Fig. 3

Hypothesized cellular adaptation models. Under normoxia, β1 integrins are properly glycosylated in the ER, are subsequently trafficked to the cell surface, and associate with lipid rafts. This allows binding to Yersinia enterocolitica invasin and bacterial internalization into host intestinal epithelial cell. Under hypoxia, HIF-1/hypoxia-induced ER stress and membrane alterations result in improper glycosylation and mislocalization of β1 integrins, thus reducing binding to and internalization of Y. enterocolitica