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1. chinaXiv:201605.01248 [pdf]

The Metabolic Regulator Histone Deacetylase 9 Contributes to Glucose Homeostasis Abnormality Induced by Hepatitis C Virus Infection

Chen, Jizheng; Guo, Min; Tang, Hong; Chen, Xinwen; Wang, Ning; Dong, Mei; Li, Zhong; Han, Xiao; Wang, Qian; Zhao, Yang; Zhuo, Zhiyong; Zhang, Chao; Chi, Xiumei; Pan, Yu; Jiang, Jing; Niu, Junqi; Yang, Dongliang
Subjects: Biology >> Biophysics

Class Ila histone deacetylases (HDACs), such as HDAC4, HDAC5, and HDAC7, provide critical mechanisms for regulating glucose homeostasis. Here we report that HDAC9, another class Ila HDAC, regulates hepatic gluconeogenesis via deacetylation of a Forkhead box 0 (FoxO) family transcription factor, FoxO1, together with HDAC3. Specifically, HDAC9 expression can be strongly induced upon hepatitis C virus (HCV) infection. HCV-induced HDAC9 upregulation enhances gluconeogenesis by promoting the expression of gluconeogenic genes, including phosphoenolpyruvate carboxykinase and glucose-6-phosphatase, indicating a major role for HDAC9 in the development of HCV-associated exaggerated gluconeogenic responses. Moreover, HDAC9 expression levels and gluconeogenic activities were elevated in livers from HCV-infected patients and persistent HCV-infected mice, emphasizing the clinical relevance of these results. Our results suggest HDAC9 is involved in glucose metabolism, HCV-induced abnormal glucose homeostasis, and type 2 diabetes.

submitted time 2016-05-11 Hits540Downloads312 Comment 0

2. chinaXiv:201605.00772 [pdf]

Modeling xeroderma pigmentosum associated neurological pathologies with patients-derived iPSCs

Fu, Lina; Xu, Xiuling; Ren, Ruotong; Zhang, Weiqi; Yang, Jiping; Ren, Xiaoqing; Wang, Si; Zhao, Yang; Liu, Guang-Hui; Ren, Ruotong; Zhang, Weiqi; Liu, Guang-Hui; Qu, Jing; Wu, Jun; Belmonte, Juan Carlos Izpisua; Wu, Jun; Sun, Liang; Yang, Ze; Yu, Yang; Qiao, Jie
Subjects: Biology >> Biophysics >> Cell Biology

Xeroderma pigmentosum (XP) is a group of genetic disorders caused by mutations of XP-associated genes, resulting in impairment of DNA repair. XP patients frequently exhibit neurological degeneration, but the underlying mechanism is unknown, in part due to lack of proper disease models. Here, we generated patient-specific induced pluripotent stem cells (iPSCs) harboring mutations in five different XP genes including XPA, XPB, XPC, XPG, and XPV. These iPSCs were further differentiated to neural cells, and their susceptibility to DNA damage stress was investigated. Mutation of XPA in either neural stem cells (NSCs) or neurons resulted in severe DNA damage repair defects, and these neural cells with mutant XPA were hyper-sensitive to DNA damage-induced apoptosis. Thus, XP-mutant neural cells represent valuable tools to clarify the molecular mechanisms of neurological abnormalities in the XP patients.

submitted time 2016-05-05 Hits788Downloads442 Comment 0

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