Evidence map›Paper›PMID 18710939›Full record

ArticleMolecular and cellular biology2008

Quantitative proteomic identification of MAZ as a transcriptional regulator of muscle-specific genes in skeletal and cardiac myocytes.

Charis L Himeda, Jeffrey A Ranish, Stephen D Hauschka

Abstract read
In one paragraph

Article in Molecular and cellular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
2.8field-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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.

  1. Pooled it
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  8. CRISPR Deletion of a SVA Retrotransposon Demonstrates Function as aInternational journal of molecular sciences · 2021
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  9. A Muscle Hybrid Promoter as a Novel Tool for Gene Therapy.Molecular therapy. Methods & clinical development · 2019
    Article
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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

3 authors at 2 institutions in 1 country.

Charis L HimedaDepartment of Biochemistry, University of Washington, Seattle, WA 98195, USA.
Jeffrey A Ranish
Stephen D Hauschka
University of Washington · USInstitute for Systems Biology · US

Funding

Quantitative Systems BiologyP50GM076547 · NIGMS · INSTITUTE FOR SYSTEMS BIOLOGY · PI BALIGA, NITIN S · 2006 to 2016
$30.6M
EXPERIMENTAL PATHOLOGY OF CARDIOVASCULAR DISEASET32HL007312 · NHLBI · UNIVERSITY OF WASHINGTON · PI MAJESKY, MARK W., SCHWARTZ, STEPHEN MARK · 1985 to 2019
$11.8M
Striated Muscle Gene Transcription and Regulatory Gene Cassettes for Gene TherapyR01AR018860 · NIAMS · UNIVERSITY OF WASHINGTON · PI HAUSCHKA, STEPHEN DENISON · 1986 to 2012
$3.4M
NHLBI PROTEOMICS INITIATIVE-268028179N01HV028179 · HV · INSTITUTE FOR SYSTEMS BIOLOGY · 2002 to 2002
–
NHLBI NIH HHS N01 HV028179NHLBI NIH HHS N01-HV-28179NHLBI NIH HHS T32 HL007312NHLBI NIH HHS T32-HL007312NIAMS NIH HHS R01 AR018860NIAMS NIH HHS R01-AR18860NIGMS NIH HHS P50 GM076547NIGMS NIH HHS P50GM076547
6 · The paper itself

Abstract

We identified a conserved sequence within the Muscle creatine kinase (MCK) promoter that is critical for high-level activity in skeletal and cardiac myocytes (MCK Promoter Element X [MPEX]). After selectively enriching for MPEX-binding factor(s) (MPEX-BFs), ICAT-based quantitative proteomics was used to identify MPEX-BF candidates, one of which was MAZ (Myc-associated zinc finger protein). MAZ transactivates the MCK promoter and binds the MPEX site in vitro, and chromatin immunoprecipitation analysis demonstrates enrichment of MAZ at the endogenous MCK promoter and other muscle gene promoters (Skeletal alpha-actin, Desmin, and alpha-Myosin heavy chain) in skeletal and cardiac myocytes. Consistent with its role in muscle gene transcription, MAZ transcripts and DNA-binding activity are upregulated during skeletal myocyte differentiation. Furthermore, MAZ was shown to bind numerous sequences (e.g., CTCCTCCC and CTCCACCC) that diverge from the GA box binding motif. Alternate motifs were identified in many muscle promoters, including Myogenin and MEF2C, and one motif was shown to be critical for Six4 promoter activity in both skeletal and cardiac myocytes. Interestingly, MAZ occupies and is able to transactivate the Six4 promoter in skeletal but not cardiac myocytes. Taken together, these findings are consistent with a previously unrecognized role for MAZ in muscle gene regulation.

Indexed as

ProteomicsTranscription, GeneticAmino Acid MotifsAnimalsBase SequenceCell DifferentiationCell ExtractsCell NucleusCells, CulturedCreatine Kinase, MM FormDNA-Binding ProteinsHomeodomain ProteinsMiceMolecular Sequence DataMuscle ProteinsMuscle, SkeletalCell Extractsc-MYC-associated zinc finger proteinCreatine Kinase, MM FormDNA-Binding ProteinsHomeodomain ProteinsMuscle ProteinsRNA, MessengerSix4 protein, mouseTrans-ActivatorsTranscription Factors

Identifiers

PMID18710939
PMCPMC2577440
OpenAlexW2137609813

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.