重庆大学微观经济学考研近年考试真题笔记2016考研近年考试真题.docx

Bacteria-Induced Uroplakin Signaling Mediates Bladder
Response to Infection
Praveen Thumbikat1, Ruth E. Berry1, Ge Zhou3, Benjamin K. Billips1, Ryan E. Yaggie1, Tetiana Zaichuk1,
Tung-Tien Sun3, Anthony J. Schaeffer1, David J. Klumpp1,2*
1 Department of Urology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, United States of America, 2 Department of Microbiology-Immunology,
Feinberg School of Medicine, Northwestern University, Chicago, Illinois, United States of America, 3 Departments of Cell Biology, Dermatology, Pharmacology and
Urology, New York University School of Medicine, New York, New York, United States of America
Abstract
Urinary tract infections are the second mon infectious disease in humans and are predominantly caused by
uropathogenic E. coli (UPEC). A majority of UPEC isolates express the type 1 pilus adhesin, FimH, and cell culture and murine
studies demonstrate that FimH is involved in invasion and apoptosis of urothelial cells. FimH initiates bladder pathology by
binding to the uroplakin plex, but the subsequent events mediating pathogenesis have not been fully
characterized. We report a hitherto undiscovered signaling role for the UPIIIa protein, the only major uroplakin with a
potential cytoplasmic signaling domain, in bacterial invasion and apoptosis. In response to FimH adhesin binding, the UPIIIa
cytoplasmic