Year: 2014
Type: book-chapter
Abstract: A B Color Plate 1 (chapter 1).(A) Electron micrograph of an A / E lesion caused by EPEC.(B) Model of protein secretion and Tir-intimin binding.The LEE-encoded Esc proteins form the secretion apparatus, and EspA-containing filaments form a channel through which secreted proteins are translocated into the host cytosol.EspB and EspD are thought to form a translocation pore in the host plasma membrane.Tir is one effector protein translocated into the host, where it is phosphorylated on tyrosine.It is then inserted into the plasma and serves as the receptor for the EPEC outer membrane protein, intimin, through its extracellular intimin binding domain (IBD).The Tir-intimin interaction triggers pedestal formation and A / E lesion induction.Electron micrograph courtesy of F. Ebel, Institut Pasteur, Paris, France.Model reproduced from Celli et al. (2000) with
Source: ASM Press eBooks
Authors: Stefan H. E. Kaufmann, Alan Sher, Rafi Ahmed
Language: English
Subfield: Endocrinology
Domain: Life Sciences
Open Access status: bronze
OpenAlex ID: W4243188444