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Rev Diabet Stud. 2007 Fall;4(3):147-58. doi: 10.1900/RDS.2007.4.147. Epub 2007 Nov 10.
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本文引用的文献

1
The emerging role of FOXO transcription factors in pancreatic beta cells.FOXO转录因子在胰腺β细胞中的新作用。
J Endocrinol. 2007 May;193(2):195-207. doi: 10.1677/JOE-06-0191.
2
The role of arachidonic acid and its metabolites in insulin secretion from human islets of langerhans.花生四烯酸及其代谢产物在人胰岛胰岛素分泌中的作用。
Diabetes. 2007 Jan;56(1):197-203. doi: 10.2337/db06-0490.
3
Tip60-dependent acetylation of p53 modulates the decision between cell-cycle arrest and apoptosis.依赖Tip60的p53乙酰化作用调节细胞周期停滞与凋亡之间的抉择。
Mol Cell. 2006 Dec 28;24(6):827-39. doi: 10.1016/j.molcel.2006.11.021.
4
Cellular functions of TIP60.TIP60的细胞功能
Int J Biochem Cell Biol. 2006;38(9):1496-509. doi: 10.1016/j.biocel.2006.03.003. Epub 2006 Mar 28.
5
Histone acetylation by Trrap-Tip60 modulates loading of repair proteins and repair of DNA double-strand breaks.由Trrap-Tip60介导的组蛋白乙酰化作用可调节修复蛋白的加载以及DNA双链断裂的修复。
Nat Cell Biol. 2006 Jan;8(1):91-9. doi: 10.1038/ncb1343. Epub 2005 Dec 11.
6
A role for the Tip60 histone acetyltransferase in the acetylation and activation of ATM.Tip60组蛋白乙酰转移酶在ATM的乙酰化和激活过程中的作用。
Proc Natl Acad Sci U S A. 2005 Sep 13;102(37):13182-7. doi: 10.1073/pnas.0504211102. Epub 2005 Sep 2.
7
cPLA2-interacting protein, PLIP, causes apoptosis and decreases G1 phase in mesangial cells.
Am J Physiol Renal Physiol. 2006 Jan;290(1):F70-9. doi: 10.1152/ajprenal.00358.2004. Epub 2005 Jun 28.
8
NKX6 transcription factor activity is required for alpha- and beta-cell development in the pancreas.NKX6转录因子活性是胰腺中α细胞和β细胞发育所必需的。
Development. 2005 Jul;132(13):3139-49. doi: 10.1242/dev.01875.
9
Minireview: transcriptional regulation in pancreatic development.小型综述:胰腺发育中的转录调控
Endocrinology. 2005 Mar;146(3):1025-34. doi: 10.1210/en.2004-1576. Epub 2004 Dec 16.
10
Acetylation by Tip60 is required for selective histone variant exchange at DNA lesions.Tip60介导的乙酰化作用是DNA损伤处组蛋白变体选择性交换所必需的。
Science. 2004 Dec 17;306(5704):2084-7. doi: 10.1126/science.1103455. Epub 2004 Nov 4.

糖尿病KKAy小鼠和非糖尿病C57BL野生型小鼠中与cPLA2α相互作用的TIP60的表达分析:瞬时和稳定过表达TIP60对胰腺β细胞葡萄糖刺激的胰岛素分泌无影响。

Expression Analysis of cPLA2 Alpha Interacting TIP60 in Diabetic KKAy and Non-Diabetic C57BL Wild-Type Mice: No Impact of Transient and Stable TIP60 Overexpression on Glucose-Stimulated Insulin Secretion in Pancreatic Beta-Cells.

作者信息

Nordentoft Iver, Jeppesen Per B, Nielsen Anders L, Jorgensen Poul, Hermansen Kjeld

机构信息

Department of Endocrinology and Metabolism C, Aarhus Sygehus THG, Aarhus University Hospital, Tage-Hansens Gade 2, DK-8000 Aarhus C, Denmark.

出版信息

Rev Diabet Stud. 2007 Fall;4(3):147-58. doi: 10.1900/RDS.2007.4.147. Epub 2007 Nov 10.

DOI:10.1900/RDS.2007.4.147
PMID:18084672
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2174065/
Abstract

UNLABELLED

In the present study we investigate the expression levels of cytosolic phospholipase A2 alpha (cPLA2alpha) interacting histone acetyl transferase proteins TIP60alpha and TIP60beta in non-diabetic C57BL wild-type mice and obese type 2 diabetic KKAy model mice. The aim was to test our hypothesis that TIP60 plays a regulatory role in glucose-stimulated insulin secretion from pancreatic beta-cells.

MATERIAL AND METHODS

Ten obese diabetic KKAy mice and ten non-diabetic C57BL mice were fed a standard chow diet. After nine weeks, islet RNA was purified and used to measure TIP60 expression. We investigated the effect of TIP60alpha and TIP60beta on glucose-stimulated insulin secretion by transient and stable overexpression in the pancreatic mouse beta-cell line MIN6 and the rat beta-cell line INS-1E.

RESULTS

We found that non-diabetic C57BL mice and diabetic KKAy mice have the same level of both the alpha and beta splice forms of TIP60. Furthermore, we demonstrated that transient and stable expression of TIP60 in INS-1E cells affects neither glucose-stimulated insulin secretion, insulin output nor cell insulin content. Also susceptibility to developing gluco-toxicity was unaffected.

CONCLUSION

TIP60 over-expression does not affect glucose stimulated insulin secretion, insulin content or abnormal beta-cell function during glucotoxicity.

摘要

未标记

在本研究中,我们调查了非糖尿病C57BL野生型小鼠和肥胖2型糖尿病KKAy模型小鼠中,胞质磷脂酶A2α(cPLA2α)相互作用的组蛋白乙酰转移酶蛋白TIP60α和TIP60β的表达水平。目的是检验我们的假设,即TIP60在胰腺β细胞的葡萄糖刺激胰岛素分泌中起调节作用。

材料与方法

给10只肥胖糖尿病KKAy小鼠和10只非糖尿病C57BL小鼠喂食标准普通饲料。9周后,纯化胰岛RNA并用于测量TIP60表达。我们通过在小鼠胰腺β细胞系MIN6和大鼠β细胞系INS-1E中瞬时和稳定过表达,研究了TIP60α和TIP60β对葡萄糖刺激胰岛素分泌的影响。

结果

我们发现非糖尿病C57BL小鼠和糖尿病KKAy小鼠中TIP60的α和β剪接形式水平相同。此外,我们证明,TIP60在INS-1E细胞中的瞬时和稳定表达既不影响葡萄糖刺激的胰岛素分泌、胰岛素产量,也不影响细胞胰岛素含量。对发生糖毒性的易感性也未受影响。

结论

TIP60过表达不影响葡萄糖刺激的胰岛素分泌、胰岛素含量或糖毒性期间β细胞的异常功能。