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Mol. Cells 2012; 33(6): 575-581

Published online May 18, 2012

https://doi.org/10.1007/s10059-012-0002-9

© The Korean Society for Molecular and Cellular Biology

Differentiated Embryo Chondrocyte 1 (DEC1) Represses PPARγ2 Gene through Interacting with CCAAT/Enhancer Binding Protein β(C/EBPβ)

Young-Kwon Park, and Hyunsung Park*

Department of Life Science, University of Seoul, Seoul 130-743, Korea

Correspondence to : *Correspondence: hspark@uos.ac.kr

Received: January 3, 2012; Revised: March 20, 2012; Accepted: March 28, 2012

Abstract

DEC1 is a transcription repressor that is induced by Hy-poxia-Inducible Factor-alpha/beta (HIF-alpha/beta). In this study, we found that either hypoxic treatment or ectopic expression of DEC1 blocks induction of a master adipogenic transactivator, peroxisome proliferative activated receptor-gamma2 (PPAR gamma 2) in 3T3-L1 cells. DEC1 did not prevent C/EBP beta, which is an upstream transactivator for PPAR gamma 2, from occupy-ing the PPARgamma2 promoter. DEC1 occupied the PPAR gamma 2 promoter by interacting with DNA-bound C/EBP beta. DEC1 occupancy was accompanied by a reduction of acetylated histones and an increase in histone deacetylase 1 (HDAC1) occupancy on the PPAR gamma 2 promoter. Based on the fact that DEC1 interacts with HDAC1, this study suggests that DEC1 blocks adipogenesis by reinforcing HDAC1 recruitment to the PPAR gamma 2 promoter. This study implies that DEC1 is one of the mediators that reset the pattern of PPAR gamma 2 expression in response to hypoxia.

Keywords adipogenesis, C/EBP beta, DEC1, hypoxia, PPAR gamma

Article

Research Article

Mol. Cells 2012; 33(6): 575-581

Published online June 30, 2012 https://doi.org/10.1007/s10059-012-0002-9

Copyright © The Korean Society for Molecular and Cellular Biology.

Differentiated Embryo Chondrocyte 1 (DEC1) Represses PPARγ2 Gene through Interacting with CCAAT/Enhancer Binding Protein β(C/EBPβ)

Young-Kwon Park, and Hyunsung Park*

Department of Life Science, University of Seoul, Seoul 130-743, Korea

Correspondence to:*Correspondence: hspark@uos.ac.kr

Received: January 3, 2012; Revised: March 20, 2012; Accepted: March 28, 2012

Abstract

DEC1 is a transcription repressor that is induced by Hy-poxia-Inducible Factor-alpha/beta (HIF-alpha/beta). In this study, we found that either hypoxic treatment or ectopic expression of DEC1 blocks induction of a master adipogenic transactivator, peroxisome proliferative activated receptor-gamma2 (PPAR gamma 2) in 3T3-L1 cells. DEC1 did not prevent C/EBP beta, which is an upstream transactivator for PPAR gamma 2, from occupy-ing the PPARgamma2 promoter. DEC1 occupied the PPAR gamma 2 promoter by interacting with DNA-bound C/EBP beta. DEC1 occupancy was accompanied by a reduction of acetylated histones and an increase in histone deacetylase 1 (HDAC1) occupancy on the PPAR gamma 2 promoter. Based on the fact that DEC1 interacts with HDAC1, this study suggests that DEC1 blocks adipogenesis by reinforcing HDAC1 recruitment to the PPAR gamma 2 promoter. This study implies that DEC1 is one of the mediators that reset the pattern of PPAR gamma 2 expression in response to hypoxia.

Keywords: adipogenesis, C/EBP beta, DEC1, hypoxia, PPAR gamma

Mol. Cells
Mar 31, 2023 Vol.46 No.3, pp. 131~189
COVER PICTURE
The physiologically important cytoprotective signaling in normal cells (background area in turquoise) mediated by NRF2 (blue chain) is often hijacked by cancer cells (red ball) in the tumor microenvironment (yellow area). However, the differential roles of NRF2 throughout the multistage carcinogenesis remains largely unresolved (white-colored overlapping misty areas).

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