Work

Death versus survival: functional interaction between the apoptotic and stress-inducible heat shock protein pathways

Year: 2005

Type: review

Abstract: Induction of heat shock proteins (Hsps) following cellular damage can prevent apoptosis induced by both the intrinsic and the extrinsic pathways. The intrinsic pathway is characterized by mitochondrial outer membrane permeabilization (MOMP), cytochrome c release, apoptosome assembly, and caspase activation. Hsps promote cell survival by preventing MOMP or apoptosome formation as well as via regulation of Akt and JNK activities. Engagement of the TNF death receptors induces the extrinsic pathway that is characterized by Fas-associated death domain-dependent (FADD-dependent) caspase-8 activation or induction of NF-kappaB to promote cellular survival. Hsps can directly suppress proapoptotic signaling events or stabilizing elements of the NF-kappaB pathway to promote cellular survival.

Source: Journal of Clinical Investigation

DOI: 10.1172/jci26471

Author: H. M. Beere

Institution: St. Jude Children's Research Hospital

Language: English

Topic: Heat shock proteins research

Subfield: Molecular Biology

Field: Biochemistry, Genetics and Molecular Biology

Domain: Life Sciences

SDG: Good health and well-being

Open Access status: bronze

Funders: St. Jude Children's Research Hospital, National Institutes of Health, National Institute of General Medical Sciences, National Institute of Allergy and Infectious Diseases