Evidence map›Paper›PMID 18467525›Full record

ArticleMolecular endocrinology (Baltimore, Md.)2008

CCAAT/enhancer binding protein-beta is a transcriptional regulator of peroxisome-proliferator-activated receptor-gamma coactivator-1alpha in the regenerating liver.

Haitao Wang, T Harshani Peiris, A Mowery, John Le Lay, Yan Gao, Linda E Greenbaum

Open access · greenAbstract read
In one paragraph

Article in Molecular endocrinology (Baltimore, Md.), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.4field-weighted citation impact, top 9% 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

33 citing papers in PubMed, 51 citations in OpenAlex.

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  9. Selective inhibition of low-affinity memory CD8The Journal of experimental medicine · 2019
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  13. Endoplasmic Reticulum Stress-Induced CHOP Inhibits PGC-1α and Causes Mitochondrial Dysfunction in Diabetic Embryopathy.Toxicological sciences : an official journal of the Society of Toxicology · 2017
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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

6 authors at 1 institution in 1 country.

Haitao WangDepartment of Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA.
T Harshani Peiris
A Mowery
John Le Lay
Yan Gao
Linda E Greenbaum
University of Pennsylvania · US

Funding

Transcriptional Control in Hepatocyte ProliferationR01DK056669 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI GREENBAUM, LINDA E · 2001 to 2011
$2.8M
NIDDK NIH HHS R01 DK 056669NIDDK NIH HHS R01 DK056669
6 · The paper itself

Abstract

The transcriptional coactivator peroxisome-proliferator-activated receptor-gamma coactivator-1alpha (PGC-1alpha) is induced in the liver in response to fasting and coordinates the activation of targets necessary for increasing energy production for gluconeogenesis and ketogenesis. After partial hepatectomy, the liver must restore its mass while maintaining metabolic homeostasis to ensure survival. Here we report that PGC-1alpha is rapidly and dramatically induced after hepatectomy, with an amplitude of induction that exceeds the fasting response. Maximal activation of PGC-1alpha after hepatectomy is dependent on the basic leucine zipper transcription factor, CCAAT/enhancer binding protein-beta (C/EBPbeta), a critical factor in hepatocyte proliferation. We demonstrate in vivo C/EBPbeta binding to C/EBP and cAMP response element sites in the PGC-1alpha promoter and show that the C/EBP site is essential for PGC-1alpha activation. Expression of the PGC-1alpha target, carnitine palmitoyl transferase 1a, the rate-limiting enzyme in fatty acid beta-oxidation, and of long-chain acyl-coenzyme A dehydrogenase, an enzyme involved in beta-oxidation of long chain fatty acids, was significantly reduced in C/EBPbeta(-/-) livers after hepatectomy. These findings identify C/EBPbeta as a direct activator of PGC-1alpha in the regenerating liver. The demonstration of a functional link between C/EBPbeta and PGC-1alpha activation provides a likely mechanism for how upstream signaling pathways in the regenerating liver can enable the adaptation to the changed metabolic status.

Indexed as

Liver RegenerationTranscription, GeneticAnimalsBinding SitesCCAAT-Enhancer-Binding Protein-betaCell LineCricetinaeGlucoseHomozygoteHumansLiverMiceOxygenPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaTrans-ActivatorsTranscription FactorsCCAAT-Enhancer-Binding Protein-betaGlucoseOxygenPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPpargc1a protein, mouseTrans-ActivatorsTranscription Factors

Identifiers

PMID18467525
PMCPMC2453599
OpenAlexW1970107943

What OpenQuestion holds

Textmetadata
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.