Protein arginine methyltransferase 1 regulates hepatic glucose production in a FoxO1-dependent manner

Hepatology ◽  
2012 ◽  
Vol 56 (4) ◽  
pp. 1546-1556 ◽  
Author(s):  
Dahee Choi ◽  
Kyoung-Jin Oh ◽  
Hye-Sook Han ◽  
Young-Sil Yoon ◽  
Chang-Yun Jung ◽  
...  
2013 ◽  
Vol 455 (2) ◽  
pp. 207-216 ◽  
Author(s):  
Kenneth K. Y. Cheng ◽  
Karen S. L. Lam ◽  
Yu Wang ◽  
Donghai Wu ◽  
Mingliang Zhang ◽  
...  

The adaptor protein APPL1 undergoes ubiquitination upon insulin stimulation in a TRAF6-dependent manner. Abrogation of APPL1 ubiquitination blocks insulin-evoked membrane localization of the APPL1–Akt complex, leading to impaired insulin actions on Akt activation and suppression of hepatic glucose production.


2014 ◽  
Vol 24 (3) ◽  
pp. 773-786 ◽  
Author(s):  
Michael Tibshirani ◽  
Miranda L. Tradewell ◽  
Katie R. Mattina ◽  
Sandra Minotti ◽  
Wencheng Yang ◽  
...  

2016 ◽  
Vol 119 (suppl_1) ◽  
Author(s):  
Olan Jackson-Weaver ◽  
Jian Wu ◽  
Yongchao Gou ◽  
Shihong Shi ◽  
Henry Sucov ◽  
...  

Rationale: Epicardial epithelial-to-mesenchymal trasition (EMT) is a vital process in embryonic heart development. During EMT, epicardial cells acquire migratory and invasive properties, and differentiate into new cell types, including cardiac fibroblasts and coronary smooth muscle cells. EMT is characterized by an increase in mesenchymal proteins such as Slug and Fibronectin, and a decrease in cell-junction proteins such as E-Cadherin, and is dependent on TGF-β signaling. We have recently demonstrated that protein arginine methyltransferase-1 (PRMT1) is necessary for TGF-β family signaling and EMT in non-epicardial cell types. Objective: To determine the role of PRMT1 in epicardial EMT. Methods and Results: We investigated the role of PRMT1 in epicardial EMT in mouse epicardial cells. PRMT1 siRNA prevented the increase in Slug and Fibronectin and the decrease in E-Cadherin in TGF-β treatment-induced EMT of mouse epicardial cell line MEC1. PRMT1 siRNA also reduced the migration and invasion of MEC1 cells. These results demonstrate that PRMT1 is required for epicardial EMT. In WT1-Cre ERT ;ROSA-YFP fl/fl mouse embryos, PRMT1 siRNA reduced epicardial EMT in a thorax culture model. Among the key transcription factors that regulate the EMT program, Slug, but not Snail, is specifically regulated by PRMT1. We further identified that PRMT1 siRNA also increased the expression of p53, a key regulator of the Slug degradation pathway. PRMT1 siRNA increases p53 expression by decreasing p53 degradation, and shifted p53 localization to the cytoplasm. In vitro methylation assays further demonstrated that PRMT1 methylates p53. Knockdown of p53 increased Slug levels and enhanced EMT, establishing p53 as a regulator of epicardial EMT through controlling Slug expression. Conclusions: The PRMT1-p53-Slug pathway is necessary for epicardial EMT in cultured MEC1 cells as well as in the epicardium ex vivo .


Biochemistry ◽  
2008 ◽  
Vol 47 (39) ◽  
pp. 10420-10427 ◽  
Author(s):  
Obiamaka Obianyo ◽  
Tanesha C. Osborne ◽  
Paul R. Thompson

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