Selenoprotein T Promotes Proliferation and G1-to-S Transition in SK-N-SH Cells: Implications in Parkinson's Disease
Selenium is prioritized to the brain mainly for selenoprotein expression. Selenoprotein T (SELENOT) protects dopaminergic, postmitotic neurons in a mouse model of Parkinson's disease (PD). We hypothesized a proliferative role of SELENOT in neural cells. To assess SELENOT status in PD, sedated m...
Saved in:
| Published in | The Journal of nutrition Vol. 149; no. 12; pp. 2110 - 2119 |
|---|---|
| Main Authors | , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Elsevier Inc
01.12.2019
Oxford University Press American Institute of Nutrition |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0022-3166 1541-6100 1541-6100 |
| DOI | 10.1093/jn/nxz199 |
Cover
| Abstract | Selenium is prioritized to the brain mainly for selenoprotein expression. Selenoprotein T (SELENOT) protects dopaminergic, postmitotic neurons in a mouse model of Parkinson's disease (PD).
We hypothesized a proliferative role of SELENOT in neural cells.
To assess SELENOT status in PD, sedated male C57BL/6 mice at 10–12 wk of age were injected with 6-hydroxydopamine in neurons, and human peripheral blood mononuclear cells were isolated from 9 healthy subjects (56% men, 68-y-old) and 11 subjects with PD (64% men, 63-y-old). Dopaminergic neural progenitor–like SK-N-SH cells with transient SELENOT overexpression or knockdown were maintained in the presence or absence of the antioxidant N-acetyl-l-cysteine and the calcium channel blocker nimodipine. Cell cycle, proliferation, and signaling parameters were determined by immunoblotting, qPCR, and flow cytometry.
SELENOT mRNA abundance was increased (P < 0.05) in SK-N-SH cells treated with 1-methyl-4-phenylpyrefidinium iodide (3.5-fold) and peripheral blood mononuclear cells from PD patients (1.6-fold). Likewise, SELENOT was expressed in tyrosine hydroxylase–positive dopaminergic neurons of 6-hydroxydopamine–injected mice. Knockdown of SELENOT in SK-N-SH cells suppressed (54%; P < 0.05) 5-ethynyl-2′-deoxyurefidine incorporation but induced (17–47%; P < 0.05) annexin V–positive cells, CASPASE-3 cleavage, and G1/S cell cycle arrest. SELENOT knockdown and overexpression increased (88–120%; P < 0.05) and reduced (37–42%; P < 0.05) both forkhead box O3 and p27, but reduced (51%; P < 0.05) and increased (1.2-fold; P < 0.05) cyclin-dependent kinase 4 protein abundance, respectively. These protein changes were diminished by nimodipine or N-acetyl-l-cysteine treatment (24 h) at steady-state levels. While the N-acetyl-l-cysteine treatment did not influence the reduction in the amount of calcium (13%; P < 0.05) by SELENOT knockdown, the nimodipine treatment reversed the decreased amount of reactive oxygen species (33%; P < 0.05) by SELENOT overexpression.
These cellular and mouse data link SELENOT to neural proliferation, expanding our understanding of selenium protection in PD. |
|---|---|
| AbstractList | Selenium is prioritized to the brain mainly for selenoprotein expression. Selenoprotein T (SELENOT) protects dopaminergic, postmitotic neurons in a mouse model of Parkinson's disease (PD).
We hypothesized a proliferative role of SELENOT in neural cells.
To assess SELENOT status in PD, sedated male C57BL/6 mice at 10–12 wk of age were injected with 6-hydroxydopamine in neurons, and human peripheral blood mononuclear cells were isolated from 9 healthy subjects (56% men, 68-y-old) and 11 subjects with PD (64% men, 63-y-old). Dopaminergic neural progenitor–like SK-N-SH cells with transient SELENOT overexpression or knockdown were maintained in the presence or absence of the antioxidant N-acetyl-l-cysteine and the calcium channel blocker nimodipine. Cell cycle, proliferation, and signaling parameters were determined by immunoblotting, qPCR, and flow cytometry.
SELENOT mRNA abundance was increased (P < 0.05) in SK-N-SH cells treated with 1-methyl-4-phenylpyrefidinium iodide (3.5-fold) and peripheral blood mononuclear cells from PD patients (1.6-fold). Likewise, SELENOT was expressed in tyrosine hydroxylase–positive dopaminergic neurons of 6-hydroxydopamine–injected mice. Knockdown of SELENOT in SK-N-SH cells suppressed (54%; P < 0.05) 5-ethynyl-2′-deoxyurefidine incorporation but induced (17–47%; P < 0.05) annexin V–positive cells, CASPASE-3 cleavage, and G1/S cell cycle arrest. SELENOT knockdown and overexpression increased (88–120%; P < 0.05) and reduced (37–42%; P < 0.05) both forkhead box O3 and p27, but reduced (51%; P < 0.05) and increased (1.2-fold; P < 0.05) cyclin-dependent kinase 4 protein abundance, respectively. These protein changes were diminished by nimodipine or N-acetyl-l-cysteine treatment (24 h) at steady-state levels. While the N-acetyl-l-cysteine treatment did not influence the reduction in the amount of calcium (13%; P < 0.05) by SELENOT knockdown, the nimodipine treatment reversed the decreased amount of reactive oxygen species (33%; P < 0.05) by SELENOT overexpression.
These cellular and mouse data link SELENOT to neural proliferation, expanding our understanding of selenium protection in PD. Background: Selenium is prioritized to the brain mainly for selenoprotein expression. Selenoprotein T (SELENOT) protects dopaminergic, postmitotic neurons in a mouse model of Parkinson's disease (PD). Objective: We hypothesized a proliferative role of SELENOT in neural cells. Methods: To assess SELENOT status in PD, sedated male C57BL/6 mice at 10-12 wk of age were injected with 6-hydroxydopamine in neurons, and human peripheral blood mononuclear cells were isolated from 9 healthy subjects (56% men, 68-y-old) and 11 subjects with PD (64% men, 63-y-old). Dopaminergic neural progenitor-like SK-N-SH cells with transient SELENOT overexpression or knockdown were maintained in the presence or absence of the antioxidant N-acetyl-l-cysteine and the calcium channel blocker nimodipine. Cell cycle, proliferation, and signaling parameters were determined by immunoblotting, qPCR, and flow cytometry. Results: SELENOT mRNA abundance was increased (P < 0.05) in SK-N-SH cells treated with 1-methyl-4-phenylpyridinium iodide (3.5-fold) and peripheral blood mononuclear cells from PD patients (1.6-fold). Likewise, SELENOT was expressed in tyrosine hydroxylase-positive dopaminergic neurons of 6-hydroxydopamine-injected mice. Knockdown of SELENOT in SK-N-SH cells suppressed (54%; P < 0.05) 5-ethynyl-2'-deoxyuridine incorporation but induced (17-47%; P < 0.05) annexin V-positive cells, CASPASE-3 cleavage, and G1/S cell cycle arrest. SELENOT knockdown and overexpression increased (88-120%; P < 0.05) and reduced (37-42%; P < 0.05) both forkhead box O3 and p27, but reduced (51%; P < 0.05) and increased (1.2-fold; P < 0.05) cyclin-dependent kinase 4 protein abundance, respectively. These protein changes were diminished by nimodipine or N-acetyl-l-cysteine treatment (24 h) at steady-state levels. While the N-acetyl-l-cysteine treatment did not influence the reduction in the amount of calcium (13%; P < 0.05) by SELENOT knockdown, the nimodipine treatment reversed the decreased amount of reactive oxygen species (33%; P < 0.05) by SELENOT overexpression. Conclusions: These cellular and mouse data link SELENOT to neural proliferation, expanding our understanding of selenium protection in PD. Selenium is prioritized to the brain mainly for selenoprotein expression. Selenoprotein T (SELENOT) protects dopaminergic, postmitotic neurons in a mouse model of Parkinson's disease (PD).BACKGROUNDSelenium is prioritized to the brain mainly for selenoprotein expression. Selenoprotein T (SELENOT) protects dopaminergic, postmitotic neurons in a mouse model of Parkinson's disease (PD).We hypothesized a proliferative role of SELENOT in neural cells.OBJECTIVEWe hypothesized a proliferative role of SELENOT in neural cells.To assess SELENOT status in PD, sedated male C57BL/6 mice at 10-12 wk of age were injected with 6-hydroxydopamine in neurons, and human peripheral blood mononuclear cells were isolated from 9 healthy subjects (56% men, 68-y-old) and 11 subjects with PD (64% men, 63-y-old). Dopaminergic neural progenitor-like SK-N-SH cells with transient SELENOT overexpression or knockdown were maintained in the presence or absence of the antioxidant N-acetyl-l-cysteine and the calcium channel blocker nimodipine. Cell cycle, proliferation, and signaling parameters were determined by immunoblotting, qPCR, and flow cytometry.METHODSTo assess SELENOT status in PD, sedated male C57BL/6 mice at 10-12 wk of age were injected with 6-hydroxydopamine in neurons, and human peripheral blood mononuclear cells were isolated from 9 healthy subjects (56% men, 68-y-old) and 11 subjects with PD (64% men, 63-y-old). Dopaminergic neural progenitor-like SK-N-SH cells with transient SELENOT overexpression or knockdown were maintained in the presence or absence of the antioxidant N-acetyl-l-cysteine and the calcium channel blocker nimodipine. Cell cycle, proliferation, and signaling parameters were determined by immunoblotting, qPCR, and flow cytometry.SELENOT mRNA abundance was increased (P < 0.05) in SK-N-SH cells treated with 1-methyl-4-phenylpyridinium iodide (3.5-fold) and peripheral blood mononuclear cells from PD patients (1.6-fold). Likewise, SELENOT was expressed in tyrosine hydroxylase-positive dopaminergic neurons of 6-hydroxydopamine-injected mice. Knockdown of SELENOT in SK-N-SH cells suppressed (54%; P < 0.05) 5-ethynyl-2'-deoxyuridine incorporation but induced (17-47%; P < 0.05) annexin V-positive cells, CASPASE-3 cleavage, and G1/S cell cycle arrest. SELENOT knockdown and overexpression increased (88-120%; P < 0.05) and reduced (37-42%; P < 0.05) both forkhead box O3 and p27, but reduced (51%; P < 0.05) and increased (1.2-fold; P < 0.05) cyclin-dependent kinase 4 protein abundance, respectively. These protein changes were diminished by nimodipine or N-acetyl-l-cysteine treatment (24 h) at steady-state levels. While the N-acetyl-l-cysteine treatment did not influence the reduction in the amount of calcium (13%; P < 0.05) by SELENOT knockdown, the nimodipine treatment reversed the decreased amount of reactive oxygen species (33%; P < 0.05) by SELENOT overexpression.RESULTSSELENOT mRNA abundance was increased (P < 0.05) in SK-N-SH cells treated with 1-methyl-4-phenylpyridinium iodide (3.5-fold) and peripheral blood mononuclear cells from PD patients (1.6-fold). Likewise, SELENOT was expressed in tyrosine hydroxylase-positive dopaminergic neurons of 6-hydroxydopamine-injected mice. Knockdown of SELENOT in SK-N-SH cells suppressed (54%; P < 0.05) 5-ethynyl-2'-deoxyuridine incorporation but induced (17-47%; P < 0.05) annexin V-positive cells, CASPASE-3 cleavage, and G1/S cell cycle arrest. SELENOT knockdown and overexpression increased (88-120%; P < 0.05) and reduced (37-42%; P < 0.05) both forkhead box O3 and p27, but reduced (51%; P < 0.05) and increased (1.2-fold; P < 0.05) cyclin-dependent kinase 4 protein abundance, respectively. These protein changes were diminished by nimodipine or N-acetyl-l-cysteine treatment (24 h) at steady-state levels. While the N-acetyl-l-cysteine treatment did not influence the reduction in the amount of calcium (13%; P < 0.05) by SELENOT knockdown, the nimodipine treatment reversed the decreased amount of reactive oxygen species (33%; P < 0.05) by SELENOT overexpression.These cellular and mouse data link SELENOT to neural proliferation, expanding our understanding of selenium protection in PD.CONCLUSIONSThese cellular and mouse data link SELENOT to neural proliferation, expanding our understanding of selenium protection in PD. Selenium is prioritized to the brain mainly for selenoprotein expression. Selenoprotein T (SELENOT) protects dopaminergic, postmitotic neurons in a mouse model of Parkinson's disease (PD). We hypothesized a proliferative role of SELENOT in neural cells. To assess SELENOT status in PD, sedated male C57BL/6 mice at 10-12 wk of age were injected with 6-hydroxydopamine in neurons, and human peripheral blood mononuclear cells were isolated from 9 healthy subjects (56% men, 68-y-old) and 11 subjects with PD (64% men, 63-y-old). Dopaminergic neural progenitor-like SK-N-SH cells with transient SELENOT overexpression or knockdown were maintained in the presence or absence of the antioxidant N-acetyl-l-cysteine and the calcium channel blocker nimodipine. Cell cycle, proliferation, and signaling parameters were determined by immunoblotting, qPCR, and flow cytometry. SELENOT mRNA abundance was increased (P < 0.05) in SK-N-SH cells treated with 1-methyl-4-phenylpyridinium iodide (3.5-fold) and peripheral blood mononuclear cells from PD patients (1.6-fold). Likewise, SELENOT was expressed in tyrosine hydroxylase-positive dopaminergic neurons of 6-hydroxydopamine-injected mice. Knockdown of SELENOT in SK-N-SH cells suppressed (54%; P < 0.05) 5-ethynyl-2'-deoxyuridine incorporation but induced (17-47%; P < 0.05) annexin V-positive cells, CASPASE-3 cleavage, and G1/S cell cycle arrest. SELENOT knockdown and overexpression increased (88-120%; P < 0.05) and reduced (37-42%; P < 0.05) both forkhead box O3 and p27, but reduced (51%; P < 0.05) and increased (1.2-fold; P < 0.05) cyclin-dependent kinase 4 protein abundance, respectively. These protein changes were diminished by nimodipine or N-acetyl-l-cysteine treatment (24 h) at steady-state levels. While the N-acetyl-l-cysteine treatment did not influence the reduction in the amount of calcium (13%; P < 0.05) by SELENOT knockdown, the nimodipine treatment reversed the decreased amount of reactive oxygen species (33%; P < 0.05) by SELENOT overexpression. These cellular and mouse data link SELENOT to neural proliferation, expanding our understanding of selenium protection in PD. ABSTRACT Background Selenium is prioritized to the brain mainly for selenoprotein expression. Selenoprotein T (SELENOT) protects dopaminergic, postmitotic neurons in a mouse model of Parkinson's disease (PD). Objective We hypothesized a proliferative role of SELENOT in neural cells. Methods To assess SELENOT status in PD, sedated male C57BL/6 mice at 10–12 wk of age were injected with 6-hydroxydopamine in neurons, and human peripheral blood mononuclear cells were isolated from 9 healthy subjects (56% men, 68-y-old) and 11 subjects with PD (64% men, 63-y-old). Dopaminergic neural progenitor–like SK-N-SH cells with transient SELENOT overexpression or knockdown were maintained in the presence or absence of the antioxidant N-acetyl-l-cysteine and the calcium channel blocker nimodipine. Cell cycle, proliferation, and signaling parameters were determined by immunoblotting, qPCR, and flow cytometry. Results SELENOT mRNA abundance was increased (P < 0.05) in SK-N-SH cells treated with 1-methyl-4-phenylpyridinium iodide (3.5-fold) and peripheral blood mononuclear cells from PD patients (1.6-fold). Likewise, SELENOT was expressed in tyrosine hydroxylase–positive dopaminergic neurons of 6-hydroxydopamine–injected mice. Knockdown of SELENOT in SK-N-SH cells suppressed (54%; P < 0.05) 5-ethynyl-2′-deoxyuridine incorporation but induced (17–47%; P < 0.05) annexin V–positive cells, CASPASE-3 cleavage, and G1/S cell cycle arrest. SELENOT knockdown and overexpression increased (88–120%; P < 0.05) and reduced (37–42%; P < 0.05) both forkhead box O3 and p27, but reduced (51%; P < 0.05) and increased (1.2-fold; P < 0.05) cyclin-dependent kinase 4 protein abundance, respectively. These protein changes were diminished by nimodipine or N-acetyl-l-cysteine treatment (24 h) at steady-state levels. While the N-acetyl-l-cysteine treatment did not influence the reduction in the amount of calcium (13%; P < 0.05) by SELENOT knockdown, the nimodipine treatment reversed the decreased amount of reactive oxygen species (33%; P < 0.05) by SELENOT overexpression. Conclusions These cellular and mouse data link SELENOT to neural proliferation, expanding our understanding of selenium protection in PD. |
| Author | Fan, Hui-Hui Wang, Xiao-Shuang Zhu, Jian-Hong Wu, Hong-Mei Zhang, Li Shao, Zi-Qiang Cheng, Wen-Hsing Zhang, Xiong |
| Author_xml | – sequence: 1 givenname: Zi-Qiang surname: Shao fullname: Shao, Zi-Qiang organization: Department of Geriatrics and Neurology, the Second Affiliated Hospital and Yuying Children's Hospital, Wenzhou Medical University,Wenzhou, Zhejiang,China – sequence: 2 givenname: Xiong surname: Zhang fullname: Zhang, Xiong organization: Department of Geriatrics and Neurology, the Second Affiliated Hospital and Yuying Children's Hospital, Wenzhou Medical University,Wenzhou, Zhejiang,China – sequence: 3 givenname: Hui-Hui surname: Fan fullname: Fan, Hui-Hui organization: Department of Preventive Medicine, Wenzhou Medical University,Wenzhou,Zhejiang,China – sequence: 4 givenname: Xiao-Shuang surname: Wang fullname: Wang, Xiao-Shuang organization: Department of Preventive Medicine, Wenzhou Medical University,Wenzhou,Zhejiang,China – sequence: 5 givenname: Hong-Mei surname: Wu fullname: Wu, Hong-Mei organization: Department of Preventive Medicine, Wenzhou Medical University,Wenzhou,Zhejiang,China – sequence: 6 givenname: Li surname: Zhang fullname: Zhang, Li organization: Department of Food Science, Nutrition and Health Promotion, Mississippi State University,Mississippi State,MS,USA – sequence: 7 givenname: Wen-Hsing orcidid: 0000-0003-2720-5164 surname: Cheng fullname: Cheng, Wen-Hsing email: wcheng@fsnhp.msstate.edu organization: Department of Food Science, Nutrition and Health Promotion, Mississippi State University,Mississippi State,MS,USA – sequence: 8 givenname: Jian-Hong surname: Zhu fullname: Zhu, Jian-Hong email: jhzhu@wmu.edu.cn organization: Department of Geriatrics and Neurology, the Second Affiliated Hospital and Yuying Children's Hospital, Wenzhou Medical University,Wenzhou, Zhejiang,China |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/31504723$$D View this record in MEDLINE/PubMed |
| BookMark | eNqFkU9v1DAQxS1URLeFA18ARQKpgBTW_-LE3NACbUUFlXY5W44zkbwkdmonlPLp8W4Kh6oqJ4_Gvzf2vHeEDpx3gNBzgt8RLNly65bu128i5SO0IAUnuSAYH6AFxpTmjAhxiI5i3GKMCZfVE3TISIF5SdkCxTV04PwQ_AjWZZvsMvg-1XFXdLaFoEfrXaZdk52SfPT5OtsE7aLdt5Nk_SX_mq_PshV0XXyfnfdDZ81eFHfXlzr8sC56dxKzjzaCjvAUPW51F-HZ7XmMvn_-tFmd5RffTs9XHy5ywws-5tBKzqmkVAiKwZRVzSmtoSnLmpEKN7htCS1NajLGQAvZSGY0kaUoWI05Zcfo7Tx3coO-udZdp4Zgex1uFMFq55zaOjU7l-DXM5ysuJogjqq30aSdtAM_RUVlJQpMuSz-j9KqKomoOE_oyzvo1k_Bpa0VZVRUgrNq9_aLW2qqe2j-_fJvTAl4MwMm-BgDtA8usrzDGjvu8xiDtt29ilezwk_Dg4PZjEHK7KeFoKKx4Aw0NoAZVePtPao_YkTQJQ |
| CitedBy_id | crossref_primary_10_1186_s43043_024_00212_7 crossref_primary_10_3390_ijms24076469 crossref_primary_10_1016_j_intimp_2021_107790 crossref_primary_10_1007_s12011_023_03894_8 crossref_primary_10_1002_mds_28197 crossref_primary_10_1038_s41416_022_02002_2 crossref_primary_10_1007_s12011_025_04568_3 crossref_primary_10_1016_j_phymed_2024_156103 crossref_primary_10_3390_ijms241210109 crossref_primary_10_3389_fnins_2021_646518 crossref_primary_10_3390_biology11060811 crossref_primary_10_1186_s12940_023_01007_5 crossref_primary_10_1016_j_ajhg_2024_02_016 crossref_primary_10_2139_ssrn_3924148 |
| Cites_doi | 10.1016/j.resp.2015.07.002 10.1128/MCB.02171-06 10.3945/an.110.000240 10.1038/35008115 10.1038/ncomms6906 10.1016/j.cell.2006.11.047 10.1016/j.cell.2011.12.037 10.1371/journal.pone.0163372 10.1093/jn/137.3.690 10.1074/jbc.M113.526863 10.1096/fj.09-143974 10.1007/s12035-015-9505-7 10.18632/oncotarget.9667 10.1038/nrc1073 10.1007/s12035-018-1352-x 10.15252/embr.201643504 10.1016/j.mad.2019.04.004 10.1128/MCB.22.22.7842-7852.2002 10.1152/physrev.00039.2013 10.1096/fj.14-252874 10.1080/15548627.2016.1203484 10.1042/BJ20100779 10.1186/1750-1326-6-8 10.1523/JNEUROSCI.2724-15.2015 10.1096/fj.06-075820 10.3390/molecules21101406 10.1186/s12943-017-0661-4 10.3233/JPD-2012-11052 10.1101/gad.13.12.1501 10.1038/onc.2014.250 10.1172/JCI96765 10.3389/fnmol.2018.00236 10.1093/jn/127.7.1304 10.1093/emboj/20.11.2690 10.1523/JNEUROSCI.1153-07.2007 10.1371/journal.pone.0001813 10.1089/ars.2015.6478 10.3945/jn.117.247775 10.1111/acel.12523 10.1016/S0140-6736(14)61393-3 10.1210/en.2013-1167 10.3389/fncel.2017.00170 10.1038/nature13992 10.1016/j.redox.2015.08.010 10.1021/bi602462q 10.1016/j.ceca.2012.02.008 10.1097/NEN.0b013e318160f347 |
| ContentType | Journal Article |
| Copyright | 2019 American Society for Nutrition. Copyright © American Society for Nutrition 2019. 2019 Copyright © American Society for Nutrition 2019. Copyright American Institute of Nutrition Dec 2019 |
| Copyright_xml | – notice: 2019 American Society for Nutrition. – notice: Copyright © American Society for Nutrition 2019. 2019 – notice: Copyright © American Society for Nutrition 2019. – notice: Copyright American Institute of Nutrition Dec 2019 |
| DBID | 6I. AAFTH AAYXX CITATION CGR CUY CVF ECM EIF NPM K9. NAPCQ 7X8 7S9 L.6 ADTOC UNPAY |
| DOI | 10.1093/jn/nxz199 |
| DatabaseName | ScienceDirect Open Access Titles Elsevier:ScienceDirect:Open Access CrossRef Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed ProQuest Health & Medical Complete (Alumni) Nursing & Allied Health Premium MEDLINE - Academic AGRICOLA AGRICOLA - Academic Unpaywall for CDI: Periodical Content Unpaywall |
| DatabaseTitle | CrossRef MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) ProQuest Health & Medical Complete (Alumni) Nursing & Allied Health Premium MEDLINE - Academic AGRICOLA AGRICOLA - Academic |
| DatabaseTitleList | AGRICOLA ProQuest Health & Medical Complete (Alumni) MEDLINE - Academic MEDLINE |
| 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 – sequence: 3 dbid: UNPAY name: Unpaywall url: https://proxy.k.utb.cz/login?url=https://unpaywall.org/ sourceTypes: Open Access Repository |
| DeliveryMethod | fulltext_linktorsrc |
| Discipline | Diet & Clinical Nutrition |
| EISSN | 1541-6100 |
| EndPage | 2119 |
| ExternalDocumentID | 10.1093/jn/nxz199 31504723 10_1093_jn_nxz199 S002231662216517X |
| Genre | Research Support, Non-U.S. Gov't Journal Article |
| GrantInformation_xml | – fundername: Science and Technology Department of Zhejiang Province grantid: 2018C37111 funderid: 10.13039/501100008990 – fundername: National Institute of Food and Agriculture grantid: NE1439; 1008124; MIS-384050 funderid: 10.13039/100005825 – fundername: Zhejiang Provincial Medical Technology Program grantid: 2018KY120; 2018KY506; 2018KY509 – fundername: Wenzhou Municipal Science and Technology Bureau grantid: Y20170146; C20170003 funderid: 10.13039/501100007194 – fundername: Zhejiang Provincial Natural Science Foundation grantid: LD19H090001; LZ19H090002 funderid: 10.13039/501100004731 – fundername: National Natural Science Foundation of China grantid: 81571087; 81771380; 81771510; 31701080 funderid: 10.13039/501100001809 |
| GroupedDBID | --- -ET -~X .55 .GJ 0R~ 18M 29L 2WC 34G 39C 3O- 4.4 48X 53G 5GY 5RE 5VS 6I. 85S A8Z AABJS AABMN AABZA AACZT AAFTH AAJQQ AAPGJ AAPQZ AAUQX AAVAP AAWDT AAWTL AAXUO AAYJJ ABBTP ABJNI ABPTD ABSAR ABSGY ABWST ACFRR ACGFO ACGOD ACIHN ACIMA ACKIV ACNCT ACUFI ACUTJ ADBBV ADEIU ADGZP ADRTK ADVEK AEAQA AENEX AETBJ AETEA AFDAS AFFNX AFFZL AFMIJ AFOFC AFRAH AFXAL AGINJ AGQXC AGUTN AHMBA AHPSJ AIKOY AIMBJ AJEEA ALEEW ALMA_UNASSIGNED_HOLDINGS AMRAJ AQDSO AQKUS ASMCH AZQFJ BAWUL BAYMD BCR BCRHZ BES BEYMZ BKOMP BLC BTRTY BYORX C1A CASEJ CDBKE DAKXR DIK DPPUQ DU5 E3Z EBS EIHJH EJD ENERS EX3 F5P F9R FDB FECEO FLUFQ FOEOM FOTVD FQBLK FRP G8K GAUVT GJXCC GX1 HF~ HZ~ IH2 K-O KBUDW KOP KQ8 KSI KSN L7B MBLQV MHKGH MV1 MVM NHB NHCRO NOMLY NOYVH NVLIB O9- OAUYM ODMLO OHT OJZSN OK1 OPAEJ OVD P-O P2P PEA PQQKQ PRG R0Z RHF RHI ROL ROX SV3 TAE TEORI TMA TN5 TNT TR2 TWZ UCJ UHB UKR UPT W2D W8F WH7 WHG WOQ WOW X7M XFK XOL XSW Y6R YBU YHG YKV YQJ YQT YSK ZGI ZHY ZXP ~KM 0SF ADUKH ADVLN AFRQD AITUG AKRWK H13 UIG AAGQS AALRI AAYWO AAYXX ABDPE ACVFH ADCNI ADMTO AEUPX AFJKZ AFPUW AGKRT AIGII AKBMS AKYEP APXCP CITATION EFKBS NU- YR5 CGR CUY CVF ECM EIF NPM Z5M AGCQF K9. NAPCQ 7X8 7S9 L.6 ADTOC UNPAY |
| ID | FETCH-LOGICAL-c454t-ef94429226620ec78b422bed77b3180d0ff127c422333ea69d93ca197653b0423 |
| IEDL.DBID | UNPAY |
| ISSN | 0022-3166 1541-6100 |
| IngestDate | Wed Oct 01 16:55:20 EDT 2025 Sun Sep 28 00:55:21 EDT 2025 Sat Sep 27 23:00:03 EDT 2025 Fri Jul 25 23:22:12 EDT 2025 Wed Feb 19 02:25:09 EST 2025 Wed Oct 01 04:09:29 EDT 2025 Thu Apr 24 23:12:43 EDT 2025 Wed Sep 11 04:40:42 EDT 2024 Fri Feb 23 02:35:29 EST 2024 |
| IsDoiOpenAccess | true |
| IsOpenAccess | true |
| IsPeerReviewed | true |
| IsScholarly | true |
| Issue | 12 |
| Keywords | Parkinson's disease CDKN1B 6-OHDA CDK FOXO3 MPP SELENOH selenium CCND1 siSELT CDKN2D calcium CDKN2C GPX1 GPX4 TXNRD1 siRNA PBMC selenoprotein NAC PD CCNE1 EdU ROS SELENOP SELENOT oxidative stress |
| Language | English |
| License | http://www.elsevier.com/open-access/userlicense/1.0 This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model) Copyright © American Society for Nutrition 2019. publisher-specific-oa |
| LinkModel | DirectLink |
| MergedId | FETCHMERGED-LOGICAL-c454t-ef94429226620ec78b422bed77b3180d0ff127c422333ea69d93ca197653b0423 |
| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 |
| ORCID | 0000-0003-2720-5164 |
| OpenAccessLink | https://proxy.k.utb.cz/login?url=https://academic.oup.com/jn/article-pdf/149/12/2110/31165064/nxz199.pdf |
| PMID | 31504723 |
| PQID | 2326864389 |
| PQPubID | 34400 |
| PageCount | 10 |
| ParticipantIDs | unpaywall_primary_10_1093_jn_nxz199 proquest_miscellaneous_2986502495 proquest_miscellaneous_2288716844 proquest_journals_2326864389 pubmed_primary_31504723 crossref_primary_10_1093_jn_nxz199 crossref_citationtrail_10_1093_jn_nxz199 oup_primary_10_1093_jn_nxz199 elsevier_sciencedirect_doi_10_1093_jn_nxz199 |
| ProviderPackageCode | CITATION AAYXX |
| PublicationCentury | 2000 |
| PublicationDate | December 2019 20191201 2019-12-00 2019-12-01 |
| PublicationDateYYYYMMDD | 2019-12-01 |
| PublicationDate_xml | – month: 12 year: 2019 text: December 2019 |
| PublicationDecade | 2010 |
| PublicationPlace | United States |
| PublicationPlace_xml | – name: United States – name: Bethesda |
| PublicationTitle | The Journal of nutrition |
| PublicationTitleAlternate | J Nutr |
| PublicationYear | 2019 |
| Publisher | Elsevier Inc Oxford University Press American Institute of Nutrition |
| Publisher_xml | – name: Elsevier Inc – name: Oxford University Press – name: American Institute of Nutrition |
| References | Prevost, Arabo, Jian, Quelennec, Cartier, Hassan, Falluel-Morel, Tanguy, Gargani, Lihrmann (bib19) 2013; 154 Zhang, Liu, Cheng, Zhu (bib45) 2019; 180 Haque, Banerjee, De, Maity, Sarkar, Majumdar, Jha, McGragor, Banerjee (bib36) 2015; 34 Castex, Arabo, Benard, Roy, Le Joncour, Prevost, Bonnet, Anouar, Falluel-Morel (bib10) 2016; 53 Lai, Zhang, Liu, Yang, Li, Zhu, Zou, Cheng, Zhu (bib24) 2016; 7 The, Ruijtenberg, Bouchet, Cristobal, Prinsen, van Mourik, Koreth, Xu, Heck, Akhmanova (bib30) 2015; 6 Abid, Cartier, Hamieh, Francois-Bellan, Bucharles, Pothion, Manecka, Leprince, Adriouch, Boyer (bib43) 2019; 56 Bellinger, Bellinger, Seale, Takemoto, Raman, Miki, Manning-Bog, Berry, White, Ross (bib14) 2011; 6 Dikiy, Novoselov, Fomenko, Sengupta, Carlson, Cerny, Ginalski, Grishin, Hatfield, Gladyshev (bib16) 2007; 46 Salcher, Hermann, Kiechl-Kohlendorfer, Ausserlechner, Obexer (bib38) 2017; 16 Medema, Kops, Bos, Burgering (bib28) 2000; 404 Grimmler, Wang, Mund, Cilensek, Keidel, Waddell, Jakel, Kullmann, Kriwacki, Hengst (bib34) 2007; 128 Legrain, Touat-Hamici, Chavatte (bib32) 2014; 289 Weiss, Sunde (bib33) 1997; 127 Zhang, Yang, Hu, Lu, Zhou, He, Wu, Zhu (bib25) 2017; 11 Burk, Hill, Motley, Winfrey, Kurokawa, Mitchell, Zhang (bib3) 2014; 28 Zhang, Ye, Zhu, Sun, Zheng, Fan, Wu, Chen, Cheng, Zhu (bib15) 2016; 11 Nakayama, Hill, Austin, Motley, Burk (bib1) 2007; 137 Labunskyy, Hatfield, Gladyshev (bib11) 2014; 94 Sherr, Roberts (bib29) 1999; 13 Campisi (bib37) 2003; 3 Burk, Hill, Olson, Weeber, Motley, Winfrey, Austin (bib2) 2007; 27 Kalia, Lang (bib12) 2015; 386 Gomez-Puerto, Verhagen, Braat, Lam, Coffer, Lorenowicz (bib40) 2016; 12 Boukhzar, Hamieh, Cartier, Tanguy, Alsharif, Castex, Arabo, El Hajji, Bonnet, Errami (bib9) 2016; 24 Schmidt, Fernandez de Mattos, van der Horst, Klompmaker, Kops, Lam, Burgering, Medema (bib27) 2002; 22 Bellinger, Raman, Rueli, Bellinger, Dewing, Seale, Andres, Uyehara-Lock, White, Ross (bib13) 2012; 2 Soerensen, Jakupoglu, Beck, Forster, Schmidt, Schmahl, Schweizer, Conrad, Brielmeier (bib8) 2008; 3 Valentine, Abel, Hill, Austin, Burk (bib6) 2008; 67 Edamakanti, Do, Didonna, Martina, Opal (bib21) 2018; 128 Pinton, Ferrari, Rapizzi, Di Virgilio, Pozzan, Rizzuto (bib46) 2001; 20 Gorlach, Bertram, Hudecova, Krizanova (bib41) 2015; 6 Sadee, Yu, Richards, Preis, Schwab, Brodsky, Biedler (bib22) 1987; 47 Cao, Zhang, Zeng, Wu, Wu, Cheng (bib23) 2017; 147 Giorgi, Baldassari, Bononi, Bonora, De Marchi, Marchi, Missiroli, Patergnani, Rimessi (bib47) 2012; 52 James, Ray, Leznova, Blain (bib35) 2008; 28 Ishii, Takanashi, Sugita, Miyazawa, Yanagihara, Yasuda, Onouchi, Kawabe, Nakata, Yamamoto (bib42) 2017; 16 de Campos, Hasegawa, Kumei, Zeredo (bib26) 2015; 218 Sunde, Raines (bib31) 2011; 2 Kim, Liu, Zhang, Duan, Wen, Song, Feighery, Lu, Rujescu, St Clair (bib48) 2012; 148 Wirth, Conrad, Winterer, Wozny, Carlson, Roth, Schmitz, Bornkamm, Coppola, Tessarollo (bib7) 2010; 24 Hamieh, Cartier, Abid, Calas, Burel, Bucharles, Jehan, Grumolato, Landry, Lerouge (bib20) 2017; 18 Pitts, Kremer, Hashimoto, Torres, Byrns, Williams, Berry (bib5) 2015; 35 Chiu-Ugalde, Theilig, Behrends, Drebes, Sieland, Subbarayal, Kohrle, Hammes, Schomburg, Schweizer (bib4) 2010; 431 Wei, Li, Li, Liu, Cheng (bib44) 2018; 11 Yue, Cheng, Breschi, Vierstra, Wu, Ryba, Sandstrom, Ma, Davis, Pope (bib18) 2014; 515 Qian, Wang, Cao, Liu, Qian, Guan, Guo, Xiao, Wang (bib39) 2016; 21 Grumolato, Ghzili, Montero-Hadjadje, Gasman, Lesage, Tanguy, Galas, Ait-Ali, Leprince, Guérineau (bib17) 2008; 22 Burk (10.1093/jn/nxz199_bib2) 2007; 27 Prevost (10.1093/jn/nxz199_bib19) 2013; 154 Pitts (10.1093/jn/nxz199_bib5) 2015; 35 Qian (10.1093/jn/nxz199_bib39) 2016; 21 Sadee (10.1093/jn/nxz199_bib22) 1987; 47 Wei (10.1093/jn/nxz199_bib44) 2018; 11 Pinton (10.1093/jn/nxz199_bib46) 2001; 20 Labunskyy (10.1093/jn/nxz199_bib11) 2014; 94 Zhang (10.1093/jn/nxz199_bib15) 2016; 11 Zhang (10.1093/jn/nxz199_bib45) 2019; 180 Grumolato (10.1093/jn/nxz199_bib17) 2008; 22 James (10.1093/jn/nxz199_bib35) 2008; 28 Burk (10.1093/jn/nxz199_bib3) 2014; 28 Hamieh (10.1093/jn/nxz199_bib20) 2017; 18 Giorgi (10.1093/jn/nxz199_bib47) 2012; 52 Wirth (10.1093/jn/nxz199_bib7) 2010; 24 Gorlach (10.1093/jn/nxz199_bib41) 2015; 6 Castex (10.1093/jn/nxz199_bib10) 2016; 53 Schmidt (10.1093/jn/nxz199_bib27) 2002; 22 Boukhzar (10.1093/jn/nxz199_bib9) 2016; 24 Dikiy (10.1093/jn/nxz199_bib16) 2007; 46 Sherr (10.1093/jn/nxz199_bib29) 1999; 13 Bellinger (10.1093/jn/nxz199_bib13) 2012; 2 Haque (10.1093/jn/nxz199_bib36) 2015; 34 Ishii (10.1093/jn/nxz199_bib42) 2017; 16 Yue (10.1093/jn/nxz199_bib18) 2014; 515 Sunde (10.1093/jn/nxz199_bib31) 2011; 2 Zhang (10.1093/jn/nxz199_bib25) 2017; 11 Grimmler (10.1093/jn/nxz199_bib34) 2007; 128 The (10.1093/jn/nxz199_bib30) 2015; 6 Medema (10.1093/jn/nxz199_bib28) 2000; 404 Gomez-Puerto (10.1093/jn/nxz199_bib40) 2016; 12 Chiu-Ugalde (10.1093/jn/nxz199_bib4) 2010; 431 Abid (10.1093/jn/nxz199_bib43) 2019; 56 Soerensen (10.1093/jn/nxz199_bib8) 2008; 3 Salcher (10.1093/jn/nxz199_bib38) 2017; 16 Cao (10.1093/jn/nxz199_bib23) 2017; 147 Weiss (10.1093/jn/nxz199_bib33) 1997; 127 Kim (10.1093/jn/nxz199_bib48) 2012; 148 Edamakanti (10.1093/jn/nxz199_bib21) 2018; 128 Campisi (10.1093/jn/nxz199_bib37) 2003; 3 Valentine (10.1093/jn/nxz199_bib6) 2008; 67 Kalia (10.1093/jn/nxz199_bib12) 2015; 386 Legrain (10.1093/jn/nxz199_bib32) 2014; 289 Bellinger (10.1093/jn/nxz199_bib14) 2011; 6 Lai (10.1093/jn/nxz199_bib24) 2016; 7 de Campos (10.1093/jn/nxz199_bib26) 2015; 218 Nakayama (10.1093/jn/nxz199_bib1) 2007; 137 |
| References_xml | – volume: 12 start-page: 1804 year: 2016 end-page: 1816 ident: bib40 article-title: Activation of autophagy by FOXO3 regulates redox homeostasis during osteogenic differentiation publication-title: Autophagy – volume: 24 start-page: 557 year: 2016 end-page: 574 ident: bib9 article-title: Selenoprotein T exerts an essential oxidoreductase activity that protects dopaminergic neurons in mouse models of Parkinson's disease publication-title: Antioxid Redox Signal – volume: 180 start-page: 89 year: 2019 end-page: 96 ident: bib45 article-title: Prioritized brain selenium retention and selenoprotein expression: nutritional insights into Parkinson's disease publication-title: Mech Ageing Dev – volume: 2 start-page: 138 year: 2011 end-page: 150 ident: bib31 article-title: Selenium regulation of the selenoprotein and nonselenoprotein transcriptomes in rodents publication-title: Adv Nutr – volume: 6 start-page: 8 year: 2011 ident: bib14 article-title: Glutathione peroxidase 4 is associated with neuromelanin in substantia nigra and dystrophic axons in putamen of Parkinson's brain publication-title: Mol Neurodegener – volume: 21 start-page: E1406 year: 2016 ident: bib39 article-title: Capsaicin suppresses cell proliferation, induces cell cycle arrest and ROS production in bladder cancer cells through FOXO3a-mediated pathways publication-title: Molecules – volume: 6 start-page: 5906 year: 2015 ident: bib30 article-title: Rb and FZR1/Cdh1 determine CDK4/6-cyclin D requirement in C. elegans and human cancer cells publication-title: Nat Commun – volume: 28 start-page: 498 year: 2008 end-page: 510 ident: bib35 article-title: Differential modification of p27Kip1 controls its cyclin D-cdk4 inhibitory activity publication-title: Mol Cell Biol – volume: 127 start-page: 1304 year: 1997 end-page: 1310 ident: bib33 article-title: Selenium regulation of classical glutathione peroxidase expression requires the 3' untranslated region in Chinese hamster ovary cells publication-title: J Nutr – volume: 24 start-page: 844 year: 2010 end-page: 852 ident: bib7 article-title: Neuronal selenoprotein expression is required for interneuron development and prevents seizures and neurodegeneration publication-title: FASEB J – volume: 47 start-page: 5207 year: 1987 end-page: 5212 ident: bib22 article-title: Expression of neurotransmitter receptors and myc protooncogenes in subclones of a human neuroblastoma cell line publication-title: Cancer Res – volume: 35 start-page: 15326 year: 2015 end-page: 15338 ident: bib5 article-title: Competition between the brain and testes under selenium-compromise: insight into sex differences in selenium metabolism and risk of neurodevelopmental disease publication-title: J Neurosci – volume: 7 start-page: 43731 year: 2016 ident: bib24 article-title: Redox-sensitive MAPK and Notch3 regulate fibroblast differentiation and activation: a dual role of ERK1/2 publication-title: Oncotarget – volume: 20 start-page: 2690 year: 2001 end-page: 2701 ident: bib46 article-title: The Ca2+ concentration of the endoplasmic reticulum is a key determinant of ceramide-induced apoptosis: significance for the molecular mechanism of Bcl-2 action publication-title: EMBO J – volume: 46 start-page: 6871 year: 2007 end-page: 6882 ident: bib16 article-title: SelT, SelW, SelH, and Rdx12: genomics and molecular insights into the functions of selenoproteins of a novel thioredoxin-like family publication-title: Biochemistry – volume: 137 start-page: 690 year: 2007 end-page: 693 ident: bib1 article-title: All regions of mouse brain are dependent on selenoprotein P for maintenance of selenium publication-title: J Nutr – volume: 147 start-page: 1858 year: 2017 end-page: 1866 ident: bib23 article-title: Analyses of selenotranscriptomes and selenium concentrations in response to dietary selenium deficiency and age reveal common and distinct patterns by tissue and sex in telomere-sysfunctional mice publication-title: J Nutr – volume: 67 start-page: 68 year: 2008 end-page: 77 ident: bib6 article-title: Neurodegeneration in mice resulting from loss of functional selenoprotein P or its receptor apolipoprotein E receptor 2 publication-title: J Neuropathol Exp Neurol – volume: 128 start-page: 269 year: 2007 end-page: 280 ident: bib34 article-title: Cdk-inhibitory activity and stability of p27Kip1 are directly regulated by oncogenic tyrosine kinases publication-title: Cell – volume: 53 start-page: 5818 year: 2016 end-page: 5832 ident: bib10 article-title: Selenoprotein T deficiency leads to neurodevelopmental abnormalities and hyperactive behavior in mice publication-title: Mol Neurobiol – volume: 56 start-page: 4086 year: 2019 end-page: 4101 ident: bib43 article-title: AMPK activation of PGC-1alpha/NRF-1-dependent SELENOT gene transcription promotes PACAP-induced neuroendocrine cell differentiation through tolerance to oxidative stress publication-title: Mol Neurobiol – volume: 16 start-page: 39 year: 2017 end-page: 51 ident: bib42 article-title: Endogenous reactive oxygen species cause astrocyte defects and neuronal dysfunctions in the hippocampus: a new model for aging brain publication-title: Aging Cell – volume: 11 start-page: e0163372 year: 2016 ident: bib15 article-title: Selenotranscriptomic analyses identify signature selenoproteins in brain regions in a mouse model of Parkinson's disease publication-title: PLoS One – volume: 148 start-page: 1051 year: 2012 end-page: 1064 ident: bib48 article-title: Interplay between DISC1 and GABA signaling regulates neurogenesis in mice and risk for schizophrenia publication-title: Cell – volume: 154 start-page: 3796 year: 2013 end-page: 3806 ident: bib19 article-title: The PACAP-regulated gene selenoprotein T is abundantly expressed in mouse and human beta-cells and its targeted inactivation impairs glucose tolerance publication-title: Endocrinology – volume: 13 start-page: 1501 year: 1999 end-page: 1512 ident: bib29 article-title: CDK inhibitors: positive and negative regulators of G1-phase progression publication-title: Genes Dev – volume: 404 start-page: 782 year: 2000 end-page: 787 ident: bib28 article-title: AFX-like forkhead transcription factors mediate cell-cycle regulation by Ras and PKB through p27kip1 publication-title: Nature – volume: 16 start-page: 95 year: 2017 ident: bib38 article-title: C10ORF10/DEPP-mediated ROS accumulation is a critical modulator of FOXO3-induced autophagy publication-title: Mol Cancer – volume: 18 start-page: 1935 year: 2017 end-page: 1946 ident: bib20 article-title: Selenoprotein T is a novel OST subunit that regulates UPR signaling and hormone secretion publication-title: EMBO Rep – volume: 128 start-page: 2252 year: 2018 end-page: 2265 ident: bib21 article-title: Mutant ataxin1 disrupts cerebellar development in spinocerebellar ataxia type 1 publication-title: J Clin Invest – volume: 289 start-page: 6299 year: 2014 end-page: 6310 ident: bib32 article-title: Interplay between selenium levels, selenoprotein expression, and replicative senescence in WI-38 human fibroblasts publication-title: J Biol Chem – volume: 28 start-page: 3579 year: 2014 end-page: 3588 ident: bib3 article-title: Selenoprotein P and apolipoprotein E receptor-2 interact at the blood-brain barrier and also within the brain to maintain an essential selenium pool that protects against neurodegeneration publication-title: FASEB J – volume: 34 start-page: 3152 year: 2015 end-page: 3163 ident: bib36 article-title: CCN5/WISP-2 promotes growth arrest of triple-negative breast cancer cells through accumulation and trafficking of p27(Kip1) via Skp2 and FOXO3a regulation publication-title: Oncogene – volume: 3 start-page: e1813 year: 2008 ident: bib8 article-title: The role of thioredoxin reductases in brain development publication-title: PLoS One – volume: 11 start-page: 236 year: 2018 ident: bib44 article-title: Oxidative stress in Parkinson's disease: a systematic review and meta-analysis publication-title: Front Mol Neurosci – volume: 27 start-page: 6207 year: 2007 end-page: 6211 ident: bib2 article-title: Deletion of apolipoprotein E receptor-2 in mice lowers brain selenium and causes severe neurological dysfunction and death when a low-selenium diet is fed publication-title: J Neurosci – volume: 218 start-page: 40 year: 2015 end-page: 45 ident: bib26 article-title: Cineradiographic analysis of respiratory movements in a mouse model for early Parkinson's disease publication-title: Respir Physiol Neurobiol – volume: 2 start-page: 115 year: 2012 end-page: 126 ident: bib13 article-title: Changes in selenoprotein P in substantia nigra and putamen in Parkinson's disease publication-title: J Parkinsons Dis – volume: 52 start-page: 36 year: 2012 end-page: 43 ident: bib47 article-title: Mitochondrial Ca2+ and apoptosis publication-title: Cell Calcium – volume: 22 start-page: 1756 year: 2008 end-page: 1768 ident: bib17 article-title: Selenoprotein T is a PACAP-regulated gene involved in intracellular Ca2+ mobilization and neuroendocrine secretion publication-title: FASEB J – volume: 22 start-page: 7842 year: 2002 end-page: 7852 ident: bib27 article-title: Cell cycle inhibition by FoxO forkhead transcription factors involves downregulation of cyclin D publication-title: Mol Cell Biol – volume: 431 start-page: 103 year: 2010 end-page: 111 ident: bib4 article-title: Mutation of megalin leads to urinary loss of selenoprotein P and selenium deficiency in serum, liver, kidneys and brain publication-title: Biochem J – volume: 3 start-page: 339 year: 2003 end-page: 349 ident: bib37 article-title: Cancer and ageing: rival demons? publication-title: Nat Rev Cancer – volume: 6 start-page: 260 year: 2015 end-page: 271 ident: bib41 article-title: Calcium and ROS: a mutual interplay publication-title: Redox Biol – volume: 515 start-page: 355 year: 2014 end-page: 364 ident: bib18 article-title: A comparative encyclopedia of DNA elements in the mouse genome publication-title: Nature – volume: 94 start-page: 739 year: 2014 end-page: 777 ident: bib11 article-title: Selenoproteins: molecular pathways and physiological roles publication-title: Physiol Rev – volume: 11 start-page: 170 year: 2017 ident: bib25 article-title: Reduced circulating levels of miR-433 and miR-133b are potential biomarkers for Parkinson's disease publication-title: Front Cell Neurosci – volume: 386 start-page: 896 year: 2015 end-page: 912 ident: bib12 article-title: Parkinson's disease publication-title: Lancet – volume: 218 start-page: 40 year: 2015 ident: 10.1093/jn/nxz199_bib26 article-title: Cineradiographic analysis of respiratory movements in a mouse model for early Parkinson's disease publication-title: Respir Physiol Neurobiol doi: 10.1016/j.resp.2015.07.002 – volume: 28 start-page: 498 year: 2008 ident: 10.1093/jn/nxz199_bib35 article-title: Differential modification of p27Kip1 controls its cyclin D-cdk4 inhibitory activity publication-title: Mol Cell Biol doi: 10.1128/MCB.02171-06 – volume: 2 start-page: 138 year: 2011 ident: 10.1093/jn/nxz199_bib31 article-title: Selenium regulation of the selenoprotein and nonselenoprotein transcriptomes in rodents publication-title: Adv Nutr doi: 10.3945/an.110.000240 – volume: 404 start-page: 782 year: 2000 ident: 10.1093/jn/nxz199_bib28 article-title: AFX-like forkhead transcription factors mediate cell-cycle regulation by Ras and PKB through p27kip1 publication-title: Nature doi: 10.1038/35008115 – volume: 6 start-page: 5906 year: 2015 ident: 10.1093/jn/nxz199_bib30 article-title: Rb and FZR1/Cdh1 determine CDK4/6-cyclin D requirement in C. elegans and human cancer cells publication-title: Nat Commun doi: 10.1038/ncomms6906 – volume: 128 start-page: 269 year: 2007 ident: 10.1093/jn/nxz199_bib34 article-title: Cdk-inhibitory activity and stability of p27Kip1 are directly regulated by oncogenic tyrosine kinases publication-title: Cell doi: 10.1016/j.cell.2006.11.047 – volume: 148 start-page: 1051 year: 2012 ident: 10.1093/jn/nxz199_bib48 article-title: Interplay between DISC1 and GABA signaling regulates neurogenesis in mice and risk for schizophrenia publication-title: Cell doi: 10.1016/j.cell.2011.12.037 – volume: 11 start-page: e0163372 year: 2016 ident: 10.1093/jn/nxz199_bib15 article-title: Selenotranscriptomic analyses identify signature selenoproteins in brain regions in a mouse model of Parkinson's disease publication-title: PLoS One doi: 10.1371/journal.pone.0163372 – volume: 137 start-page: 690 year: 2007 ident: 10.1093/jn/nxz199_bib1 article-title: All regions of mouse brain are dependent on selenoprotein P for maintenance of selenium publication-title: J Nutr doi: 10.1093/jn/137.3.690 – volume: 289 start-page: 6299 year: 2014 ident: 10.1093/jn/nxz199_bib32 article-title: Interplay between selenium levels, selenoprotein expression, and replicative senescence in WI-38 human fibroblasts publication-title: J Biol Chem doi: 10.1074/jbc.M113.526863 – volume: 24 start-page: 844 year: 2010 ident: 10.1093/jn/nxz199_bib7 article-title: Neuronal selenoprotein expression is required for interneuron development and prevents seizures and neurodegeneration publication-title: FASEB J doi: 10.1096/fj.09-143974 – volume: 53 start-page: 5818 year: 2016 ident: 10.1093/jn/nxz199_bib10 article-title: Selenoprotein T deficiency leads to neurodevelopmental abnormalities and hyperactive behavior in mice publication-title: Mol Neurobiol doi: 10.1007/s12035-015-9505-7 – volume: 7 start-page: 43731 year: 2016 ident: 10.1093/jn/nxz199_bib24 article-title: Redox-sensitive MAPK and Notch3 regulate fibroblast differentiation and activation: a dual role of ERK1/2 publication-title: Oncotarget doi: 10.18632/oncotarget.9667 – volume: 3 start-page: 339 year: 2003 ident: 10.1093/jn/nxz199_bib37 article-title: Cancer and ageing: rival demons? publication-title: Nat Rev Cancer doi: 10.1038/nrc1073 – volume: 56 start-page: 4086 year: 2019 ident: 10.1093/jn/nxz199_bib43 article-title: AMPK activation of PGC-1alpha/NRF-1-dependent SELENOT gene transcription promotes PACAP-induced neuroendocrine cell differentiation through tolerance to oxidative stress publication-title: Mol Neurobiol doi: 10.1007/s12035-018-1352-x – volume: 18 start-page: 1935 year: 2017 ident: 10.1093/jn/nxz199_bib20 article-title: Selenoprotein T is a novel OST subunit that regulates UPR signaling and hormone secretion publication-title: EMBO Rep doi: 10.15252/embr.201643504 – volume: 180 start-page: 89 year: 2019 ident: 10.1093/jn/nxz199_bib45 article-title: Prioritized brain selenium retention and selenoprotein expression: nutritional insights into Parkinson's disease publication-title: Mech Ageing Dev doi: 10.1016/j.mad.2019.04.004 – volume: 22 start-page: 7842 year: 2002 ident: 10.1093/jn/nxz199_bib27 article-title: Cell cycle inhibition by FoxO forkhead transcription factors involves downregulation of cyclin D publication-title: Mol Cell Biol doi: 10.1128/MCB.22.22.7842-7852.2002 – volume: 94 start-page: 739 year: 2014 ident: 10.1093/jn/nxz199_bib11 article-title: Selenoproteins: molecular pathways and physiological roles publication-title: Physiol Rev doi: 10.1152/physrev.00039.2013 – volume: 28 start-page: 3579 year: 2014 ident: 10.1093/jn/nxz199_bib3 article-title: Selenoprotein P and apolipoprotein E receptor-2 interact at the blood-brain barrier and also within the brain to maintain an essential selenium pool that protects against neurodegeneration publication-title: FASEB J doi: 10.1096/fj.14-252874 – volume: 12 start-page: 1804 year: 2016 ident: 10.1093/jn/nxz199_bib40 article-title: Activation of autophagy by FOXO3 regulates redox homeostasis during osteogenic differentiation publication-title: Autophagy doi: 10.1080/15548627.2016.1203484 – volume: 431 start-page: 103 year: 2010 ident: 10.1093/jn/nxz199_bib4 article-title: Mutation of megalin leads to urinary loss of selenoprotein P and selenium deficiency in serum, liver, kidneys and brain publication-title: Biochem J doi: 10.1042/BJ20100779 – volume: 6 start-page: 8 year: 2011 ident: 10.1093/jn/nxz199_bib14 article-title: Glutathione peroxidase 4 is associated with neuromelanin in substantia nigra and dystrophic axons in putamen of Parkinson's brain publication-title: Mol Neurodegener doi: 10.1186/1750-1326-6-8 – volume: 35 start-page: 15326 year: 2015 ident: 10.1093/jn/nxz199_bib5 article-title: Competition between the brain and testes under selenium-compromise: insight into sex differences in selenium metabolism and risk of neurodevelopmental disease publication-title: J Neurosci doi: 10.1523/JNEUROSCI.2724-15.2015 – volume: 22 start-page: 1756 year: 2008 ident: 10.1093/jn/nxz199_bib17 article-title: Selenoprotein T is a PACAP-regulated gene involved in intracellular Ca2+ mobilization and neuroendocrine secretion publication-title: FASEB J doi: 10.1096/fj.06-075820 – volume: 21 start-page: E1406 year: 2016 ident: 10.1093/jn/nxz199_bib39 article-title: Capsaicin suppresses cell proliferation, induces cell cycle arrest and ROS production in bladder cancer cells through FOXO3a-mediated pathways publication-title: Molecules doi: 10.3390/molecules21101406 – volume: 16 start-page: 95 year: 2017 ident: 10.1093/jn/nxz199_bib38 article-title: C10ORF10/DEPP-mediated ROS accumulation is a critical modulator of FOXO3-induced autophagy publication-title: Mol Cancer doi: 10.1186/s12943-017-0661-4 – volume: 2 start-page: 115 year: 2012 ident: 10.1093/jn/nxz199_bib13 article-title: Changes in selenoprotein P in substantia nigra and putamen in Parkinson's disease publication-title: J Parkinsons Dis doi: 10.3233/JPD-2012-11052 – volume: 13 start-page: 1501 year: 1999 ident: 10.1093/jn/nxz199_bib29 article-title: CDK inhibitors: positive and negative regulators of G1-phase progression publication-title: Genes Dev doi: 10.1101/gad.13.12.1501 – volume: 34 start-page: 3152 year: 2015 ident: 10.1093/jn/nxz199_bib36 article-title: CCN5/WISP-2 promotes growth arrest of triple-negative breast cancer cells through accumulation and trafficking of p27(Kip1) via Skp2 and FOXO3a regulation publication-title: Oncogene doi: 10.1038/onc.2014.250 – volume: 128 start-page: 2252 year: 2018 ident: 10.1093/jn/nxz199_bib21 article-title: Mutant ataxin1 disrupts cerebellar development in spinocerebellar ataxia type 1 publication-title: J Clin Invest doi: 10.1172/JCI96765 – volume: 11 start-page: 236 year: 2018 ident: 10.1093/jn/nxz199_bib44 article-title: Oxidative stress in Parkinson's disease: a systematic review and meta-analysis publication-title: Front Mol Neurosci doi: 10.3389/fnmol.2018.00236 – volume: 127 start-page: 1304 year: 1997 ident: 10.1093/jn/nxz199_bib33 article-title: Selenium regulation of classical glutathione peroxidase expression requires the 3' untranslated region in Chinese hamster ovary cells publication-title: J Nutr doi: 10.1093/jn/127.7.1304 – volume: 20 start-page: 2690 year: 2001 ident: 10.1093/jn/nxz199_bib46 article-title: The Ca2+ concentration of the endoplasmic reticulum is a key determinant of ceramide-induced apoptosis: significance for the molecular mechanism of Bcl-2 action publication-title: EMBO J doi: 10.1093/emboj/20.11.2690 – volume: 27 start-page: 6207 year: 2007 ident: 10.1093/jn/nxz199_bib2 article-title: Deletion of apolipoprotein E receptor-2 in mice lowers brain selenium and causes severe neurological dysfunction and death when a low-selenium diet is fed publication-title: J Neurosci doi: 10.1523/JNEUROSCI.1153-07.2007 – volume: 3 start-page: e1813 year: 2008 ident: 10.1093/jn/nxz199_bib8 article-title: The role of thioredoxin reductases in brain development publication-title: PLoS One doi: 10.1371/journal.pone.0001813 – volume: 24 start-page: 557 year: 2016 ident: 10.1093/jn/nxz199_bib9 article-title: Selenoprotein T exerts an essential oxidoreductase activity that protects dopaminergic neurons in mouse models of Parkinson's disease publication-title: Antioxid Redox Signal doi: 10.1089/ars.2015.6478 – volume: 147 start-page: 1858 year: 2017 ident: 10.1093/jn/nxz199_bib23 article-title: Analyses of selenotranscriptomes and selenium concentrations in response to dietary selenium deficiency and age reveal common and distinct patterns by tissue and sex in telomere-sysfunctional mice publication-title: J Nutr doi: 10.3945/jn.117.247775 – volume: 16 start-page: 39 year: 2017 ident: 10.1093/jn/nxz199_bib42 article-title: Endogenous reactive oxygen species cause astrocyte defects and neuronal dysfunctions in the hippocampus: a new model for aging brain publication-title: Aging Cell doi: 10.1111/acel.12523 – volume: 386 start-page: 896 year: 2015 ident: 10.1093/jn/nxz199_bib12 article-title: Parkinson's disease publication-title: Lancet doi: 10.1016/S0140-6736(14)61393-3 – volume: 154 start-page: 3796 year: 2013 ident: 10.1093/jn/nxz199_bib19 article-title: The PACAP-regulated gene selenoprotein T is abundantly expressed in mouse and human beta-cells and its targeted inactivation impairs glucose tolerance publication-title: Endocrinology doi: 10.1210/en.2013-1167 – volume: 11 start-page: 170 year: 2017 ident: 10.1093/jn/nxz199_bib25 article-title: Reduced circulating levels of miR-433 and miR-133b are potential biomarkers for Parkinson's disease publication-title: Front Cell Neurosci doi: 10.3389/fncel.2017.00170 – volume: 515 start-page: 355 year: 2014 ident: 10.1093/jn/nxz199_bib18 article-title: A comparative encyclopedia of DNA elements in the mouse genome publication-title: Nature doi: 10.1038/nature13992 – volume: 6 start-page: 260 year: 2015 ident: 10.1093/jn/nxz199_bib41 article-title: Calcium and ROS: a mutual interplay publication-title: Redox Biol doi: 10.1016/j.redox.2015.08.010 – volume: 46 start-page: 6871 year: 2007 ident: 10.1093/jn/nxz199_bib16 article-title: SelT, SelW, SelH, and Rdx12: genomics and molecular insights into the functions of selenoproteins of a novel thioredoxin-like family publication-title: Biochemistry doi: 10.1021/bi602462q – volume: 52 start-page: 36 year: 2012 ident: 10.1093/jn/nxz199_bib47 article-title: Mitochondrial Ca2+ and apoptosis publication-title: Cell Calcium doi: 10.1016/j.ceca.2012.02.008 – volume: 67 start-page: 68 year: 2008 ident: 10.1093/jn/nxz199_bib6 article-title: Neurodegeneration in mice resulting from loss of functional selenoprotein P or its receptor apolipoprotein E receptor 2 publication-title: J Neuropathol Exp Neurol doi: 10.1097/NEN.0b013e318160f347 – volume: 47 start-page: 5207 year: 1987 ident: 10.1093/jn/nxz199_bib22 article-title: Expression of neurotransmitter receptors and myc protooncogenes in subclones of a human neuroblastoma cell line publication-title: Cancer Res |
| SSID | ssj0001498 |
| Score | 2.4057481 |
| Snippet | Selenium is prioritized to the brain mainly for selenoprotein expression. Selenoprotein T (SELENOT) protects dopaminergic, postmitotic neurons in a mouse model... ABSTRACT Background Selenium is prioritized to the brain mainly for selenoprotein expression. Selenoprotein T (SELENOT) protects dopaminergic, postmitotic... Background Selenium is prioritized to the brain mainly for selenoprotein expression. Selenoprotein T (SELENOT) protects dopaminergic, postmitotic neurons in a... Background: Selenium is prioritized to the brain mainly for selenoprotein expression. Selenoprotein T (SELENOT) protects dopaminergic, postmitotic neurons in a... |
| SourceID | unpaywall proquest pubmed crossref oup elsevier |
| SourceType | Open Access Repository Aggregation Database Index Database Enrichment Source Publisher |
| StartPage | 2110 |
| SubjectTerms | 6-Hydroxydopamine acetylcysteine Aged Animals Annexin V Antioxidants Blood brain Calcium Calcium - metabolism Calcium channel blockers Calcium channels Caspase-3 Cell cycle cell cycle checkpoints Cell Line Cell proliferation Cell Proliferation - physiology Cyclin-dependent kinase Cyclin-dependent kinase 4 Cyclin-dependent kinase inhibitor p27 Cysteine Dopamine receptors Female Flow cytometry Forkhead protein G1 Phase - physiology Humans Hydroxylase Immunoblotting Iodides Kinases Leukocytes (mononuclear) Male males Mice Mice, Inbred C57BL Middle Aged Movement disorders mRNA Neurodegenerative diseases Neurons Nimodipine nutrition oxidative stress Parkinson disease Parkinson Disease - metabolism Parkinson Disease - pathology Parkinson's disease Proteins Reactive oxygen species Reactive Oxygen Species - metabolism S Phase - physiology Selenium selenoprotein selenoproteins Selenoproteins - physiology Tyrosine Up-Regulation Vitamins |
| Title | Selenoprotein T Promotes Proliferation and G1-to-S Transition in SK-N-SH Cells: Implications in Parkinson's Disease |
| URI | https://dx.doi.org/10.1093/jn/nxz199 https://www.ncbi.nlm.nih.gov/pubmed/31504723 https://www.proquest.com/docview/2326864389 https://www.proquest.com/docview/2288716844 https://www.proquest.com/docview/2986502495 https://academic.oup.com/jn/article-pdf/149/12/2110/31165064/nxz199.pdf |
| UnpaywallVersion | publishedVersion |
| Volume | 149 |
| hasFullText | 1 |
| inHoldings | 1 |
| isFullTextHit | |
| isPrint | |
| journalDatabaseRights | – providerCode: PRVLSH databaseName: Elsevier Journals customDbUrl: mediaType: online eissn: 1541-6100 dateEnd: 99991231 omitProxy: true ssIdentifier: ssj0001498 issn: 1541-6100 databaseCode: AKRWK dateStart: 19280901 isFulltext: true providerName: Library Specific Holdings |
| link | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV1Zb9QwEB6V3QfEA_cR1FbmEPBANontHOZt1dIurFhVbFe0T5HjOKIlyq5IVkB_PeNcWlBb8cBbFI9z2OOZbzQXwEuZMIQhitlSBD4aKHiVqEjZyB5CUS4ZjUzu8KdZMFnwjyf-yRYcdrkwso0KH3UpDeeF066hvUozBwG941HHmC0OM6VjUKU6xc8LT4gRjt-AYWA8TQMYLmZH49O-VrhXey0RL3hoLLluV2NIMPOCZv5VmumPxLcN_HkLbq6Llfz1Q-b5hk46uANfu79pQlG-jdZVMlIXfxV6_A-_exdut7iVjJtZ92BLF_fB2j_TFXlF2uKiOZl1tf0fQDk3Cm1Z14E4K8gxOaoD_3RpLnITUFPzBJFFSg49u1rac1Irzno-wSnzqY3ifkL2dJ6X78iHjdh3M2zytevUtdcl2W_cTA9hcfD-eG9itx0ebMV9Xtk6E9z0y0KUQF2twijhlCY6DcMEZY2bulnm0VDhTcaYloFIBVPSQwjls8RE9DyCQbEs9BMgQZgaLy7NGD45QzGOZoNPU0VFgnKGMwvedLsbq7b8uenCkceNG57F50XcrKwFz3vSVVPz4zKitx2LxC1YaUBIjLroMvId3OLrHrfdMVjcSpEyRrQbRIHpT2_Bs34Yz79x6shCL9dIQyNj80acX0MjIuQc02XcgscN8_ZfwtAi4CHF9XnRc_PVn_n0n6i2YVB9X-sdhGtVsgvD8fTzl-lueyR_A2MpPng |
| linkProvider | Unpaywall |
| linkToUnpaywall | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV1Lb9QwEB6V7QFx4E1J1SLzEHAgm8R2HuZWtbQLiFWl7UrlFDmOI1oi76rJCuivZ5yXFtRWHLhF8TgPezzzjeYF8EpmDGGIYq4UUYgGCl5lKlEusodQlEtGE5s7_GUaTeb802l4ugFHfS6M7KLCx31Kw7nxujV0l3nhIaD3AupZs8VjtnQMqlTP_LwMhBjj-C3YjKynaQSb8-nx3tehVnjQeC0RLwRoLPl-X2NIMPuCdv51mumPxLc1_HkHbq_MUv76IctyTScd3oNv_d-0oSjfx6s6G6vLvwo9_offvQ93O9xK9tpZD2BDm4fgHJzpmrwmXXHRkkz72v6PoJpZhbZo6kCcGXJCjpvAP13Zi9IG1DQ8QaTJyVHg1gt3RhrF2cwnOGX22UVxPyH7uiyr9-TjWuy7Hbb52k3q2puKHLRupscwP_xwsj9xuw4PruIhr11dCG77ZSFKoL5WcZJxSjOdx3GGssbP_aIIaKzwJmNMy0jkgikZIIQKWWYjep7AyCyMfgokinPrxaUFwycXKMbRbAhprqjIUM5w5sDbfndT1ZU_t104yrR1w7P03KTtyjrwYiBdtjU_riJ617NI2oGVFoSkqIuuIt_FLb7pcTs9g6WdFKlSRLtREtn-9A48H4bx_FunjjR6sUIamlibN-H8BhqRIOfYLuMObLXMO3wJQ4uAxxTX5-XAzdd_5vY_Ue3AqL5Y6V2Ea3X2rDuKvwF3XTzV |
| 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=Selenoprotein+T+Promotes+Proliferation+and+G1-to-S+Transition+in+SK-N-SH+Cells%3A+Implications+in+Parkinson%27s+Disease&rft.jtitle=The+Journal+of+nutrition&rft.au=Shao%2C+Zi-Qiang&rft.au=Zhang%2C+Xiong&rft.au=Fan%2C+Hui-Hui&rft.au=Wang%2C+Xiao-Shuang&rft.date=2019-12-01&rft.pub=American+Institute+of+Nutrition&rft.issn=0022-3166&rft.eissn=1541-6100&rft.volume=149&rft.issue=12&rft.spage=2110&rft_id=info:doi/10.1093%2Fjn%2Fnxz199&rft.externalDBID=NO_FULL_TEXT |
| thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=0022-3166&client=summon |
| thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=0022-3166&client=summon |
| thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=0022-3166&client=summon |