A mouse model for functional dissection of TAB1 O-GlcNAcylation.

ABSTRACT: Background: O-GlcNAcylation is a posttranslational modification associated with various physiological and pathophysiological processes including diabetes, cancer, neurodegeneration and inflammation. However, the biological mechanisms underlying the role of specific O-GlcNAc sites and their link to phenotypes remain largely unexplored due to lack of suitable in vivo models. TGF-β activated kinase-1 binding protein-1 (TAB1) is a scaffolding protein required for TGF-β activated kinase-1 (TAK1) mediated signalling. A single O-GlcNAc site has been identified on human TAB1 that modulates TAK1-mediated cytokine release in cells. Methods: Here, we report the generation of the Tab1 ^S393A mouse model using a constitutive knock-in strategy. The Tab1 ^S39

SUBMITTER: Authier F 

PROVIDER: S-EPMC7333360 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature