دورية أكاديمية
Tcf19 is a novel islet factor necessary for proliferation and survival in the INS-1 β-cell line.
| العنوان: | Tcf19 is a novel islet factor necessary for proliferation and survival in the INS-1 β-cell line. |
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| المؤلفون: | Krautkramer KA; Department of Medicine, Division of Endocrinology, Diabetes, and Metabolism, University of Wisconsin, Madison, Wisconsin;, Linnemann AK, Fontaine DA, Whillock AL, Harris TW, Schleis GJ, Truchan NA, Marty-Santos L, Lavine JA, Cleaver O, Kimple ME, Davis DB |
| المصدر: | American journal of physiology. Endocrinology and metabolism [Am J Physiol Endocrinol Metab] 2013 Sep 01; Vol. 305 (5), pp. E600-10. Date of Electronic Publication: 2013 Jul 16. |
| نوع المنشور: | Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't |
| اللغة: | English |
| بيانات الدورية: | Publisher: American Physiological Society Country of Publication: United States NLM ID: 100901226 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1522-1555 (Electronic) Linking ISSN: 01931849 NLM ISO Abbreviation: Am J Physiol Endocrinol Metab Subsets: MEDLINE |
| أسماء مطبوعة: | Original Publication: Bethesda, MD. : American Physiological Society |
| مواضيع طبية MeSH: | Cell Cycle/*physiology , Diabetes Mellitus/*metabolism , Endoplasmic Reticulum Stress/*physiology , Insulin-Secreting Cells/*metabolism , Transcription Factors/*metabolism, Animals ; Cell Cycle/genetics ; Cell Line, Tumor ; Cell Survival/physiology ; Diabetes Mellitus/genetics ; Diabetes Mellitus/pathology ; Humans ; In Situ Hybridization ; Male ; Mice ; Mice, Inbred C57BL ; RNA/chemistry ; RNA/genetics ; RNA, Small Interfering/pharmacology ; Real-Time Polymerase Chain Reaction ; Transcription Factors/biosynthesis ; Transcription Factors/genetics |
| مستخلص: | Recently, a novel type 1 diabetes association locus was identified at human chromosome 6p31.3, and transcription factor 19 (TCF19) is a likely causal gene. Little is known about Tcf19, and we now show that it plays a role in both proliferation and apoptosis in insulinoma cells. Tcf19 is expressed in mouse and human islets, with increasing mRNA expression in nondiabetic obesity. The expression of Tcf19 is correlated with β-cell mass expansion, suggesting that it may be a transcriptional regulator of β-cell mass. Increasing proliferation and decreasing apoptotic cell death are two strategies to increase pancreatic β-cell mass and prevent or delay diabetes. siRNA-mediated knockdown of Tcf19 in the INS-1 insulinoma cell line, a β-cell model, results in a decrease in proliferation and an increase in apoptosis. There was a significant reduction in the expression of numerous cell cycle genes from the late G1 phase through the M phase, and cells were arrested at the G1/S checkpoint. We also observed increased apoptosis and susceptibility to endoplasmic reticulum (ER) stress after Tcf19 knockdown. There was a reduction in expression of genes important for the maintenance of ER homeostasis (Bip, p58(IPK), Edem1, and calreticulin) and an increase in proapoptotic genes (Bim, Bid, Nix, Gadd34, and Pdia2). Therefore, Tcf19 is necessary for both proliferation and survival and is a novel regulator of these pathways. |
| References: | Dev Dyn. 2012 May;241(5):1008-19. (PMID: 22434763) Mol Endocrinol. 2013 Jan;27(1):162-71. (PMID: 23204325) Proc Natl Acad Sci U S A. 2010 May 18;107(20):9035-42. (PMID: 20418503) Mol Endocrinol. 2010 Sep;24(9):1822-34. (PMID: 20660304) Mol Cell. 1999 Sep;4(3):387-94. (PMID: 10518219) Diabetes. 2010 Dec;59(12):3131-8. (PMID: 20876711) J Biol Chem. 2011 Jan 14;286(2):1292-300. (PMID: 21062743) J Mol Endocrinol. 2007 Feb;38(1-2):193-206. (PMID: 17293440) J Biol Chem. 2007 Jan 26;282(4):2450-5. (PMID: 17142463) Surv Synth Pathol Res. 1985;4(2):110-25. (PMID: 3901180) Nucleic Acids Res. 2004 Jan 1;32(Database issue):D552-6. (PMID: 14681479) Diabetologia. 2007 Apr;50(4):752-63. (PMID: 17268797) Electrophoresis. 2009 Jun;30(11):1845-55. (PMID: 19517440) Genome Biol. 2009;10(11):R130. (PMID: 19919682) FEBS Lett. 2007 Jul 31;581(19):3658-64. (PMID: 17499246) Diabetologia. 2007 May;50(5):1006-14. (PMID: 17333111) Mol Cell Proteomics. 2008 Aug;7(8):1434-51. (PMID: 18448419) Anal Biochem. 1976 May 7;72:248-54. (PMID: 942051) Exp Diabetes Res. 2012;2012:618396. (PMID: 21915177) Diabetologia. 2010 Sep;53(9):2020-8. (PMID: 20532863) Diabetes. 2008 Oct;57(10):2718-27. (PMID: 18599523) J Biol Chem. 2012 Jan 2;287(1):43-47. (PMID: 22105075) Adv Exp Med Biol. 2010;654:447-62. (PMID: 20217509) Diabetes. 2008 Sep;57(9):2371-81. (PMID: 18544709) Annu Rev Biochem. 2000;69:69-93. (PMID: 10966453) Diabetes. 2005 Apr;54(4):1074-81. (PMID: 15793246) Diabetes. 2011 May;60(5):1370-9. (PMID: 21525508) Dev Dyn. 2008 Nov;237(11):3270-9. (PMID: 18924236) FASEB J. 2003 Aug;17(11):1573-5. (PMID: 12824288) Diabetes. 1995 Mar;44(3):249-56. (PMID: 7883109) Mol Cell Biol. 2003 Feb;23(4):1292-303. (PMID: 12556489) J Clin Invest. 2010 Nov;120(11):4031-9. (PMID: 20978346) J Biol Chem. 2009 Mar 13;284(11):6661-73. (PMID: 19131336) Science. 2004 Dec 24;306(5705):2255-7. (PMID: 15618518) Science. 2003 Feb 28;299(5611):1397-400. (PMID: 12610306) J Cell Sci. 2000 Dec;113 Pt 23:4143-9. (PMID: 11069759) Cell Growth Differ. 1991 Apr;2(4):179-86. (PMID: 1868030) Endocr Rev. 2008 Feb;29(1):42-61. (PMID: 18048764) J Diabetes. 2011 Mar;3(1):48-57. (PMID: 21073664) EMBO Rep. 2010 Jan;11(1):45-51. (PMID: 20010802) Endocrinology. 2010 Apr;151(4):1462-72. (PMID: 20176718) Endocrinology. 2010 Aug;151(8):3577-88. (PMID: 20534724) Cell Death Differ. 2006 Mar;13(3):374-84. (PMID: 16397578) Hum Genet. 2011 Feb;129(2):161-76. (PMID: 21076979) Science. 2003 Feb 28;299(5611):1394-7. (PMID: 12610305) Autophagy. 2009 Jul;5(5):690-8. (PMID: 19363302) J Biol Chem. 2009 Feb 20;284(8):5289-98. (PMID: 19103594) J Cell Biol. 2001 May 28;153(5):1011-22. (PMID: 11381086) Nat Neurosci. 2010 Jun;13(6):767-75. (PMID: 20436479) Mol Cell. 2009 Jun 12;34(5):627-33. (PMID: 19524542) Diabetes Obes Metab. 2010 Oct;12 Suppl 2:48-57. (PMID: 21029300) Mol Cell Biol. 2008 May;28(10):3465-76. (PMID: 18347054) Genome Res. 2008 May;18(5):706-16. (PMID: 18347327) Diabetes. 2003 Jan;52(1):102-10. (PMID: 12502499) |
| معلومات مُعتمدة: | 3R01-DK-079862-S1 United States DK NIDDK NIH HHS; T32GM08692 United States GM NIGMS NIH HHS; UL1TR0000427 United States TR NCATS NIH HHS; 5-R01-DK-079862 United States DK NIDDK NIH HHS; UL1 TR000427 United States TR NCATS NIH HHS; F31-DK-092098 United States DK NIDDK NIH HHS; K08-DK-083442 United States DK NIDDK NIH HHS; T32 GM008692 United States GM NIGMS NIH HHS; K08 DK083442 United States DK NIDDK NIH HHS |
| فهرسة مساهمة: | Keywords: apoptosis; diabetes; endoplasmic reticulum stress; islet; proliferation; transcription; transcription factor 19; β-cell |
| المشرفين على المادة: | 0 (RNA, Small Interfering) 0 (TCF19 protein, human) 0 (Transcription Factors) 63231-63-0 (RNA) |
| تواريخ الأحداث: | Date Created: 20130718 Date Completed: 20140228 Latest Revision: 20211021 |
| رمز التحديث: | 20221213 |
| مُعرف محوري في PubMed: | PMC3761170 |
| DOI: | 10.1152/ajpendo.00147.2013 |
| PMID: | 23860123 |
| قاعدة البيانات: | MEDLINE |
| تدمد: | 1522-1555 |
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| DOI: | 10.1152/ajpendo.00147.2013 |