Format

Send to:

Choose Destination
See comment in PubMed Commons below
J Biol Chem. 2003 Jul 18;278(29):27072-9. Epub 2003 May 7.

SINK is a p65-interacting negative regulator of NF-kappaB-dependent transcription.

Author information

  • 1Department of Cell Biology and Genetics, College of Life Sciences, Peking University, Beijing 100871, China.

Abstract

The transcription factor NF-kappaB plays important roles in inflammation and cell survival. In this study, we identified SINK, an NF-kappaB-inducible protein. Overexpression of SINK inhibited NF-kappaB-dependent transcription induced by tumor necrosis factor (TNF) stimulation or its downstream signaling proteins but did not inhibit NF-kappaB translocation to the nucleus and binding to DNA. Co-immunoprecipitation and in vitro kinase assays indicated that SINK specifically interacted with the NF-kappaB transactivator p65 and inhibited p65 phosphorylation by the catalytic subunit of protein kinase A, which has previously been shown to regulate NF-kappaB activation. Consistent with its role in inhibition of NF-kappaB-dependent transcription, SINK also sensitized cells to apoptosis induced by TNF and TRAIL (TNF-related apoptosis-inducing ligand). Taken together, these data suggest that SINK is critically involved in a novel negative feedback control pathway of NF-kappaB-induced gene expression.

PMID:
12736262
[PubMed - indexed for MEDLINE]
Free full text
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for HighWire
    Loading ...
    Write to the Help Desk