PuSH - Publication Server of Helmholtz Zentrum München: The TBLR1/TBL1 co-factor complex acts as a transcriptional checkpoint in the brown adipose tissue response to prolonged cold exposure.

Information

Clues to quality of journals

Open Access Policy of Helmholtz Association 2016

CC Licencences

Publication Metrics

Navigation

Home

Deutsch

EVA: Electronic Publishing

New EVA Application

Research

Advanced Search

Browse by ...

... HMGU-Authors/Consortia

... Organizational Structure

... Journal

... Publication Type

... Research Data

... Arbeitsgruppen

... Publication Year

Publication overview

Statistics

Statistics (last 5 years)

OA Publications

Publish

Submit Publication

Import publication from...

...EVA

Report missing publication

Highlights

Support & Contact

Contact persons

Help

Data protection

Helmholtz Open Science

JANE Journal Estimator

SHERPA/RoMEO

DOAJ

Export:

Text

Endnote (RIS) BIB

BibTeX

Köker, S.C. ; Tsokanos, F.-F. ; El-Merahbi, R. ; Jha, A.K. ; Cicatelli, K. ; Weber, P. ; Mhamane, A. ; Kaltenecker, D. ; Morigny, P. ; Loft, A. ; Klepac, K. ; Maida, A. ; Molocea, C.-E. ; Hass, D, ; Vogl, E.S. ; Alfaro, A.J. ; Sun, W.* ; Zitzelsberger, H. ; Unger, K. ; Szendrödi, J.* ; Li, Y.* ; Diaz, M.B. ; Wolfrum, C.* ; Bartelt, A. ; Herzig, S. ; Georgiadi, A.

The TBLR1/TBL1 co-factor complex acts as a transcriptional checkpoint in the brown adipose tissue response to prolonged cold exposure.

FASEB J. 39:e70886 (2025)

Publ. Version/Full Text

Research data

DOI

PMC

	Open Access Hybrid

Abstract
Metrics
Extra information

Brown adipose tissue (BAT) is a key thermogenic organ, whose activation in response to cold environmental temperatures and β-adrenergic stimulation requires the proper function of the NCOR/HDAC3 corepressor complex in brown adipocytes. The NCOR/HDAC3 complex is large and multi-component, including the transducin beta-like 1 (TBL1) and TBL1-related 1 (TBLR1) proteins. Loss of TBL1 in the hepatocytes and TBLR1 in the white adipocytes has been shown to impair fasting- and β-adrenergic-induced lipolysis. However, their roles in BAT thermogenesis remain unknown. Here, we report that deletion of TBLR1 alone in brown adipocytes does not impair the adaptive thermogenic response to prolonged cold exposure. In contrast, simultaneous deletion of TBL1 and TBLR1 dampens β-adrenergic-induced lipolysis and mitochondrial respiration in cultured mouse brown adipocytes. Transgenic mice with UCP1-Cre mediated double deletion of TBLR1 and TBL1 exhibit reduced whole-body energy expenditure during prolonged cold exposure, lower core body temperature, increased appearance of unilocular adipocytes in BAT, and suppressed expression of metabolic and myogenic PRDM16 target genes. Also, we present some evidence that TBLR1 and TBL1 interact with HDAC3 and PRDM16 in brown adipocytes, potentially suggesting a direct involvement in the PRDM16-controlled transcriptional program. These findings identify the TBLR1/TBL1 complex as a critical regulator of BAT adaptation to prolonged cold and systemic energy homeostasis, shedding light on the context-dependent functions of corepressor complexes.

Impact Factor

Scopus SNIP

Altmetric

4.200

0.000