Requirement for translocon-associated protein (TRAP) α in insulin biogenesis
Xin Li(University of Michigan), Omar A. Itani(University of Michigan), Leena Haataja(University of Michigan), Kathleen J. Dumas(University of Michigan), Jing Yang(Tianjin Medical University General Hospital), Jeeyeon Cha(Vanderbilt University Medical Center), Stéphane Flibotte(University of British Columbia), Hung‐Jen Shih(University of Michigan), Colin Delaney(University of Michigan), Jialu Xu(Tianjin Medical University General Hospital), Ling Qi(University of Michigan), Peter Arvan(University of Michigan), Ming Liu(University of Michigan), Patrick J Hu(University of Michigan)
Cited by 37Open Access
Abstract
and biochemical studies in pancreatic β cells reveal that TRAPα deletion impairs preproinsulin translocation while unexpectedly disrupting distal steps in insulin biogenesis including proinsulin processing and secretion. The association of common intronic single-nucleotide variants in the human TRAPα gene with susceptibility to type 2 diabetes and pancreatic β cell dysfunction suggests that impairment of preproinsulin translocation and proinsulin trafficking may contribute to the pathogenesis of type 2 diabetes.
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