Powered by OpenAIRE graph
Found an issue? Give us feedback
image/svg+xml Jakob Voss, based on art designer at PLoS, modified by Wikipedia users Nina and Beao Closed Access logo, derived from PLoS Open Access logo. This version with transparent background. http://commons.wikimedia.org/wiki/File:Closed_Access_logo_transparent.svg Jakob Voss, based on art designer at PLoS, modified by Wikipedia users Nina and Beao Biochemical and Biop...arrow_drop_down
image/svg+xml Jakob Voss, based on art designer at PLoS, modified by Wikipedia users Nina and Beao Closed Access logo, derived from PLoS Open Access logo. This version with transparent background. http://commons.wikimedia.org/wiki/File:Closed_Access_logo_transparent.svg Jakob Voss, based on art designer at PLoS, modified by Wikipedia users Nina and Beao
Biochemical and Biophysical Research Communications
Article . 1998 . Peer-reviewed
License: Elsevier TDM
Data sources: Crossref
versions View all 2 versions
addClaim

Cloning and Characterization of a Novel Transforming Growth Factor-β1-Induced TIAF1 Protein That Inhibits Tumor Necrosis Factor Cytotoxicity

Authors: N S, Chang; J, Mattison; H, Cao; N, Pratt; Y, Zhao; C, Lee;

Cloning and Characterization of a Novel Transforming Growth Factor-β1-Induced TIAF1 Protein That Inhibits Tumor Necrosis Factor Cytotoxicity

Abstract

To determine how TGF-beta1 protects L929 fibroblasts against TNF-alpha cytotoxicity, we report the isolation and characterization of a novel cDNA encoding a 12-kDa TGF-beta1-induced antiapoptotic factor, designated TIAF1. GFP-tagged TIAF1 protein is present mostly in perinuclear and nuclear locations. TIAF1 inhibits the cytotoxic effects of TNF-alpha and overexpressed TNF receptor adaptors TRADD, FADD, and RIP. L929 stable transfectants expressing TIAF1 do not have significant changes in the expression of TNF receptors and effector or regulatory proteins in apoptosis, which may account for the acquired TNF resistance in these cells. Notably, these cells have a significantly suppressed IkappaB-alpha protein expression, and IkappaB-alpha degradation is blocked when exposing these cells to TNF-alpha. Similarly, stimulation of untransfected L929 cells with TGF-beta1 results in suppression of IkappaB-alpha expression and retarded IkappaB-alpha degradation in response to TNF-alpha. Despite the fact that the mechanism for blocking TNF cytotoxicity is unknown, TIAF1 is apparently involved in TGF-beta1 inhibition of IkappaB-alpha expression and suppression of TNF-mediated IkappaB-alpha degradation.

Keywords

Base Sequence, Dose-Response Relationship, Drug, Myosin Heavy Chains, Molecular Sequence Data, Drug Resistance, Nuclear Proteins, Proteins, Apoptosis, DNA-Binding Proteins, Mice, Gene Expression Regulation, NF-KappaB Inhibitor alpha, Protein Biosynthesis, Animals, Humans, I-kappa B Proteins, Amino Acid Sequence, Cloning, Molecular, Apoptosis Regulatory Proteins, Carrier Proteins

  • BIP!
    Impact byBIP!
    selected citations
    These citations are derived from selected sources.
    This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
    35
    popularity
    This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
    Top 10%
    influence
    This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
    Top 10%
    impulse
    This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
    Top 10%
Powered by OpenAIRE graph
Found an issue? Give us feedback
selected citations
These citations are derived from selected sources.
This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Citations provided by BIP!
popularity
This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
BIP!Popularity provided by BIP!
influence
This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Influence provided by BIP!
impulse
This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
BIP!Impulse provided by BIP!
35
Top 10%
Top 10%
Top 10%
Upload OA version
Are you the author of this publication? Upload your Open Access version to Zenodo!
It’s fast and easy, just two clicks!