Tumour necrosis factor-alpha regulates expression of the CCAAT-enhancer-binding proteins (C/EBPs) alpha and beta and determines the occupation of the C/EBP site in the promoter of the insulin-responsive glucose-transporter gene in 3T3-L1 adipocytes.

ECU Author/Contributor (non-ECU co-authors, if there are any, appear on document)

Renu Jain (Creator)

Phillip H. Pekala (Creator)

Kelle Phelps (Creator)

Shailaja Police (Creator)

Institution

East Carolina University (ECU )

Web Site: http://www.ecu.edu/lib/

Abstract: We have demonstrated previously that treatment of 3T3-L1 adipocytes with tumour necrosis factor-alpha (TNF) results in a rapid (4 h) and significant (75–80%) reduction in the rate of transcription of the GLUT4 gene. Control of GLUT4 gene transcription has been suggested at least in part to reside with the CCAAT-enhancer-binding protein (C/EBP) family (alpha beta and delta isoforms) of transcription factors. Using electrophoretic mobility shift assays we have examined the ability of TNF to alter the occupation of the C!EBP site in the GLUT4 promoter. The data suggest that in fully differentiated adipocytes the C/EBP site is a ligand for predominantly alpha/alpha homodimers; however after exposure to TNF a shift in occupancy of the site occurs and the ligands become alpha/beta heterodimers and beta/beta homodimers. Partner selection in dimer formation appears to be controlled by selective translocation of the beta-isoform from the cytosol to the nucleus after exposure of the cells to TNF. Originally published Biochemical Journal Vol. 338 No. 3 Mar 1999

Additional Information

Publication

Other

Biochemical Journal. 338:3(March 1999) p. 737-743.

Language: English

Date: 2011

Keywords

Cytokines, differentiation, Gene expression, glucose transport, transcription factor

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