Evidence map›Paper›PMID 32827753›Full record

ReviewBiochimica et biophysica acta. Gene regulatory mechanisms2021

GCN5 acetyltransferase in cellular energetic and metabolic processes.

Beste Mutlu, Pere Puigserver

Open access · greenAbstract readReview
In one paragraph

Review in Biochimica et biophysica acta. Gene regulatory mechanisms, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
5.1field-weighted citation impact, top 4% of its field
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

46 citing papers in PubMed, 68 citations in OpenAlex.

  1. Article
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  10. N-acetyl cysteine through modulation of HDACIBRO neuroscience reports · 2025
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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

2 authors at 1 institution in 1 country.

Beste MutluDepartment of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA, USA; Department of Cell Biology, Harvard Medical School, Boston, MA, USA.
Pere PuigserverDepartment of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA, USA; Department of Cell Biology, Harvard Medical School, Boston, MA, USA. Electronic address: pere_puigserver@dfci.harvard.edu.
Harvard University · US

Funding

Transcriptional Control of Mitochondrial Bioenergetic FunctionR01DK081418 · NIDDK · DANA-FARBER CANCER INST · PI PUIGSERVER, PERE · 2008 to 2021
$5.2M
Insulin Signaling and Metabolic Effects through CLK2 KinaseR01DK089883 · NIDDK · DANA-FARBER CANCER INST · PI PUIGSERVER, PERE · 2011 to 2020
$3.8M
Metabolic Vulnerabilities in Melanoma TumorsR01CA181217 · NCI · DANA-FARBER CANCER INST · PI PUIGSERVER, PERE · 2014 to 2024
$3.7M
Small molecules targeting hepatic glucose production and insulin resistanceR01DK117655 · NIDDK · DANA-FARBER CANCER INST · PI GRIFFIN, PATRICK ROBERT, PUIGSERVER, PERE · 2019 to 2023
$3.3M
Metabolic and Bioenergetic Control in Mitochondrial DiseasesR01GM121452 · NIGMS · DANA-FARBER CANCER INST · PI PUIGSERVER, PERE · 2017 to 2020
$1.5M
Remodeling mitochondrial cristae to rescue bioenergetic defects in mitochondrial diseaseF32GM136019 · NIGMS · DANA-FARBER CANCER INST · PI MUTLU, BESTE · 2020 to 2022
$154k
NCI NIH HHS R01 CA181217NIDDK NIH HHS R01 DK081418NIDDK NIH HHS R01 DK089883NIDDK NIH HHS R01 DK117655NIGMS NIH HHS F32 GM136019NIGMS NIH HHS R01 GM121452
6 · The paper itself

Abstract

General Control Non-repressed 5 protein (GCN5), encoded by the mammalian gene Kat2a, is the first histone acetyltransferase discovered to link histone acetylation to transcriptional activation [1]. The enzymatic activity of GCN5 is linked to cellular metabolic and energetic states regulating gene expression programs. GCN5 has a major impact on energy metabolism by i) sensing acetyl-CoA, a central metabolite and substrate of the GCN5 catalytic reaction, and ii) acetylating proteins such as PGC-1α, a transcriptional coactivator that controls genes linked to energy metabolism and mitochondrial biogenesis. PGC-1α is biochemically associated with the GCN5 protein complex during active metabolic reprogramming. In the first part of the review, we examine how metabolism can change GCN5-dependent histone acetylation to regulate gene expression to adapt cells. In the second part, we summarize the GCN5 function as a nutrient sensor, focusing on non-histone protein acetylation, mainly the metabolic role of PGC-1α acetylation across different tissues.

Indexed as

AcetylationAcetyl Coenzyme AAdipose TissueAnimalsEnergy MetabolismGlucoseHistonesHumansLiverMitochondriaNutrientsOrganelle Biogenesisp300-CBP-Associated Factorp300-CBP Transcription FactorsPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaThermogenesisAcetyl Coenzyme AGlucoseHistonesNutrientsp300-CBP-Associated Factorp300-CBP Transcription FactorsPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaTrans-ActivatorsAcetylationAcetyl-CoAGCN5Glucose homeostasisMetabolismMitochondriaPGC-1α

Identifiers

PMID32827753
PMCPMC7854474
OpenAlexW3079804098

What OpenQuestion holds

Textmetadata
LicenceTDM
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.