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An Anti-Inflammatory Approach to Treating Diabetes and Atherosclerosis Using Salicylate
Steven E. Shoelson,Ju Ho Youn,Giulio Romeo,Tanya Ignjatovic,Dongsheng Cai,Minsheng Yuan,Nicky Konstantoupolos,Laura Herrero,Myrlene Staten,Vivan Fonseca,Allison Goldfine,Jongsoon Lee 한국식품영양과학회 2014 한국식품영양과학회 학술대회발표집 Vol.2014 No.10
The carboxy-terminal region of the TBC1D4 (AS160) RabGAP mediates protein homodimerization
Woo, Ju Rang,Kim, Soon-Jong,Kim, Keon Young,Jang, Hyonchol,Shoelson, Steven E.,Park, SangYoun ELSEVIER 2017 INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES Vol.103 No.-
<P><B>Abstract</B></P> <P>TBC1D4 (also known as AS160) is a Rab·GTPase-activating protein (RabGAP) which functions in insulin signaling. TBC1D4 is critical for translocation of glucose transporter 4 (GLUT4), from an inactive, intracellular, vesicle-bound site to the plasma membrane, where it promotes glucose entry into cells. The TBC1D4 protein is structurally subdivided into two N-terminal phosphotyrosine-binding (PTB) domains, a C-terminal catalytic RabGAP domain, and a disordered segment in between containing potential Akt phosphorylation sites. Structural predictions further suggest that a region C-terminal to the RabGAP domain adopts a coiled-coil motif. We show that C-terminal region (CTR) region is largely α-helical and mediates TBC1D4 RabGAP dimerization. RabGAP catalytic activity and thermal stability appear to be independent of CTR-mediated dimerization.</P>
Lee, B.C.,Kim, M.S.,Pae, M.,Yamamoto, Y.,Eberle, D.,Shimada, T.,Kamei, N.,Park, H.S.,Sasorith, S.,Woo, J.,You, J.,Mosher, W.,Brady, Hugh J.M.,Shoelson, Steven E.,Lee, J. Cell Press 2016 Cell metabolism Vol.23 No.4
<P>Obesity-induced inflammation mediated by immune cells in adipose tissue appears to participate in the pathogenesis of insulin resistance. We show that natural killer (NK) cells in adipose tissue play an important role. High-fat diet (HFD) increases NK cell numbers and the production of proinflammatory cytokines, notably TNF alpha, in epididymal, but not subcutaneous, fat depots. When NK cells were depleted either with neutralizing antibodies or genetic ablation in E4bp4(+/-) mice, obesity-induced insulin resistance improved in parallel with decreases in both adipose tissue macrophage (ATM) numbers, and ATM and adipose tissue inflammation. Conversely, expansion of NK cells following IL-15 administration or reconstitution of NK cells into E4bp4(-/-) mice increased both ATM numbers and adipose tissue inflammation and exacerbated HFD-induced insulin resistance. These results indicate that adipose NK cells control ATMs as an upstream regulator potentially by producing proinflammatory mediators, including TNF alpha, and thereby contribute to the development of obesity-induced insulin resistance.</P>