Publication: Signaling pathways mediated by tumor necrosis factor a
Authors
Leong, K.G. ; Karsan, A.
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Publisher
Murcia : F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
Abstract
Tumor necrosis factor a (TNFa) has been
shown to trigger many signaling pathways. Following
oligomerization by TNFa, the receptors TNF-RI and
TNF-RI1 associate with adapter molecules via specific
protein-protein interactions. The subsequent recruitment
of downstream molecules to the receptor complex
enables propagation of the TNFa signal. l k o cellular
responses to TNFa have been well documented, the
induction of cell death and the activation of gene
transcription for cell survival. TNFa-induced apoptosis
involves the activation of caspase cascades, which
culminate in the cleavage of specific cellular substrates
to effect cell death. TNFa has also been implicated in
various caspase-independent cell death processes. Two
transcription factors activated by TNFa are nuclear
factor KB (NFKB) and activating protein 1 (AP-1).
Pathways that promote the activation of these
transcription factors involve signaling molecules such as
kinases, phospholipases, and sphingomyelinases. In
addition to increased survival (anti-apoptotic) gene
expression, NFKB and AP-1 also induce the expression
of genes involved in inflammation, cell growth, and
signal regulation. The past decade has witnessed the
identification of numerous signaling intermediates
implicated in TNFa cellular responses. This article
reviews the molecular mechanisms of TNFa signal
transduction. In particular, pathways involved in cell
death and transcription factor activation are discussed.
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