Cloning and characterization of a novel transforming growth factor-β1-induced TIAF1 protein that inhibits tumor necrosis factor cytotoxicity

被引：33

作者：

Chang, NS ^{[1
]}

Mattison, J ^{[1
]}

Cao, H ^{[1
]}

Pratt, N ^{[1
]}

Zhao, Y ^{[1
]}

Lee, C ^{[1
]}

机构：

[1] Guthrie Med Ctr, Lab Mol Immunol, Guthrie Res Inst, Sayre, PA 18840 USA

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 1998年 / 253卷 / 03期

关键词：

D O I：

10.1006/bbrc.1998.9846

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

To determine how TGF-beta 1 protects L929 fibroblasts against TNF-alpha cytotoxicity, we report the isolation and characterization of a novel cDNA encoding a 12-kDa TGF-beta 1-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 I kappa B-alpha protein expression, and I kappa B-alpha degradation is blocked when exposing these cells to TNF-alpha. Similarly, stimulation of untransfected L929 cells with TGF-beta 1 results in suppression of I kappa B-alpha expression and retarded I kappa B-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-beta 1 inhibition of I kappa B-alpha expression and suppression of TNF-mediated I kappa B-alpha degradation. (C) 1998 Academic Press.

引用

页码：743 / 749

页数：7

共 31 条

[11] CHATURVEDI MM, 1994, LYMPHOKINE CYTOK RES, V13, P309
[12] Apoptosis and the cell cycle: the p53 connection
Choisy-Rossi, C
Yonish-Rouach, E
[J]. CELL DEATH AND DIFFERENTIATION, 1998, 5 (02) : 129 - 131
[13] SINGLE-STEP METHOD OF RNA ISOLATION BY ACID GUANIDINIUM THIOCYANATE PHENOL CHLOROFORM EXTRACTION
CHOMCZYNSKI, P
SACCHI, N
[J]. ANALYTICAL BIOCHEMISTRY, 1987, 162 (01) : 156 - 159
[14] Early events in TNF signaling: A story of associations and dissociations
Darnay, BG
Aggarwal, BB
[J]. JOURNAL OF LEUKOCYTE BIOLOGY, 1997, 61 (05) : 559 - 566
[15] Cleavage of poly(ADP-ribose) polymerase: a sensitive parameter to study cell death
Duriez, PJ
Shah, GM
[J]. BIOCHEMISTRY AND CELL BIOLOGY-BIOCHIMIE ET BIOLOGIE CELLULAIRE, 1997, 75 (04): : 337 - 349
[16] NF-κB and rel proteins:: Evolutionarily conserved mediators of immune responses
Ghosh, S
May, MJ
Kopp, EB
[J]. ANNUAL REVIEW OF IMMUNOLOGY, 1998, 16 : 225 - 260
[17] Superior performance in protein homology detection with the Blocks Database servers
Henikoff, S
Pietrokovski, S
Henikoff, JG
[J]. NUCLEIC ACIDS RESEARCH, 1998, 26 (01) : 309 - 312
[18] HENNET T, 1993, CANCER RES, V53, P1456
[19] TNF-Dependent recruitment of the protein kinase RIP to the TNF receptor-1 signaling complex
Hsu, HL
Huang, JN
Shu, HB
Baichwal, V
Goeddel, DV
[J]. IMMUNITY, 1996, 4 (04) : 387 - 396
[20] TRADD-TRAF2 and TRADD-FADD interactions define two distinct TNF receptor 1 signal transduction pathways
Hsu, HL
Shu, HB
Pan, MG
Goeddel, DV
[J]. CELL, 1996, 84 (02) : 299 - 308

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