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Sam68 is required for both NF-κB activation and apoptosis signaling by the TNF receptor.

Abstract：

:The RNA-binding protein Sam68 is implicated in various cellular processes including RNA metabolism, apoptosis, and signal transduction. Here we identify a role of Sam68 in TNF-induced NF-κB activation and apoptosis. We found that Sam68 is recruited to the TNF receptor, and its deficiency dramatically reduces RIP recruitment and ubiquitylation. It also impairs cIAP1 recruitment and maintenance of recruited TRAF2 at the TNF receptor. In its absence, activation of the TAK1-IKK kinase complex is defective, greatly reducing signal transduction. Sam68 is also found as a part of the TNF-induced cytoplasmic caspase-8-FADD complex. RIP is not recruited to this complex in Sam68 knockout cells, and caspase activation is virtually absent. These findings delineate previously unknown functions for Sam68 in the TNF signaling pathway, where it acts as a signaling adaptor both in the membrane-associated complex I and in the cytoplasmic complex II, regulating both NF-κB activation and apoptosis.

journal_name

Mol Cell

journal_title

Molecular cell

authors

Ramakrishnan P,Baltimore D

doi

10.1016/j.molcel.2011.05.007

subject

Has Abstract

pub_date

2011-07-22 00:00:00

pages

167-79

issue

2

eissn

1097-2765

issn

1097-4164

pii

S1097-2765(11)00339-X

journal_volume

43

pub_type

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