States. J. Occup. Environ. Med. 48: 478-488.
– reference: Huang YK, Huang YL, Hsueh YM, Yang MH, Wu MM, Chen SY, Hsu LI, Chen CJ. 2008. Arsenic exposure, urinary arsenic speciation, and the incidence of urothelial carcinoma: a twelve-year follow-up study. Cancer Causes Control 19: 829-839.
– reference: Eblin KE, Bredfeldt TG, Buffington S, Gandolfi AJ. 2007. Mitogenic signal transduction caused by monomethylarsonous acid in human bladder cells: role in arsenic-induced carcinogenesis. Toxicol. Sci. 95: 321-330.
– reference: Heck JE, Gamble MV, Chen Y, Graziano JH, Slavkovich V, Parvez F, Baron JA, Howe GR, Ahsan H. 2007. Consumption of folate-related nutrients and metabolism of arsenic in Bangladesh. Am. J. Clin. Nutr. 85: 1367-1374.
– reference: Thomas DJ, Li J, Waters SB, Xing W, Adair BM, Drobna Z, Devesa V, Styblo M. 2007. Arsenic (+3 oxidation state) methyltransferase and the methylation of arsenicals. Exp. Biol. Med. (Maywood) 232: 3-13.
– reference: Meza MM, Yu L, Rodriguez YY, Guild M, Thompson D, Gandolfi AJ, Klimecki WT. 2005. Developmentally restricted genetic determinants of human arsenic metabolism: association between urinary methylated arsenic and CYT19 polymorphisms in children. Environ. Health Perspect. 113: 775-781.
– volume: 55
  start-page: 1296
  year: 1995
  end-page: 1300
  article-title: Incidence of internal cancers and ingested inorganic arsenic: a seven‐year follow‐up study in Taiwan
  publication-title: Cancer Res
– volume: 107
  start-page: 312
  year: 2009
  end-page: 323
  article-title: Arsenic and cardiovascular disease
  publication-title: Toxicol. Sci
– volume: 74
  start-page: 289
  year: 2000
  end-page: 299
  article-title: Comparative toxicity of trivalent and pentavalent inorganic and methylated arsenicals in rat and human cells
  publication-title: Arch. Toxicol
– volume: 111
  start-page: 1888
  year: 2003
  end-page: 1891
  article-title: Profile of urinary arsenic metabolites during pregnancy
  publication-title: Environ. Health Perspect
– volume: 113
  start-page: 775
  year: 2005
  end-page: 781
  article-title: Developmentally restricted genetic determinants of human arsenic metabolism: association between urinary methylated arsenic and CYT19 polymorphisms in children
  publication-title: Environ. Health Perspect
– volume: 11
  start-page: 576
  year: 2001
  end-page: 579
  article-title: Population genomics: linkage disequilibrium holds the key
  publication-title: Curr. Biol
– year: 2005
– volume: 115
  start-page: 599
  year: 2007
  end-page: 605
  article-title: Genetic polymorphisms influencing arsenic metabolism: evidence from Argentina
  publication-title: Environ. Health Perspect
– volume: 95
  start-page: 321
  year: 2007
  end-page: 330
  article-title: Mitogenic signal transduction caused by monomethylarsonous acid in human bladder cells: role in arsenic‐induced carcinogenesis
  publication-title: Toxicol. Sci
– volume: 78
  start-page: 299
  year: 2001
  end-page: 312
  article-title: 17‐Hydroxylase: an evaluation of the present view of its catalytic role in steroidogenesis
  publication-title: J. Steroid Biochem. Mol. Biol
– volume: 133
  start-page: 69
  year: 2002
  end-page: 76
  article-title: Epidemiologic evidence of diabetogenic effect of arsenic
  publication-title: Toxicol. Lett
– volume: 218
  start-page: 99
  year: 2007
  end-page: 106
  article-title: Urinary arsenic profile affects the risk of urothelial carcinoma even at low arsenic exposure
  publication-title: Toxicol. Appl. Pharmacol
– volume: 70
  start-page: 42
  year: 2008
  end-page: 47
  article-title: Health and socioeconomic effects of groundwater arsenic contamination in rural Bangladesh: new evidence from field surveys
  publication-title: J. Environ. Health
– volume: 77
  start-page: 57
  year: 2002
  end-page: 74
  article-title: The use of MassARRAY technology for high throughput genotyping
  publication-title: Adv. Biochem. Eng. Biotechnol
– volume: 44
  start-page: 185
  year: 1998
  end-page: 190
  article-title: Exposure to inorganic arsenic metabolites during early human development
  publication-title: Toxicol. Sci
– volume: 19
  start-page: 894
  year: 2006
  end-page: 898
  article-title: shRNA Silencing of AS3MT expression minimizes arsenic methylation capacity of HepG2 cells
  publication-title: Chem. Res. Toxicol
– volume: 79
  start-page: 183
  year: 2005
  end-page: 191
  article-title: A new metabolic pathway of arsenite: arsenic‐glutathione complexes are substrates for human arsenic methyltransferase Cyt19
  publication-title: Arch. Toxicol
– volume: 113
  start-page: 1153
  year: 2005
  end-page: 1159
  article-title: Dietary intake and arsenic methylation in a U.S. population
  publication-title: Environ. Health Perspect
– volume: 47
  start-page: 778
  year: 2005
  end-page: 784
  article-title: Association between arsenic exposure and a measure of subclinical sensory neuropathy in Bangladesh
  publication-title: J. Occup. Environ. Med
– volume: 637
  start-page: 80
  year: 2008
  end-page: 92
  article-title: Role of the Met(287)Thr polymorphism in the AS3MT gene on the metabolic arsenic profile
  publication-title: Mutat. Res
– volume: 48
  start-page: 478
  year: 2006
  end-page: 488
  article-title: Arsenic methylation and bladder cancer risk in case–control studies in Argentina and the United States
  publication-title: J. Occup. Environ. Med
– volume: 115
  start-page: 1081
  year: 2007
  end-page: 1086
  article-title: Metabolism of low‐dose inorganic arsenic in a central European population: influence of sex and genetic polymorphisms
  publication-title: Environ. Health Perspect
– volume: 198
  start-page: 377
  year: 2004
  end-page: 384
  article-title: Animal models for arsenic carcinogenesis: inorganic arsenic is a transplacental carcinogen in mice
  publication-title: Toxicol. Appl. Pharmacol
– volume: 4
  start-page: 587
  year: 2003
  end-page: 597
  article-title: Haplotype blocks and linkage disequilibrium in the human genome
  publication-title: Nat. Rev. Genet
– volume: 81
  start-page: 559
  year: 2007
  end-page: 575
  article-title: PLINK: a tool set for whole‐genome association and population‐based linkage analyses
  publication-title: Am. J. Hum. Genet
– volume: 218
  start-page: 135
  year: 2007
  end-page: 142
  article-title: Arsenic methylation capability and hypertension risk in subjects living in arseniasis‐hyperendemic areas in southwestern Taiwan
  publication-title: Toxicol. Appl. Pharmacol
– volume: 88
  start-page: 293
  year: 1994
  end-page: 297
  article-title: Estimation and test for linkage between markers: a comparison of lod score and χ test in a linkage study of maritime pine ( Ait.)
  publication-title: Theor. Appl. Genet
– volume: 14
  start-page: 62
  year: 2004
  end-page: 66
  article-title: An abundance of bidirectional promoters in the human genome
  publication-title: Genome Res
– volume: 667
  start-page: 4
  year: 2009
  end-page: 14
  article-title: Arsenic metabolism is influenced by polymorphisms in genes involved in one‐carbon metabolism and reduction reactions
  publication-title: Mutat. Res
– volume: 163
  start-page: 203
  year: 2000
  end-page: 207
  article-title: Monomethylarsonous acid (MMA(III)) is more toxic than arsenite in Chang human hepatocytes
  publication-title: Toxicol. Appl. Pharmacol
– volume: 206
  start-page: 299
  year: 2005
  end-page: 308
  article-title: Arsenic exposure, urinary arsenic speciation, and peripheral vascular disease in blackfoot disease‐hyperendemic villages in Taiwan
  publication-title: Toxicol. Appl. Pharmacol
– volume: 85
  start-page: 1367
  year: 2007
  end-page: 1374
  article-title: Consumption of folate‐related nutrients and metabolism of arsenic in Bangladesh
  publication-title: Am. J. Clin. Nutr
– volume: 19
  start-page: 829
  year: 2008
  end-page: 839
  article-title: Arsenic exposure, urinary arsenic speciation, and the incidence of urothelial carcinoma: a twelve‐year follow‐up study
  publication-title: Cancer Causes Control
– volume: 198
  start-page: 319
  year: 2004
  end-page: 326
  article-title: Elucidating the pathway for arsenic methylation
  publication-title: Toxicol. Appl. Pharmacol
– volume: 659
  start-page: 293
  year: 2008
  end-page: 301
  article-title: Toxicogenomics of arsenic: classical ideas and recent advances
  publication-title: Mutat. Res
– volume: 31
  start-page: 189
  year: 2009
  end-page: 200
  article-title: Chronic exposure of arsenic via drinking water and its adverse health impacts on humans
  publication-title: Environ. Geochem. Health
– volume: 45
  start-page: 241
  year: 2003
  end-page: 248
  article-title: Arsenic methylation and skin cancer risk in southwestern Taiwan
  publication-title: J. Occup. Environ. Med
– volume: 104
  start-page: 620
  year: 1996
  end-page: 628
  article-title: Methylation study of a population environmentally exposed to arsenic in drinking water
  publication-title: Environ. Health Perspect
– volume: 26
  start-page: 484
  year: 2006
  end-page: 492
  article-title: Steroidogenic gene expression in H295R cells and the human adrenal gland: adrenotoxic effects of lindane in vitro
  publication-title: J. Appl. Toxicol
– volume: 21
  start-page: 263
  year: 2005
  end-page: 265
  article-title: Haploview: analysis and visualization of LD and haplotype maps
  publication-title: Bioinformatics
– volume: 108
  start-page: 655
  year: 2000
  end-page: 661
  article-title: Risk of internal cancers from arsenic in drinking water
  publication-title: Environ. Health Perspect
– volume: 28
  start-page: 359
  year: 2007
  end-page: 365
  article-title: Arsenic in the environment: effects on human health and possible prevention
  publication-title: J. Environ. Biol
– volume: 232
  start-page: 3
  year: 2007
  end-page: 13
  article-title: Arsenic (+3 oxidation state) methyltransferase and the methylation of arsenicals
  publication-title: Exp. Biol. Med. (Maywood)
– volume: 239
  start-page: 200
  year: 2009
  end-page: 207
  article-title: Association of AS3MT polymorphisms and the risk of premalignant arsenic skin lesions
  publication-title: Toxicol. Appl. Pharmacol
– volume: 76
  start-page: 887
  year: 2005
  end-page: 893
  article-title: A note on exact tests of Hardy–Weinberg equilibrium
  publication-title: Am. J. Hum. Genet
– volume: 232
  start-page: 3
  year: 2007
  ident: e_1_2_1_39_1
  article-title: Arsenic (+3 oxidation state) methyltransferase and the methylation of arsenicals
  publication-title: Exp. Biol. Med. (Maywood)
– ident: e_1_2_1_32_1
  doi: 10.1016/j.mrfmmm.2008.07.003
– ident: e_1_2_1_34_1
  doi: 10.1093/toxsci/kfn236
– ident: e_1_2_1_16_1
  doi: 10.1289/ehp.96104620
– ident: e_1_2_1_12_1
  doi: 10.1007/s00204-004-0620-x
– volume: 70
  start-page: 42
  year: 2008
  ident: e_1_2_1_24_1
  article-title: Health and socioeconomic effects of groundwater arsenic contamination in rural Bangladesh: new evidence from field surveys
  publication-title: J. Environ. Health
– ident: e_1_2_1_13_1
  doi: 10.1093/ajcn/85.5.1367
– volume: 55
  start-page: 1296
  year: 1995
  ident: e_1_2_1_4_1
  article-title: Incidence of internal cancers and ingested inorganic arsenic: a seven‐year follow‐up study in Taiwan
  publication-title: Cancer Res
– ident: e_1_2_1_40_1
  doi: 10.1101/gr.1982804
– ident: e_1_2_1_10_1
  doi: 10.1016/S0960-9822(01)00348-7
– ident: e_1_2_1_15_1
  doi: 10.1289/ehp.6254
– ident: e_1_2_1_29_1
  doi: 10.1086/519795
– ident: e_1_2_1_41_1
  doi: 10.1016/S0378-4274(02)00085-1
– ident: e_1_2_1_14_1
  doi: 10.1016/j.mrfmmm.2007.07.004
– volume: 28
  start-page: 359
  year: 2007
  ident: e_1_2_1_33_1
  article-title: Arsenic in the environment: effects on human health and possible prevention
  publication-title: J. Environ. Biol
– ident: e_1_2_1_28_1
  doi: 10.1016/j.taap.2006.09.021
– ident: e_1_2_1_45_1
  doi: 10.1038/nrg1123
– ident: e_1_2_1_43_1
  doi: 10.1016/j.taap.2009.06.007
– ident: e_1_2_1_20_1
  doi: 10.1016/S0960-0760(01)00105-4
– ident: e_1_2_1_42_1
  doi: 10.1016/j.taap.2004.11.022
– ident: e_1_2_1_3_1
  doi: 10.1097/01.jom.0000058336.05741.e8
– ident: e_1_2_1_8_1
  doi: 10.1007/BF00223635
– volume: 77
  start-page: 57
  year: 2002
  ident: e_1_2_1_19_1
  article-title: The use of MassARRAY technology for high throughput genotyping
  publication-title: Adv. Biochem. Eng. Biotechnol
– ident: e_1_2_1_27_1
  doi: 10.1006/taap.1999.8872
– ident: e_1_2_1_9_1
  doi: 10.1016/j.mrrev.2008.06.003
– ident: e_1_2_1_22_1
  doi: 10.1289/ehp.7780
– ident: e_1_2_1_21_1
  doi: 10.1289/ehp.10026
– ident: e_1_2_1_30_1
  doi: 10.1007/s10653-008-9235-0
– ident: e_1_2_1_18_1
  doi: 10.1007/s10552-008-9146-5
– ident: e_1_2_1_2_1
  doi: 10.1093/bioinformatics/bth457
– ident: e_1_2_1_25_1
– ident: e_1_2_1_11_1
  doi: 10.1097/01.jom.0000169089.54549.db
– ident: e_1_2_1_37_1
  doi: 10.1007/s002040000134
– ident: e_1_2_1_23_1
  doi: 10.1289/ehp.00108655
– ident: e_1_2_1_38_1
  doi: 10.1016/j.taap.2003.10.020
– ident: e_1_2_1_31_1
  doi: 10.1289/ehp.9734
– ident: e_1_2_1_46_1
  doi: 10.1086/429864
– ident: e_1_2_1_35_1
  doi: 10.1289/ehp.7907
– ident: e_1_2_1_5_1
  doi: 10.1093/toxsci/44.2.185
– ident: e_1_2_1_7_1
  doi: 10.1093/toxsci/kfl160
– ident: e_1_2_1_26_1
  doi: 10.1002/jat.1166
– ident: e_1_2_1_44_1
  doi: 10.1016/j.taap.2003.10.028
– ident: e_1_2_1_6_1
  doi: 10.1021/tx060076u
– ident: e_1_2_1_17_1
  doi: 10.1016/j.taap.2006.10.022
– ident: e_1_2_1_36_1
  doi: 10.1097/01.jom.0000200982.28276.70
SSID ssj0009928
Score 2.1309605
Snippet Differences in arsenic metabolism are known to play a role in individual variability in arsenic‐induced disease susceptibility. Genetic variants in genes...
Differences in arsenic metabolism are known to play a role in individual variability in arsenic-induced disease susceptibility. Genetic variants in genes...
SourceID pubmedcentral
proquest
pubmed
crossref
wiley
istex
SourceType Open Access Repository
Aggregation Database
Index Database
Enrichment Source
Publisher
StartPage 260
SubjectTerms 5'-Nucleotidase - genetics
Arsenic
Arsenic - metabolism
Arsenic - urine
Arsenic Poisoning - genetics
Arsenic Poisoning - urine
Arsenicals - urine
AS3MT
Chromosomes
Chromosomes, Human, Pair 10 - genetics
Clusters
Female
Genes
Genetic Association Studies
Genetics
Humans
Introns - genetics
Linkage Disequilibrium
Male
Metabolism
Methylation
Methyltransferases - genetics
Mexico
Mouth Mucosa - metabolism
Multigene Family
Polymorphism
Polymorphism, Single Nucleotide
SNP
Steroid 17-alpha-Hydroxylase - genetics
Title Genetic association between intronic variants in AS3MT and arsenic methylation efficiency is focused on a large linkage disequilibrium cluster in chromosome 10
URI https://api.istex.fr/ark:/67375/WNG-F9L1KJ3V-M/fulltext.pdf
https://onlinelibrary.wiley.com/doi/abs/10.1002%2Fjat.1492
https://www.ncbi.nlm.nih.gov/pubmed/20014157
https://www.proquest.com/docview/1753544685
https://www.proquest.com/docview/733932681
https://www.proquest.com/docview/869579812
https://www.proquest.com/docview/883026246
https://pubmed.ncbi.nlm.nih.gov/PMC2862143
Volume 30
hasFullText 1
inHoldings 1
isFullTextHit
isPrint
link http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV1bb9MwFLbQeEFCXMat3HSQUHlZtjTOzY8TUKZBpwk6qMRDZDu2Vtal29Igyp_hr3JO3DQUVoR4qlSfNrFzzvF34s-fGXseKpGLNLeeiKX2QusbT1mFyZDT5CURIlgqFAcH8d5RuD-KRgtWJe2FcfoQyxduFBl1vqYAl6rcaUVDv8gZhrmg9NvjMcnmv3rfKkcJUR-rSopZXsiTUaM76wc7zQ9XZqKrNKjfLoOZf7Ilf0Wx9TTUv8k-Nx1w7JOT7WqmtvX337Qd_6-Ht9iNBTqFXedOt9kVU2yy7qGTt55vwbDdrVVuQRcOW-Hr-Sa77t4BgtvadIf9IE1rNAXZ-gAsiGEwLtzpO_AVq3Ui4-A3sPuBD4Ygixyw3jbUSidczx1fD0wtd0F7RWFcgp3qqjQ5YIOECRHagVajMT8CrTqdV-N6O0N1CnpSkRwEXUAfE_2wnJ4a6Pl32VH_9fDlnrc4EMLTWBYFnpWhiDVWvGkYGaxjE8QioVK5r_Ik11FglRASp9_Qxpi5Aml5jgDORrGSVvHA5_fYRjEtzAMGqdIKm1Jfh1SzJZjzhYjwAghhYsFNh71onCPTC7V0OrRjkjmd5yDDp5PR0-mwZ0vLM6cQcolNt_avpYG8OCFGXRJlnw7eZH3xrvd2n3_MBvhnjQNmGOe0eCMLM63KjBRVI-xzGnUYrLFJOCc4nvbWm2DnokQgqvuLCUnCxUEYd9h95_nL2w5qXnCUdFiyEhNLAxIrX20pxse1aHmApTNicxyJ2uXXDlWG0xJ9PvxXw0fsmmN0EJvqMduYXVTmCQLFmXpap4Sfix1o4Q
linkProvider Wiley-Blackwell
linkToHtml http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV1bb9MwFLam7QEkxGXcyvUgofKybGnuFk8TopStrSbooA-TLNtxtLIuhbVBlD_DX-WcuEkprAjxFKk-TWLn-Pg79ufPjD0PFE95kmYOj6R2gsw1jsoUBkOfBi-JECGjRLHXjzrHwcEwHG6wl9VeGKsPUU-4Uc8o4zV1cJqQ3luqhn6SM-znHOPvVrk8R4jo3VI7ivPyYFXSzHICPx5WyrOut1f9c2Us2qJm_XYZ0PyTL_krji0HovYNdlJVwfJPznaLmdrV339Td_zPOt5k1xcAFfatR91iGybfZs0jq3A934HBcsPWdAeacLTUvp5vs2t2GhDs7qbb7AfJWqMpyKUbwIIbBqPcHsADXzFhJz4O_gL77_3eAGSeAqbchkrpkOu5peyBKRUvaLsojKaQTXQxNSlggYQxcdqBFqQxRAItPH0pRuWOhuIc9LggRQh6gD4lBuJ0cm6g5d5hx-3Xg1cdZ3EmhKMxM_KcTAY80pj0JkFoMJWNEY4ESqWuSuNUh16mOJc4AgdZhMHLk5mfIobLwkjJTPme699lm_kkN_cZJEorLEpcHVDaFmPY5zzEByCKibhvGuxF5R1CLwTT6dyOsbBSz57AryPo6zTYs9rysxUJucSmWTpYbSAvzohUF4fiY_-NaPNu6_DA_yB6eLPKAwV2dVq_kbmZFFNBoqoh1jkJGwzW2MS-T4g8aa03wcqFMUdg9xcTUoWLvCBqsHvW9evX9kpqcBg3WLzSKWoD0itfLclHp6VuuYfZM8JzbInS59c2lcCRia4P_tXwKbvSGfS6ovu2f_iQXbUEDyJXPWKbs4vCPEbcOFNPyvjwE9mYbP8
linkToPdf http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV3bbhMxELVQKyEkRKHcUm6DhMJLt93s3Y8VEErbRBGkEKkPlu211dB0U5osIvwMv8rMOhcCDUI8RYon2bV3PHNmfXzM2ItI8ZxnufV4IrUXWd94yioMhiElL4kQwVKh2Gon-8fRQS_uTVmVtBfG6UPMX7jRzKjiNU3wi9zuLkRDP8sxTnOO4Xc9SjBLEiB6v5CO4rw6V5Uks7woTHsz4Vk_2J39cikVrdOofrsKZ_5Jl_wVxlZ5qLnBTmY9cPSTs51yrHb099_EHf-vi7fZrSk8hT3nT3fYNVNssnrH6VtPtqG72K412oY6dBbK15NNdtO9BAS3t-ku-0Gi1mgKcuEEMGWGQb9wx-_AVyzXiY2D38Deh7DVBVnkgAW3oVY64nriCHtgKr0L2iwK_RHYoS5HJgdskDAgRjvQcjQGSKBlpy9lv9rPUJ6DHpSkB0EX0KfEPxwNzw00_HvsuPmm-2rfm54I4WmsiwLPyognGkveLIoNFrIpgpFIqdxXeZrrOLCKc4n5N7IJhq5A2jBHBGfjREmrwsAP77O1YliYhwwypRU2Zb6OqGhLMehzHuMFEMMkPDQ19nLmHEJP5dLp1I6BcELPgcCnI-jp1NjzueWFkwi5wqZe-dfcQF6eEaUujcWn9lvR5EeNw4Pwo2jhn80cUOBEp9UbWZhhORIkqRpjn7O4xmCFTRqGhMezxmoT7FyccoR1fzEhTbgkiJIae-A8f37bQUUMjtMaS5fmxNyA1MqXW4r-aaVaHmDtjOAcR6Jy-ZVDJTAv0efWvxo-Y9c7r5vi6F378BG74dgdxKx6zNbGl6V5gqBxrJ5W0eEnSm1rrg
openUrl ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Genetic+association+between+intronic+variants+in+AS3MT+and+arsenic+methylation+efficiency+is+focused+on+a+large+linkage+disequilibrium+cluster+in+chromosome+10&rft.jtitle=Journal+of+applied+toxicology&rft.au=Gomez%E2%80%90Rubio%2C+Paulina&rft.au=Meza%E2%80%90Montenegro%2C+Maria+M.&rft.au=Cantu%E2%80%90Soto%2C+Ernesto&rft.au=Klimecki%2C+Walter+T.&rft.date=2010-04-01&rft.issn=0260-437X&rft.eissn=1099-1263&rft.volume=30&rft.issue=3&rft.spage=260&rft.epage=270&rft_id=info:doi/10.1002%2Fjat.1492&rft.externalDBID=n%2Fa&rft.externalDocID=10_1002_jat_1492
thumbnail_l http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=0260-437X&client=summon
thumbnail_m http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=0260-437X&client=summon
thumbnail_s http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=0260-437X&client=summon