Evidence map›Paper›PMID 11073990›Full record

ArticleMolecular and cellular biology2000

A novel Rb- and p300-binding protein inhibits transactivation by MyoD.

W R MacLellan, G Xiao, M Abdellatif, M D Schneider

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

61 citing papers in PubMed, 123 citations in OpenAlex.

  1. Article
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  4. Integrative transcriptomics and cell systems analyses reveal protective pathways controlled by Igfbp-3 in anthracycline-induced cardiotoxicity.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023
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  20. Peptidic degron in EID1 is recognized by an SCF E3 ligase complex containing the orphan F-box protein FBXO21.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article

1 more citing papers are in PubMed but not listed here.

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

4 authors at 2 institutions in 2 countries.

W R MacLellanCardiovascular Research Laboratories, Department of Medicine, UCLA School of Medicine, Los Angeles, California 90095, USA. rmaclellan@mednet.ucla.edu
G Xiao
M Abdellatif
M D Schneider
University of California, Los Angeles · USBaylor College of Medicine · US

Funding

GENES THAT CONTROL CELL NUMBER--GI/S CHECKPOINTR01HL061668 · NHLBI · IMPERIAL COLLEGE OF SCIENCE, TECHNOLOGY AND MEDICINE · PI SCHNEIDER, MICHAEL DAVID · 1998 to 2007
$2.8M
MOLECULAR MECHANISMS OF CARDIAC HYPERTROPHYR01HL047567 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI SCHNEIDER, MICHAEL DAVID · 1992 to 2006
$2.1M
MOLECULAR MECHANISMS OF CARDIAC DIFFERENTIATIONK08HL003671 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI MACLELLAN, WILLIAM ROBB · 1997 to 2000
$86k
NHLBI NIH HHS K08 HL03671NHLBI NIH HHS R01 HL047567NHLBI NIH HHS R01 HL061668NHLBI NIH HHS R01 HL47567NHLBI NIH HHS R01 HL61668
6 · The paper itself

Abstract

The retinoblastoma protein (Rb) regulates both the cell cycle and tissue-specific transcription, by modulating the activity of factors that associate with its A-B and C pockets. In skeletal muscle, Rb has been reported to regulate irreversible cell cycle exit and muscle-specific transcription. To identify factors interacting with Rb in muscle cells, we utilized the yeast two-hybrid system, using the A-B and C pockets of Rb as bait. A novel protein we have designated E1A-like inhibitor of differentiation 1 (EID-1), was the predominant Rb-binding clone isolated. It is preferentially expressed in adult cardiac and skeletal muscle and encodes a 187-amino-acid protein, with a classic Rb-binding motif (LXCXE) in its C terminus. Overexpression of EID-1 in skeletal muscle inhibited tissue-specific transcription. Repression of skeletal muscle-restricted genes was mediated by a block to transactivation by MyoD independent of G(1) exit and, surprisingly, was potentiated by a mutation that prevents EID-1 binding to Rb. Inhibition of MyoD may be explained by EID-1's ability to bind and inhibit p300's histone acetylase activity, an essential MyoD coactivator. Thus, EID-1 binds both Rb and p300 and is a novel repressor of MyoD function.

Indexed as

Saccharomyces cerevisiae ProteinsTranscriptional ActivationAcetyltransferasesAdenovirus E1A ProteinsAmino Acid SequenceCell Cycle ProteinsCloning, MolecularGene Expression RegulationHistone AcetyltransferasesMolecular Sequence DataMuscle, SkeletalMyoD ProteinNuclear ProteinsProtein BindingRepressor ProteinsRetinoblastoma ProteinAcetyltransferasesAdenovirus E1A ProteinsCell Cycle ProteinsEID1 protein, humanHistone AcetyltransferasesMyoD ProteinNuclear ProteinsRepressor ProteinsRetinoblastoma ProteinSaccharomyces cerevisiae ProteinsTrans-Activators

Identifiers

PMID11073990
PMCPMC86545
OpenAlexW2129781589

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.