Regulation of nuclear translocation of HDAC3 by IkBalpha is required for TNF-inhibition of PPARgamma function

doi:10.1074/jbc.M507784200

HOME

QUICK SEARCH:

	Author:		Keyword(s):
Year:		Vol:		Page:

A more recent version of this article appeared on February 17, 2006

This Article

	Full Text (Accepted Manuscript)
	All Versions of this Article: 281/7/4540 most recent M507784200v1
	Alert me when this article is cited
	Alert me if a correction is posted

Services

	Email this article to a friend
	Similar articles in this journal
	Similar articles in PubMed
	Alert me to new issues of the journal
	Download to citation manager
	Request Permissions

Citing Articles

	Citing Articles via HighWire
	Citing Articles via Google Scholar

Google Scholar

	Articles by Gao, Z.
	Articles by Ye, J.
	Search for Related Content

PubMed

	PubMed Citation
	Articles by Gao, Z.
	Articles by Ye, J.

Social Bookmarking

	What's this?

Papers In Press, published online ahead of print December 21, 2005
J. Biol. Chem, 10.1074/jbc.M507784200
Submitted on July 18, 2005
Revised on December 16, 2005
Accepted on December 21, 2005

Regulation of nuclear translocation of HDAC3 by IkBalpha is required for TNF-inhibition of PPARgamma function

Zhangou Gao, Qing He, Bailu Peng, Paul Chiao, and Jianping Ye

Antioxidant and Gene Regulation laboratory, Pennington Biomedical Research Center, Baton Rouge, LA 70808

Corresponding Author: yej{at}pbrc.edu

Inhibition of PPARg function by TNF-a contributes to metabolic disorder in glucose and fatty acids under inflammation and cancer, but the molecular mechanism remains to be fully understood. In this study, we demonstrate that nuclear translocation of HDAC3 is regulated by TNF-a, and this event is required for inhibition of the transcriptional activity of PPARg by TNF-a. HDAC3 is associated with IkBa in the cytoplasm. After IkB degradation in response to TNF-a, HDAC3 is subject to nuclear translocation leading to an increase in HDAC3 activity in the nucleus. This mechanism determines subcellular distribution of HDAC3. Knockout of IkBa, but not p65 or p50, leads to disappearance of HDAC3 in the cytoplasm. This is associated with HDAC3 enrichment in the nucleus. The inhibition of PPARg by TNF-a happens without a reduction in the DNA-binding activity of PPAR. These results support that IkBa-dependent nuclear translocation of HDAC3 is responsible for PPARg inhibition by TNF-a.

Add to CiteULike CiteULike Add to Complore Complore Add to Connotea Connotea Add to Del.icio.us Del.icio.us Add to Digg Digg Add to Reddit Reddit Add to Technorati Technorati What's this?

This article has been cited by other articles:

J. Zhang, Z. Gao, J. Yin, M. J. Quon, and J. Ye
S6K Directly Phosphorylates IRS-1 on Ser-270 to Promote Insulin Resistance in Response to TNF-{alpha} Signaling through IKK2
J. Biol. Chem., December 19, 2008; 283(51): 35375 - 35382.
[Abstract] [Full Text] [PDF]

C. Pang, Z. Gao, J. Yin, J. Zhang, W. Jia, and J. Ye
Macrophage infiltration into adipose tissue may promote angiogenesis for adipose tissue remodeling in obesity
Am J Physiol Endocrinol Metab, August 1, 2008; 295(2): E313 - E322.
[Abstract] [Full Text] [PDF]

J. Ye, Z. Gao, J. Yin, and Q. He
Hypoxia is a potential risk factor for chronic inflammation and adiponectin reduction in adipose tissue of ob/ob and dietary obese mice
Am J Physiol Endocrinol Metab, October 1, 2007; 293(4): E1118 - E1128.
[Abstract] [Full Text] [PDF]

J. Yan, Z. Gao, G. Yu, Q. He, J. Weng, and J. Ye
Nuclear Corepressor Is Required for Inhibition of Phosphoenolpyruvate Carboxykinase Expression by Tumor Necrosis Factor-{alpha}
Mol. Endocrinol., July 1, 2007; 21(7): 1630 - 1641.
[Abstract] [Full Text] [PDF]

F. Escaffit, O. Vaute, M. Chevillard-Briet, B. Segui, Y. Takami, T. Nakayama, and D. Trouche
Cleavage and Cytoplasmic Relocalization of Histone Deacetylase 3 Are Important for Apoptosis Progression
Mol. Cell. Biol., January 15, 2007; 27(2): 554 - 567.
[Abstract] [Full Text] [PDF]