Enteropathogenic E. coli effector Map interacts with Rab13 and regulates the depletion of the tight junction proteins occludin and claudins via cathepsin B-mediated mechanisms.

ABSTRACT: Infections by enteropathogenic Escherichia coli (EPEC) cause acute diarrheal disease in infants accounting for severe morbidity and mortality. One of the underlying causes of the disease is the breakdown of the intestinal barrier maintained by the tight junctions (TJs). EPEC uses a type 3 secretion system to translocate more than 20 effectors into infected cells, which disrupt several functions of the host cells. The effectors EspF, Map, EspG1/G2 and NleA have been reported to disrupt the TJs causing the leakage of charged ions and uncharged molecules through the barrier. We have previously reported that EspF and Map cause the depletion of TJ proteins claudin-1, claudin-4 and occludin through both transcriptional and post-transcriptional mechanisms. Here, we show that the inhibition of the

SUBMITTER: Mandal A 

PROVIDER: S-EPMC11892358 | biostudies-literature | 2025 Feb

REPOSITORIES: biostudies-literature