Evidence map›Paper›PMID 40787784›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2025

The TBLR1/TBL1 Co-Factor Complex Acts as a Transcriptional Checkpoint in the Brown Adipose Tissue Response to Prolonged Cold Exposure.

Sahika Cingir Köker, Foivos-Filippos Tsokanos, Rabih El-Merahbi, Ankush Kumar Jha, Karin Cicatelli, Peter Weber, Amit Mhamane, Doris Kaltenecker, Pauline Morigny, Anne Loft and 16 more

Abstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Article
  2. The TBLR1/TBL1 Co-Factor Complex Acts as a Transcriptional Checkpoint in the Brown Adipose Tissue Response to Prolonged Cold Exposure.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

26 authors.

Sahika Cingir KökerInstitute for Diabetes and Cancer (IDC), Helmholtz Center Munich (HMGU), Neuherberg, Germany.
Foivos-Filippos TsokanosInstitute for Diabetes and Cancer (IDC), Helmholtz Center Munich (HMGU), Neuherberg, Germany.
Rabih El-MerahbiInstitute for Diabetes and Cancer (IDC), Helmholtz Center Munich (HMGU), Neuherberg, Germany.
Ankush Kumar JhaInstitute for Diabetes and Cancer (IDC), Helmholtz Center Munich (HMGU), Neuherberg, Germany.
Karin CicatelliInstitute for Diabetes and Cancer (IDC), Helmholtz Center Munich (HMGU), Neuherberg, Germany.
Peter WeberInstitute for Diabetes and Cancer (IDC), Helmholtz Center Munich (HMGU), Neuherberg, Germany.
Amit MhamaneInstitute for Diabetes and Cancer (IDC), Helmholtz Center Munich (HMGU), Neuherberg, Germany.
Doris KalteneckerInstitute for Diabetes and Cancer (IDC), Helmholtz Center Munich (HMGU), Neuherberg, Germany.
Pauline MorignyInstitute for Diabetes and Cancer (IDC), Helmholtz Center Munich (HMGU), Neuherberg, Germany.
Anne LoftInstitute for Diabetes and Cancer (IDC), Helmholtz Center Munich (HMGU), Neuherberg, Germany.
Katarina KlepacInstitute for Diabetes and Cancer (IDC), Helmholtz Center Munich (HMGU), Neuherberg, Germany.
Adriano MaidaInstitute for Diabetes and Cancer (IDC), Helmholtz Center Munich (HMGU), Neuherberg, Germany.
Claudia-Eveline MoloceaInstitute for Diabetes and Cancer (IDC), Helmholtz Center Munich (HMGU), Neuherberg, Germany.
Daniela HassInstitute for Diabetes and Cancer (IDC), Helmholtz Center Munich (HMGU), Neuherberg, Germany.
Elena Sophie VoglInstitute for Diabetes and Cancer (IDC), Helmholtz Center Munich (HMGU), Neuherberg, Germany.
Ana Jimena AlfaroInstitute for Diabetes and Cancer (IDC), Helmholtz Center Munich (HMGU), Neuherberg, Germany.
Wenfei SunInstitute of Food, Nutrition and Health (IFNH), Eidgenössische Technische Hochschule Zürich (ETH), Zurich, Switzerland.
Horst ZitzelsbergerGerman Center for Diabetes Research (DZD), Neuherberg, Germany.
Kristian UngerGerman Center for Diabetes Research (DZD), Neuherberg, Germany.
Julia SzendrödiDepartment of Endocrinology and Clinical Chemistry, Heidelberg University Hospital, Heidelberg, Germany.
Yongguo LiInstitute of Pharmacology and Toxicology, University Hospital Bonn, University Bonn, Bonn, Germany.
Mauricio Berriel DiazInstitute for Diabetes and Cancer (IDC), Helmholtz Center Munich (HMGU), Neuherberg, Germany.
Christian WolfrumInstitute of Food, Nutrition and Health (IFNH), Eidgenössische Technische Hochschule Zürich (ETH), Zurich, Switzerland.
Alexander BarteltInstitute for Diabetes and Cancer (IDC), Helmholtz Center Munich (HMGU), Neuherberg, Germany.ORCID https://orcid.org/0000-0001-7840-3991
Stephan HerzigInstitute for Diabetes and Cancer (IDC), Helmholtz Center Munich (HMGU), Neuherberg, Germany.
Anastasia GeorgiadiInstitute for Diabetes and Cancer (IDC), Helmholtz Center Munich (HMGU), Neuherberg, Germany.ORCID https://orcid.org/0000-0002-9648-8682

Funding

Austrian Science Fund (FWF) J4224-B34Deutsche Forschungsgemeinschaft (DFG) 450149205-TRR333/1Deutsches Zentrum für Herz-Kreislaufforschung (DZHK)
6 · The paper itself

Abstract

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.

Indexed as

Adipose Tissue, BrownCold TemperatureNuclear ProteinsTranscription, GeneticTransducinAdipocytes, BrownAnimalsEnergy MetabolismHistone Deacetylase 3Histone DeacetylasesLipolysisMaleMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicHistone Deacetylase 3Histone DeacetylasesNuclear ProteinsTransducinbrown adipose tissueenergy expenditureHDAC3PKAPRDM16TBLR1/TBL1thermogenesis

Identifiers

PMID40787784
PMCPMC12337241

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.