Fanconi anemia protein, FANCG, is a phosphoprotein and is upregulated with FANCA after TNF-α treatment

被引：20

作者：

Futaki, M ^{[1
]}

Watanabe, S ^{[1
]}

Kajigaya, S ^{[1
]}

Liu, JM ^{[1
]}

机构：

[1] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2001年 / 281卷 / 02期

关键词：

Fanconi anemia; phosphorylation; TNF-alpha; protein complex; protein regulation; NF-kappa B;

D O I：

10.1006/bbrc.2001.4359

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：

Fanconi anemia (FA) is a genetic syndrome characterized by bone marrow failure, birth defects, and a predisposition to malignancy. At this time, six FA genes have been identified, and several gene products have been found to interact in a protein complex. FA cells appear to overexpress the proinflammatory cytokine, tumor necrosis factor-alpha (TNF-cu), We therefore examined the effects of TNF-alpha on the regulation of FA complementation group proteins, FANCG and FANCA, We found that treatment with TNF-alpha induced FANCG; protein expression. FANCA was induced concurrently with FANCG;, and the FANCA/FANCG complex was increased in the nucleus following TNF-alpha treatment. Inactivation of inhibitory kappa B kinase-2 modulated the expression of FANCG. We also found that both nuclear and cytoplasmic FANCG fractions were phosphorylated. These results show that FANCG is a phosphoprotein and suggest that the cellular accumulation of FA proteins is subject to regulation by TNF-alpha signaling.

引用

页码：347 / 351

页数：5

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