These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.
Pubmed for Handhelds
PUBMED FOR HANDHELDS
Search MEDLINE/PubMed
Title: Shiga toxins and apoptosis. Author: Cherla RP, Lee SY, Tesh VL. Journal: FEMS Microbiol Lett; 2003 Nov 21; 228(2):159-66. PubMed ID: 14638419. Abstract: The enteric pathogens Shigella dysenteriae serotype 1 and Shiga toxin-producing Escherichia coli (STEC) cause bloody diarrheal diseases that may progress to life-threatening extraintestinal complications. Although the S. dysenteriae and STEC differ in the expression of a number of virulence determinants, they share the capacity to produce one or more potent cytotoxins, called Shiga toxins (Stxs). Following the ingestion of the organisms, the expression of Stxs is critical for the development of vascular lesions in the colon, kidneys and central nervous system. It has been known for some time that following the intracellular routing of Stxs to the endoplasmic reticulum and nuclear membrane, the toxins translocate into the cytoplasm and target ribosomes for damage. However, numerous recent studies have shown that Stxs trigger programmed cell death signaling cascades in intoxicated cells. The mechanisms of apoptosis induction by these toxins are newly emerging, and the data published to date suggest that the toxins may signal apoptosis in different cells types via different mechanisms. Here we review the Stxs and the known mechanistic aspects of Stx-induced apoptosis, and present a model of apoptosis induction.[Abstract] [Full Text] [Related] [New Search]