PARP-1 Inhibits Glycolysis in Ischemic Kidneys
After ischemic renal injury (IRI), selective damage occurs in the S(3) segments of the proximal tubules as a result of inhibition of glycolysis, but the mechanism of this inhibition is unknown. We previously reported that inhibition of poly(ADP-ribose) polymerase-1 (PARP-1) activity protects against...
Saved in:
| Published in | Journal of the American Society of Nephrology Vol. 20; no. 1; pp. 95 - 103 |
|---|---|
| Main Authors | , |
| Format | Journal Article |
| Language | English |
| Published |
Washington, DC
American Society of Nephrology
01.01.2009
|
| Subjects | |
| Online Access | Get full text |
| ISSN | 1046-6673 1533-3450 1533-3450 |
| DOI | 10.1681/ASN.2008030325 |
Cover
| Abstract | After ischemic renal injury (IRI), selective damage occurs in the S(3) segments of the proximal tubules as a result of inhibition of glycolysis, but the mechanism of this inhibition is unknown. We previously reported that inhibition of poly(ADP-ribose) polymerase-1 (PARP-1) activity protects against ischemia-induced necrosis in proximal tubules by preserving ATP levels. Here, we tested whether PARP-1 activation in proximal tubules after IRI leads to poly(ADP-ribosyl)ation of the key glycolytic enzyme glyceraldehyde-3-phosphate dehydrogenase (GAPDH), a modification that inhibits its activity. Using in vitro and in vivo models, under hypoxic conditions, we detected poly(ADP-ribosyl)ation and reduced activity of GAPDH; inhibition of PARP-1 activity restored GAPDH activity and ATP levels. Inhibition of GAPDH with iodoacetate exacerbated ATP depletion, cytotoxicity, and necrotic cell death of LLCPK(1) cells subjected to hypoxic conditions, whereas inhibition of PARP-1 activity was cytoprotective. In conclusion, these data indicate that poly(ADP-ribosyl)ation of GAPDH and the subsequent inhibition of anaerobic respiration exacerbate ATP depletion selectively in the proximal tubule after IRI. |
|---|---|
| AbstractList | After ischemic renal injury (IRI), selective damage occurs in the S(3) segments of the proximal tubules as a result of inhibition of glycolysis, but the mechanism of this inhibition is unknown. We previously reported that inhibition of poly(ADP-ribose) polymerase-1 (PARP-1) activity protects against ischemia-induced necrosis in proximal tubules by preserving ATP levels. Here, we tested whether PARP-1 activation in proximal tubules after IRI leads to poly(ADP-ribosyl)ation of the key glycolytic enzyme glyceraldehyde-3-phosphate dehydrogenase (GAPDH), a modification that inhibits its activity. Using in vitro and in vivo models, under hypoxic conditions, we detected poly(ADP-ribosyl)ation and reduced activity of GAPDH; inhibition of PARP-1 activity restored GAPDH activity and ATP levels. Inhibition of GAPDH with iodoacetate exacerbated ATP depletion, cytotoxicity, and necrotic cell death of LLCPK(1) cells subjected to hypoxic conditions, whereas inhibition of PARP-1 activity was cytoprotective. In conclusion, these data indicate that poly(ADP-ribosyl)ation of GAPDH and the subsequent inhibition of anaerobic respiration exacerbate ATP depletion selectively in the proximal tubule after IRI.After ischemic renal injury (IRI), selective damage occurs in the S(3) segments of the proximal tubules as a result of inhibition of glycolysis, but the mechanism of this inhibition is unknown. We previously reported that inhibition of poly(ADP-ribose) polymerase-1 (PARP-1) activity protects against ischemia-induced necrosis in proximal tubules by preserving ATP levels. Here, we tested whether PARP-1 activation in proximal tubules after IRI leads to poly(ADP-ribosyl)ation of the key glycolytic enzyme glyceraldehyde-3-phosphate dehydrogenase (GAPDH), a modification that inhibits its activity. Using in vitro and in vivo models, under hypoxic conditions, we detected poly(ADP-ribosyl)ation and reduced activity of GAPDH; inhibition of PARP-1 activity restored GAPDH activity and ATP levels. Inhibition of GAPDH with iodoacetate exacerbated ATP depletion, cytotoxicity, and necrotic cell death of LLCPK(1) cells subjected to hypoxic conditions, whereas inhibition of PARP-1 activity was cytoprotective. In conclusion, these data indicate that poly(ADP-ribosyl)ation of GAPDH and the subsequent inhibition of anaerobic respiration exacerbate ATP depletion selectively in the proximal tubule after IRI. After ischemic renal injury (IRI), selective damage occurs in the S(3) segments of the proximal tubules as a result of inhibition of glycolysis, but the mechanism of this inhibition is unknown. We previously reported that inhibition of poly(ADP-ribose) polymerase-1 (PARP-1) activity protects against ischemia-induced necrosis in proximal tubules by preserving ATP levels. Here, we tested whether PARP-1 activation in proximal tubules after IRI leads to poly(ADP-ribosyl)ation of the key glycolytic enzyme glyceraldehyde-3-phosphate dehydrogenase (GAPDH), a modification that inhibits its activity. Using in vitro and in vivo models, under hypoxic conditions, we detected poly(ADP-ribosyl)ation and reduced activity of GAPDH; inhibition of PARP-1 activity restored GAPDH activity and ATP levels. Inhibition of GAPDH with iodoacetate exacerbated ATP depletion, cytotoxicity, and necrotic cell death of LLCPK(1) cells subjected to hypoxic conditions, whereas inhibition of PARP-1 activity was cytoprotective. In conclusion, these data indicate that poly(ADP-ribosyl)ation of GAPDH and the subsequent inhibition of anaerobic respiration exacerbate ATP depletion selectively in the proximal tubule after IRI. After ischemic renal injury (IRI), selective damage occurs in the S 3 segments of the proximal tubules as a result of inhibition of glycolysis, but the mechanism of this inhibition is unknown. We previously reported that inhibition of poly(ADP-ribose) polymerase-1 (PARP-1) activity protects against ischemia-induced necrosis in proximal tubules by preserving ATP levels. Here, we tested whether PARP-1 activation in proximal tubules after IRI leads to poly(ADP-ribosyl)ation of the key glycolytic enzyme glyceraldehyde-3-phosphate dehydrogenase (GAPDH), a modification that inhibits its activity. Using in vitro and in vivo models, under hypoxic conditions, we detected poly(ADP-ribosyl)ation and reduced activity of GAPDH; inhibition of PARP-1 activity restored GAPDH activity and ATP levels. Inhibition of GAPDH with iodoacetate exacerbated ATP depletion, cytotoxicity, and necrotic cell death of LLCPK 1 cells subjected to hypoxic conditions, whereas inhibition of PARP-1 activity was cytoprotective. In conclusion, these data indicate that poly(ADP-ribosyl)ation of GAPDH and the subsequent inhibition of anaerobic respiration exacerbate ATP depletion selectively in the proximal tubule after IRI. |
| Author | Devalaraja-Narashimha, Kishor Padanilam, Babu J. |
| AuthorAffiliation | Department of Cellular and Integrative Physiology and † Department of Internal Medicine, Section of Nephrology, University of Nebraska Medical Center, Omaha, Nebraska |
| AuthorAffiliation_xml | – name: Department of Cellular and Integrative Physiology and † Department of Internal Medicine, Section of Nephrology, University of Nebraska Medical Center, Omaha, Nebraska |
| Author_xml | – sequence: 1 givenname: Kishor surname: Devalaraja-Narashimha fullname: Devalaraja-Narashimha, Kishor – sequence: 2 givenname: Babu J. surname: Padanilam fullname: Padanilam, Babu J. |
| BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=21036734$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/19056868$$D View this record in MEDLINE/PubMed |
| BookMark | eNp1kc9PwjAcxRuDEUGvHs0ueht-u_7aLiaEKBKJEn-cm1I6qRkdrsNk_70lIKiJpzbp572XvtdBLVc6g9AZhh7mKb7qPz_0EoAUCJCEHaBjzAiJCWXQCnegPOZckDbqeP8OgFkixBFq4wwYT3l6jHqT_tMkxtHIze3U1j4aFo0ui8ZbH1kXjbyem4XV0b2dOdP4E3SYq8Kb0-3ZRa-3Ny-Du3j8OBwN-uNY05TWId-QTAnCgGcqnaWUTRkHoDORkZxjwVTOwGSZ4gkzhBmqYAra5EaoBBKOSRddb3yXq-nCzLRxdaUKuazsQlWNLJWVv1-cncu38lMGMROhiy663BpU5cfK-FourNemKJQz5crL0EqWMkEDeP4zaRfxXVEALraA8loVeaWctn7HJRhIaHht1Ntwuiq9r0y-twK53kqGreR-qyCgfwTa1qq25fpHtvhP9gUYHJSM |
| CODEN | JASNEU |
| CitedBy_id | crossref_primary_10_1097_SLA_0b013e31828cced3 crossref_primary_10_1155_2013_486574 crossref_primary_10_1152_physrev_00029_2022 crossref_primary_10_1152_ajprenal_00144_2023 crossref_primary_10_1152_ajprenal_00239_2009 crossref_primary_10_1152_ajprenal_00275_2023 crossref_primary_10_1016_j_cellsig_2010_08_003 crossref_primary_10_1016_j_bbagen_2013_11_007 crossref_primary_10_3390_v16060910 crossref_primary_10_1016_j_jneumeth_2012_06_020 crossref_primary_10_1681_ASN_2013121270 crossref_primary_10_1016_j_kint_2019_02_009 crossref_primary_10_1038_srep06952 crossref_primary_10_1152_physrev_00001_2017 crossref_primary_10_1152_ajprenal_00271_2014 crossref_primary_10_1253_circj_CJ_15_0230 crossref_primary_10_1038_nrneph_2017_5 crossref_primary_10_1681_ASN_2012121169 crossref_primary_10_1016_j_kint_2019_10_020 crossref_primary_10_1073_pnas_1305538110 crossref_primary_10_1016_j_jss_2014_01_020 crossref_primary_10_3390_pharmaceutics12050416 crossref_primary_10_3390_app12125998 crossref_primary_10_3389_fonc_2022_979683 crossref_primary_10_1172_jci_insight_123151 crossref_primary_10_1155_2014_967826 crossref_primary_10_1152_ajprenal_00561_2015 crossref_primary_10_1016_j_celrep_2014_08_036 crossref_primary_10_1097_SHK_0b013e3181e7e9ba crossref_primary_10_1016_j_abb_2011_11_005 crossref_primary_10_1016_j_chembiol_2020_03_016 crossref_primary_10_1134_S0006297917060013 crossref_primary_10_1007_s12177_012_9085_y crossref_primary_10_1681_ASN_2015080870 crossref_primary_10_1016_j_bbadis_2017_03_012 crossref_primary_10_1681_ASN_2012070678 crossref_primary_10_1016_j_freeradbiomed_2016_02_024 crossref_primary_10_1111_jcmm_14285 crossref_primary_10_3233_JAD_151040 crossref_primary_10_3390_ijms23137292 crossref_primary_10_3390_biology7010010 crossref_primary_10_23876_j_krcp_2018_37_3_185 crossref_primary_10_1101_gad_334284_119 crossref_primary_10_1007_s00018_016_2202_5 crossref_primary_10_1016_j_semnephrol_2016_03_002 crossref_primary_10_1152_ajpendo_00328_2016 crossref_primary_10_5115_acb_2016_49_2_79 crossref_primary_10_1016_j_ijbiomac_2019_10_174 crossref_primary_10_1016_j_tem_2015_09_012 crossref_primary_10_1038_ki_2012_64 crossref_primary_10_3389_fmed_2020_00065 crossref_primary_10_1186_1477_5956_8_22 crossref_primary_10_1016_j_kint_2015_10_008 crossref_primary_10_1152_ajprenal_00459_2014 crossref_primary_10_1042_BSR20171313 |
| ContentType | Journal Article |
| Copyright | 2009 INIST-CNRS Copyright © 2009 by the American Society of Nephrology |
| Copyright_xml | – notice: 2009 INIST-CNRS – notice: Copyright © 2009 by the American Society of Nephrology |
| DBID | AAYXX CITATION IQODW CGR CUY CVF ECM EIF NPM 7X8 5PM |
| DOI | 10.1681/ASN.2008030325 |
| DatabaseName | CrossRef Pascal-Francis Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed MEDLINE - Academic PubMed Central (Full Participant titles) |
| DatabaseTitle | CrossRef MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) MEDLINE - Academic |
| DatabaseTitleList | 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 |
| DeliveryMethod | fulltext_linktorsrc |
| Discipline | Medicine |
| EISSN | 1533-3450 |
| EndPage | 103 |
| ExternalDocumentID | PMC2615730 19056868 21036734 10_1681_ASN_2008030325 |
| Genre | Research Support, Non-U.S. Gov't Journal Article |
| GroupedDBID | --- .55 .GJ 0R~ 18M 29L 2WC 34G 39C 53G 5GY 5RE 5VS 6PF AAQQT AAUIN AAWTL AAYXX ABBLC ABJNI ABOCM ABXYN ACGFO ACLDA ACZKN ADBBV AENEX AFEXH AFFNX AFNMH AHOMT AHQVU ALMA_UNASSIGNED_HOLDINGS BAWUL BTFSW BYPQX CITATION CS3 DIK DU5 E3Z EBS EJD ERAAH F5P GX1 H13 HYE HZ~ K-O KQ8 O9- OK1 OVD P0W P2P RHI RPM TEORI TNP TR2 W8F X7M XVB YFH ZGI IQODW ACIJW CGR CUY CVF ECM EIF NPM 7X8 5PM |
| ID | FETCH-LOGICAL-c484t-34e39a735069a8d845b56004d793f6175af50e99a625e35e4a0b0cefe7a202613 |
| ISSN | 1046-6673 1533-3450 |
| IngestDate | Thu Aug 21 18:32:18 EDT 2025 Fri Jul 11 03:16:46 EDT 2025 Thu Apr 03 06:58:12 EDT 2025 Mon Jul 21 09:13:53 EDT 2025 Tue Jul 01 00:49:52 EDT 2025 Thu Apr 24 23:12:45 EDT 2025 |
| IsDoiOpenAccess | false |
| IsOpenAccess | true |
| IsPeerReviewed | true |
| IsScholarly | true |
| Issue | 1 |
| Keywords | Nephrology Enzyme Transferases Glycosyltransferases Cardiovascular disease Kidney Urology NAD Urinary system Ischemia Glycolysis ADP-ribosyltransferase Inhibitor Pentosyltransferases |
| Language | English |
| License | CC BY 4.0 |
| LinkModel | OpenURL |
| MergedId | FETCHMERGED-LOGICAL-c484t-34e39a735069a8d845b56004d793f6175af50e99a625e35e4a0b0cefe7a202613 |
| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Supplemental information for this article is available at http://www.jasn.org/. Published online ahead of print. Publication date available at www.jasn.org. |
| OpenAccessLink | https://www.ncbi.nlm.nih.gov/pmc/articles/2615730 |
| PMID | 19056868 |
| PQID | 66798574 |
| PQPubID | 23479 |
| PageCount | 9 |
| ParticipantIDs | pubmedcentral_primary_oai_pubmedcentral_nih_gov_2615730 proquest_miscellaneous_66798574 pubmed_primary_19056868 pascalfrancis_primary_21036734 crossref_primary_10_1681_ASN_2008030325 crossref_citationtrail_10_1681_ASN_2008030325 |
| ProviderPackageCode | CITATION AAYXX |
| PublicationCentury | 2000 |
| PublicationDate | 2009-01-00 2009 2009-Jan 20090101 |
| PublicationDateYYYYMMDD | 2009-01-01 |
| PublicationDate_xml | – month: 01 year: 2009 text: 2009-01-00 |
| PublicationDecade | 2000 |
| PublicationPlace | Washington, DC |
| PublicationPlace_xml | – name: Washington, DC – name: United States |
| PublicationTitle | Journal of the American Society of Nephrology |
| PublicationTitleAlternate | J Am Soc Nephrol |
| PublicationYear | 2009 |
| Publisher | American Society of Nephrology |
| Publisher_xml | – name: American Society of Nephrology |
| References | 1512218 - J Biol Chem. 1992 Aug 25;267(24):16771-4 14678945 - Am J Physiol Renal Physiol. 2004 Apr;286(4):F803-9 18293416 - J Neurosci Res. 2008 Jun;86(8):1768-80 14551462 - Am J Nephrol. 2003 Nov-Dec;23(6):380-9 12004242 - Crit Care Med. 2002 May;30(5 Suppl):S235-40 1807913 - Contrib Nephrol. 1991;95:222-8 8558430 - J Pharmacol Exp Ther. 1996 Jan;276(1):194-205 10030664 - Oncogene. 1998 Dec 31;17(26):3401-15 11536009 - Cell Death Differ. 2001 Jun;8(6):588-94 8034046 - FEBS Lett. 1994 Jul 18;348(3):223-7 11251191 - Brain Res. 2001 Mar 16;894(2):181-8 3942135 - Am J Kidney Dis. 1986 Jan;7(1):76-83 7910173 - J Clin Invest. 1994 May;93(5):2175-88 3155867 - Radiat Res. 1985 Jan;101(1):4-15 10484526 - Am J Physiol. 1999 Sep;277(3 Pt 2):F428-36 9015404 - Cardiovasc Res. 1996 Dec;32(6):1016-23 682423 - Kidney Int. 1978 Jul;14(1):31-49 3953769 - Am J Pathol. 1986 Mar;122(3):462-8 11040379 - J Neurosci Methods. 2000 Jul 31;100(1-2):157-63 10494029 - Cell Physiol Biochem. 1999;9(3):150-72 11049868 - Am J Physiol Regul Integr Comp Physiol. 2000 Nov;279(5):R1834-40 9211321 - Methods Enzymol. 1997;280:255-65 9815122 - Am J Physiol. 1998 Nov;275(5 Pt 2):F623-31 14614022 - Clin Cancer Res. 2003 Nov 1;9(14):5370-9 3985159 - Am J Physiol. 1985 Apr;248(4 Pt 2):F522-6 8621564 - J Biol Chem. 1996 Apr 12;271(15):9129-34 17430886 - J Biol Chem. 2007 Jun 15;282(24):17845-54 10987849 - J Neurochem. 2000 Oct;75(4):1675-80 8161720 - J Am Soc Nephrol. 1994 Jan;4(7):1387-95 2770278 - J Surg Res. 1989 Sep;47(3):220-6 1409644 - Proc Natl Acad Sci U S A. 1992 Oct 15;89(20):9382-5 12138133 - J Am Soc Nephrol. 2002 Aug;13(8):2027-36 8510397 - Kidney Int. 1993 May;43(5):1160-78 11509754 - Toxicol Sci. 2001 Sep;63(1):143-8 3099216 - Nature. 1987 Jan 1-7;325(6099):78-81 16310767 - Eur J Pharmacol. 2005 Dec 19;527(1-3):163-71 9113237 - Adv Ren Replace Ther. 1997 Apr;4(2 Suppl 1):17-24 7925359 - Eur J Biochem. 1994 Sep 1;224(2):447-54 2375389 - Am J Physiol. 1990 Jul;259(1 Pt 2):F164-75 11316856 - J Am Soc Nephrol. 2001 May;12(5):973-82 15494543 - Am J Physiol Renal Physiol. 2005 Feb;288(2):F387-98 15911333 - Pharmacol Res. 2005 Jul;52(1):44-59 9822378 - Science. 1998 Nov 20;282(5393):1484-7 389705 - Biochem Soc Trans. 1979 Oct;7(5):1149-60 6465286 - Am J Pathol. 1984 Aug;116(2):253-61 2375390 - Am J Physiol. 1990 Jul;259(1 Pt 2):F176-85 8627159 - J Exp Med. 1996 Feb 1;183(2):463-71 7246739 - Am J Physiol. 1981 Jun;240(6):F492-500 14523042 - J Clin Invest. 2003 Oct;112(7):1049-57 |
| References_xml | – reference: 682423 - Kidney Int. 1978 Jul;14(1):31-49 – reference: 7246739 - Am J Physiol. 1981 Jun;240(6):F492-500 – reference: 11509754 - Toxicol Sci. 2001 Sep;63(1):143-8 – reference: 16310767 - Eur J Pharmacol. 2005 Dec 19;527(1-3):163-71 – reference: 7910173 - J Clin Invest. 1994 May;93(5):2175-88 – reference: 8034046 - FEBS Lett. 1994 Jul 18;348(3):223-7 – reference: 2375390 - Am J Physiol. 1990 Jul;259(1 Pt 2):F176-85 – reference: 12004242 - Crit Care Med. 2002 May;30(5 Suppl):S235-40 – reference: 11316856 - J Am Soc Nephrol. 2001 May;12(5):973-82 – reference: 12138133 - J Am Soc Nephrol. 2002 Aug;13(8):2027-36 – reference: 6465286 - Am J Pathol. 1984 Aug;116(2):253-61 – reference: 10484526 - Am J Physiol. 1999 Sep;277(3 Pt 2):F428-36 – reference: 10494029 - Cell Physiol Biochem. 1999;9(3):150-72 – reference: 15494543 - Am J Physiol Renal Physiol. 2005 Feb;288(2):F387-98 – reference: 11049868 - Am J Physiol Regul Integr Comp Physiol. 2000 Nov;279(5):R1834-40 – reference: 11251191 - Brain Res. 2001 Mar 16;894(2):181-8 – reference: 14678945 - Am J Physiol Renal Physiol. 2004 Apr;286(4):F803-9 – reference: 1807913 - Contrib Nephrol. 1991;95:222-8 – reference: 8627159 - J Exp Med. 1996 Feb 1;183(2):463-71 – reference: 8510397 - Kidney Int. 1993 May;43(5):1160-78 – reference: 10030664 - Oncogene. 1998 Dec 31;17(26):3401-15 – reference: 389705 - Biochem Soc Trans. 1979 Oct;7(5):1149-60 – reference: 14614022 - Clin Cancer Res. 2003 Nov 1;9(14):5370-9 – reference: 3099216 - Nature. 1987 Jan 1-7;325(6099):78-81 – reference: 9211321 - Methods Enzymol. 1997;280:255-65 – reference: 9015404 - Cardiovasc Res. 1996 Dec;32(6):1016-23 – reference: 9113237 - Adv Ren Replace Ther. 1997 Apr;4(2 Suppl 1):17-24 – reference: 3953769 - Am J Pathol. 1986 Mar;122(3):462-8 – reference: 8161720 - J Am Soc Nephrol. 1994 Jan;4(7):1387-95 – reference: 3985159 - Am J Physiol. 1985 Apr;248(4 Pt 2):F522-6 – reference: 1409644 - Proc Natl Acad Sci U S A. 1992 Oct 15;89(20):9382-5 – reference: 3942135 - Am J Kidney Dis. 1986 Jan;7(1):76-83 – reference: 8621564 - J Biol Chem. 1996 Apr 12;271(15):9129-34 – reference: 11536009 - Cell Death Differ. 2001 Jun;8(6):588-94 – reference: 7925359 - Eur J Biochem. 1994 Sep 1;224(2):447-54 – reference: 14523042 - J Clin Invest. 2003 Oct;112(7):1049-57 – reference: 9815122 - Am J Physiol. 1998 Nov;275(5 Pt 2):F623-31 – reference: 17430886 - J Biol Chem. 2007 Jun 15;282(24):17845-54 – reference: 3155867 - Radiat Res. 1985 Jan;101(1):4-15 – reference: 2770278 - J Surg Res. 1989 Sep;47(3):220-6 – reference: 11040379 - J Neurosci Methods. 2000 Jul 31;100(1-2):157-63 – reference: 1512218 - J Biol Chem. 1992 Aug 25;267(24):16771-4 – reference: 10987849 - J Neurochem. 2000 Oct;75(4):1675-80 – reference: 8558430 - J Pharmacol Exp Ther. 1996 Jan;276(1):194-205 – reference: 2375389 - Am J Physiol. 1990 Jul;259(1 Pt 2):F164-75 – reference: 18293416 - J Neurosci Res. 2008 Jun;86(8):1768-80 – reference: 9822378 - Science. 1998 Nov 20;282(5393):1484-7 – reference: 14551462 - Am J Nephrol. 2003 Nov-Dec;23(6):380-9 – reference: 15911333 - Pharmacol Res. 2005 Jul;52(1):44-59 |
| SSID | ssj0015277 |
| Score | 2.221706 |
| Snippet | After ischemic renal injury (IRI), selective damage occurs in the S(3) segments of the proximal tubules as a result of inhibition of glycolysis, but the... After ischemic renal injury (IRI), selective damage occurs in the S 3 segments of the proximal tubules as a result of inhibition of glycolysis, but the... |
| SourceID | pubmedcentral proquest pubmed pascalfrancis crossref |
| SourceType | Open Access Repository Aggregation Database Index Database Enrichment Source |
| StartPage | 95 |
| SubjectTerms | Adenosine Triphosphate - analysis Adenosine Triphosphate - biosynthesis Animals Basic Research Biological and medical sciences Cell Hypoxia Glyceraldehyde-3-Phosphate Dehydrogenases - metabolism Glycolysis Ischemia - metabolism Kidney - blood supply Kidney - metabolism LLC-PK1 Cells Medical sciences Mice Nephrology. Urinary tract diseases Poly (ADP-Ribose) Polymerase-1 Poly(ADP-ribose) Polymerase Inhibitors Poly(ADP-ribose) Polymerases - physiology Swine |
| Title | PARP-1 Inhibits Glycolysis in Ischemic Kidneys |
| URI | https://www.ncbi.nlm.nih.gov/pubmed/19056868 https://www.proquest.com/docview/66798574 https://pubmed.ncbi.nlm.nih.gov/PMC2615730 |
| Volume | 20 |
| hasFullText | 1 |
| inHoldings | 1 |
| isFullTextHit | |
| isPrint | |
| link | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV3db9MwELdgSAgJTXyODhh5QOIBeaSNPx8tNtaOtar2gfoWOY6jRprSibYP8NdzjvPR7EMMXtIoPcXW_S7nO9_5DqGPps-YlsJgBu4HJiS0OCGpi7nKSIBBoGXmIrrjCRtekOMZnbU9W8vTJatk3_y-9VzJ_6AKzwBXd0r2H5BtXgoP4B7whSsgDNd7YTxVp1Pch298nicuAHB0-QtwLWuM5MXnETiuZer79zwtALA77NCNsyVFk8Tp9hEs4NzZdD84_KFO1Kk6VngCP2fD0XioSk2RL-eLJst3qg7UZHSixj6ekayr0FO9t9DqrnsM6_UluNfYdQ7dVKiD8IbgeO3o22lW62y_rG1wU4Uz4VS4XpbFaQXooGhA28WqDtBfW8OazELwYCOYDnmIHg04Y66nxdGsSfpxPXy5r0_hp12V8YQxv3RH7JgpT6_0Er6YzLc6uc0XuZ5Su2GjnD9D2xWogfKS8hw9sMUL9HhcpU-8RPteYIJaYIJWYIK8CGqBCSqBeYUuvh2efx3iqmEGNkSQFY6IjaTmEQ2Z1CIVhCbOoCUpKOEMTFWqMxpaKTU4vTailugwCY3NLNcD54tHr9FWsSjsGxQYmbIwESmjhhNNmZBhFvEE7DluuDFJD-GaP7Gpqsm7piaXsfMqgZ-xOpvELT976FNDf-XrqNxJuddhd0NeQ9tDH2r-x6ALXYBLF3axXsbMhRQpB4odj0Y7lARDXzDRQ7yDU0Pgqqx3_ynyeVltHfhCYRnc_du03qInPtLotufeoa3Vz7V9DwbrKtkrZfAPv1-Slw |
| linkProvider | Geneva Foundation for Medical Education and Research |
| 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=PARP-1+Inhibits+Glycolysis+in+Ischemic+Kidneys&rft.jtitle=Journal+of+the+American+Society+of+Nephrology&rft.au=DEVALARAJA-NARASHIMHA%2C+Kishor&rft.au=PADANILAM%2C+Babu+J&rft.date=2009&rft.pub=American+Society+of+Nephrology&rft.issn=1046-6673&rft.volume=20&rft.issue=1&rft.spage=95&rft.epage=103&rft_id=info:doi/10.1681%2Fasn.2008030325&rft.externalDBID=n%2Fa&rft.externalDocID=21036734 |
| thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=1046-6673&client=summon |
| thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=1046-6673&client=summon |
| thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=1046-6673&client=summon |