Evidence map›Paper›PMID 24732800›Full record

ArticleMolecular and cellular biology2014

CtBP and associated LSD1 are required for transcriptional activation by NeuroD1 in gastrointestinal endocrine cells.

Subir K Ray, H Joyce Li, Eric Metzger, Roland Schüle, Andrew B Leiter

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

47 citing papers in PubMed, 69 citations in OpenAlex.

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  10. TGF-β in developmental and fibrogenic EMTs.Seminars in cancer biology · 2022
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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

5 authors at 2 institutions in 2 countries.

Subir K RayDepartment of Medicine, Division of Gastroenterology, University of Massachusetts Medical School, Worcester, Massachusetts, USA.
H Joyce LiDepartment of Medicine, Division of Gastroenterology, University of Massachusetts Medical School, Worcester, Massachusetts, USA.
Eric MetzgerCenter for Clinical Research, University of Freiburg Medical Center, Freiburg, Germany.
Roland SchüleCenter for Clinical Research, University of Freiburg Medical Center, Freiburg, Germany.
Andrew B LeiterDepartment of Medicine, Division of Gastroenterology, University of Massachusetts Medical School, Worcester, Massachusetts, USA andrew.leiter@umassmed.edu.
University of Massachusetts Chan Medical School · USUniversity of Freiburg · DE

Funding

CELL-SPECIFIC REGULATION OF SECRETIN GENE EXPRESSIONR01DK043673 · NIDDK · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI LEITER, ANDREW B · 1992 to 2007
$3.4M
Transcriptional regulation of enteroendocrine cell differentiation by NeuroDR01DK090000 · NIDDK · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI LEITER, ANDREW B. · 2010 to 2013
$1.6M
NIDDK NIH HHS DK43673NIDDK NIH HHS DK90000NIDDK NIH HHS R01 DK043673NIDDK NIH HHS R01 DK090000
6 · The paper itself

Abstract

Gene expression programs required for differentiation depend on both DNA-bound transcription factors and surrounding histone modifications. Expression of the basic helix-loop-helix (bHLH) protein NeuroD1 is restricted to endocrine cells in the gastrointestinal (GI) tract, where it is important for endocrine differentiation. RREB1 (RAS-responsive element binding protein 1), identified as a component of the CtBP corepressor complex, binds to nearby DNA elements to associate with NeuroD and potentiate transcription of a NeuroD1 target gene. Transcriptional activation by RREB1 depends on recruitment of CtBP with its associated proteins, including LSD1, through its PXDLS motifs. The mechanism of transcriptional activation by CtBP has not been previously characterized. Here we found that activation was dependent on the histone H3 lysine 9 (H3K9) demethylase activity of LSD1, which removes repressive methyl marks from dimethylated H3K9 (H3K9Me2), to facilitate subsequent H3K9 acetylation by the NeuroD1-associated histone acetyltransferase, P300/CBP-associated factor (PCAF). The secretin, β-glucokinase, insulin I, and insulin II genes, four known direct targets of NeuroD1 in intestinal and pancreatic endocrine cells, all show similar promoter occupancy by CtBP-associated proteins and PCAF, with acetylation of H3K9. This work may indicate a mechanism for selective regulation of transcription by CtBP and LSD1 involving their association with specific transcription factors and cofactors to drive tissue-specific transcription.

Indexed as

AcetylationAlcohol OxidoreductasesAnimalsBasic Helix-Loop-Helix ProteinsCell LineDNA-Binding ProteinsEnteroendocrine CellsHistone DemethylasesHistonesHumansLysineMethylationModels, BiologicalNerve Tissue Proteinsp300-CBP-Associated Factorp300-CBP Transcription FactorsAlcohol OxidoreductasesBasic Helix-Loop-Helix ProteinsC-terminal binding proteinDNA-Binding ProteinsHistone DemethylasesHistonesKDM1A protein, humanLysineNerve Tissue ProteinsNeurogenic differentiation factor 1p300-CBP-Associated Factorp300-CBP Transcription FactorsRREB1 protein, humanSecretinTranscription Factors

Identifiers

PMID24732800
PMCPMC4054299
OpenAlexW2111668004

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.