Affinage

MYOD1

Myoblast determination protein 1 · UniProt P15172

Length
320 aa
Mass
34.5 kDa
Annotated
2026-04-29
100 papers in source corpus 50 papers cited in narrative 50 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

MYOD1 is a master regulatory basic-helix-loop-helix (bHLH) transcription factor that specifies skeletal muscle identity by binding E-box DNA sequences as heterodimers with E-proteins, organizing muscle-specific enhancers and three-dimensional genome architecture, and activating the full myogenic transcriptional program including structural genes, fusion genes (Myomaker, Myomixer), and regulatory microRNAs (miR-206, miR-133) (PMID:1846704, PMID:23249738, PMID:35017543, PMID:33355126, PMID:17030984). The bHLH domain mediates DNA-dependent heterodimer assembly with E-proteins such as E47 and HEB-beta, while an N-terminal activation domain, cooperation between N- and C-terminal regions unique to MyoD (versus Myf5), and PBX/MEIS homeodomain co-factor interactions collectively determine muscle lineage specificity over alternative fates (PMID:9488706, PMID:16275751, PMID:25801030, PMID:17699609). MyoD activity is regulated at multiple levels: post-translationally by acetylation (CBP/p300, PCAF) that enhances transcriptional activity, methylation by G9a that triggers Cul4/Ddb1/Dcaf1-mediated proteasomal degradation, phosphorylation that selectively blocks homodimer DNA binding, and N-terminal ubiquitination by HUWE1; at target promoters, a KAP1-scaffolded switch releases corepressors (G9a, HDAC1, HP1α/β) upon MSK1 phosphorylation to permit activation (PMID:10944526, PMID:26149774, PMID:8226992, PMID:22277673, PMID:25737281). MyoD also inhibits cell proliferation through a separable myc-like domain, positively autoregulates its own transcription, and its mRNA is subject to translational repression by Staufen1 in quiescent satellite cells and m6A-dependent stabilization by METTL3 (PMID:2359457, PMID:2546677, PMID:29073096, PMID:28878038).

Mechanistic history

Synthesis pass · year-by-year structured walk · 25 steps
  1. 1989 High

    Establishing that MyoD operates in a positive autoregulatory feedback loop with myogenin resolved how a single transcription factor can initiate and sustain the myogenic program.

    Evidence cDNA transfection into 10T1/2 and Swiss 3T6 cells with Northern blot detection of endogenous MyoD1 and myogenin mRNA

    PMID:2546677

    Open questions at the time
    • Cis-regulatory elements mediating autoregulation not mapped
    • Whether autoregulation is direct or indirect not resolved
  2. 1989 High

    Placing Ras upstream of MyoD expression explained how oncogenic signaling blocks myogenesis and showed that forced MyoD expression could override this block.

    Evidence Retroviral ras transformation of myoblasts with epistasis rescue by retroviral MyoD re-expression

    PMID:2548731

    Open questions at the time
    • Intermediate signaling steps between Ras and MyoD transcription not identified
    • Whether Ras directly targets MyoD promoter or acts indirectly unknown
  3. 1990 High

    Demonstrating that MyoD inhibits cell proliferation through a domain separable from its differentiation function established that cell cycle arrest and myogenic differentiation are mechanistically uncoupled.

    Evidence Microinjection of deletion/chimeric MyoD constructs into NIH 3T3 cells measuring DNA synthesis versus differentiation markers

    PMID:2359457

    Open questions at the time
    • The 'myc-like domain' target genes and mechanism of growth arrest not identified
    • Whether cell cycle arrest requires DNA binding not resolved
  4. 1991 High

    Defining the 68-amino-acid bHLH domain as necessary and sufficient for myogenic conversion, with separable dimerization and DNA-binding functions, established the modular architecture of MyoD's core activity.

    Evidence Deletion and chimeric mutagenesis with transient transfection, DNA-binding, and cell conversion assays

    PMID:1651276 PMID:1846704

    Open questions at the time
    • Identity of the 'recognition factor' that unmasks the N-terminal activation domain remained unknown
    • Structural basis of basic-region DNA specificity not yet resolved
  5. 1992 High

    Showing that c-Jun physically contacts the MyoD HLH domain and mediates mutual transcriptional antagonism revealed a direct mechanism by which AP-1 signaling opposes myogenesis.

    Evidence Co-immunoprecipitation (in vivo and in vitro), mutagenesis of leucine zipper/HLH domains, reporter assays; extended by analysis of multiple Jun/Fos family members

    PMID:1310896 PMID:1313772

    Open questions at the time
    • Whether the Jun-MyoD interaction occurs on chromatin in muscle cells not shown
    • Stoichiometric regulation of this antagonism in vivo unknown
  6. 1993 High

    Discovering that phosphorylation selectively blocks MyoD homodimer but not MyoD-E12 heterodimer DNA binding provided a biochemical mechanism for how post-translational modification shifts the functional dimer equilibrium in muscle cells.

    Evidence Baculovirus-expressed MyoD with in vitro dephosphorylation and EMSA comparing homodimer/heterodimer binding

    PMID:8226992

    Open questions at the time
    • Identity of the kinase(s) responsible not determined
    • In vivo relevance of homodimer versus heterodimer ratio not directly tested
  7. 1993 High

    Identifying a heat-sensitive cellular factor required for MyoD-E47 heterodimer DNA binding in reconstituted systems indicated that purified bHLH proteins are insufficient for DNA recognition, pointing to an obligate co-factor.

    Evidence In vitro reconstitution with purified proteins, cell extract fractionation, EMSA

    PMID:8393567

    Open questions at the time
    • Molecular identity of the factor never established
    • Whether this factor is the same as the 'recognition factor' from activation domain studies unknown
  8. 1998 High

    Biophysical demonstration that the MyoD bHLH domain is intrinsically unfolded and that heterodimer assembly is driven by DNA contacts (not preformed protein-protein affinity) fundamentally revised the model of bHLH complex formation.

    Evidence Fluorescence quenching, equilibrium sedimentation, EMSA, and loop-swap mutagenesis between MyoD and E47

    PMID:9488706

    Open questions at the time
    • How chromatin context affects this DNA-driven assembly unknown
    • Whether the same mechanism operates in vivo in nucleosome-bound contexts not tested
  9. 2000 High

    Identifying acetylation of MyoD by CBP/p300 and PCAF at the DNA-binding domain boundary, and showing that this modification enhances transcriptional activity, established a key activating post-translational switch for MyoD function.

    Evidence In vitro acetylation assays, site-directed mutagenesis of acetylation sites, microinjection functional assays

    PMID:10944526

    Open questions at the time
    • In vivo acetylation dynamics during differentiation not tracked
    • Which deacetylase reverses this modification not identified in this study
  10. 2001 High

    Demonstrating that MyoD undergoes ubiquitin-proteasome degradation in the nucleus, predominantly through an N-terminus-dependent pathway, explained how MyoD turnover is regulated in the compartment where it is active.

    Evidence In vitro degradation in purified HeLa nucleoplasm, proteasome inhibitors, leptomycin B; extended by N-terminal mutagenesis and NLS/NES modifications

    PMID:11309375 PMID:12397066

    Open questions at the time
    • The E3 ligase for the N-terminal pathway not identified in these studies
    • How degradation is coordinated with transcriptional activity unknown
  11. 2002 High

    Identifying Cdk9/cyclin T2 as a MyoD-interacting kinase that phosphorylates MyoD and activates its transcriptional program connected MyoD to P-TEFb-mediated transcriptional elongation.

    Evidence Co-immunoprecipitation, in vitro kinase assay, dominant-negative Cdk9, reporter assays

    PMID:12037670

    Open questions at the time
    • Specific phosphorylation sites on MyoD not mapped
    • Whether Cdk9 phosphorylation of MyoD is distinct from its Pol II CTD phosphorylation function unclear
  12. 2003 High

    Showing that STAT3 directly interacts with MyoD and competes for p300/CBP coactivators to inhibit MyoD DNA binding and transactivation revealed a cytokine-responsive antagonistic pathway during myogenesis.

    Evidence Co-immunoprecipitation, EMSA, reporter assays, coactivator rescue experiments in C2C12 cells

    PMID:12947115

    Open questions at the time
    • Whether STAT3-MyoD interaction occurs at specific genomic loci not tested by ChIP
    • In vivo relevance in regenerating muscle not examined
  13. 2005 High

    Microarray-based comparison of MyoD and Myf5 target genes, combined with domain-swap mutagenesis, established that functional distinction between these MRFs depends on cooperative interaction between MyoD's N- and C-terminal regions.

    Evidence Microarray profiling with MyoD/Myf5 domain-swap mutants in myoblast differentiation

    PMID:16275751

    Open questions at the time
    • Structural basis for N-/C-terminal cooperation not resolved
    • Specific cofactors differentially recruited by MyoD versus Myf5 not identified
  14. 2006 High

    Discovery that MyoD directly activates miR-206 transcription, which then post-transcriptionally suppresses Fstl1 and Utrn, revealed a feed-forward mechanism by which MyoD indirectly represses genes during differentiation.

    Evidence ChIP showing MyoD binding to miR-206 locus, 3'UTR reporter assays for target validation, fibroblast-to-muscle conversion

    PMID:17030984

    Open questions at the time
    • Full spectrum of miR-206 targets during differentiation not defined
    • Whether miR-206 induction is essential for MyoD-driven differentiation not tested by miRNA loss-of-function
  15. 2007 High

    Demonstrating that Pbx homeodomain proteins are required for MyoD to activate fast-muscle genes in zebrafish established co-factor-dependent target selectivity as a core mechanism of bHLH lineage specification.

    Evidence Morpholino knockdown of Pbx in zebrafish with genetic epistasis and in situ hybridization

    PMID:17699609

    Open questions at the time
    • Whether PBX marks pre-existing accessible sites or is co-recruited with MyoD not determined
    • Mammalian validation of fast/slow muscle selectivity not provided in this study
  16. 2008 High

    Identifying HP1α/β as direct MyoD-binding repressors recruited to target promoters in proliferating myoblasts explained how MyoD can occupy target genes without activating them prior to differentiation.

    Evidence Recombinant protein binding, co-IP, ChIP at MyoD target promoters, HP1 overexpression/knockdown in C2C12 cells

    PMID:18599480

    Open questions at the time
    • Signal that triggers HP1 release upon differentiation not identified
    • Whether HP1 binding depends on H3K9 methylation at MyoD-bound sites not tested
  17. 2012 High

    Genome-wide ChIP-seq in MyoD-null myoblasts demonstrated that MyoD is required for assembly of muscle-specific enhancers marked by H3K4me1 and recruitment of Set7, establishing MyoD as a pioneer-like enhancer organizer rather than simply an activator of pre-existing enhancers.

    Evidence ChIP-seq for histone marks and Set7 in MyoD-null versus wild-type myoblasts with MyoD re-expression rescue

    PMID:23249738

    Open questions at the time
    • Whether MyoD directly displaces nucleosomes or requires chromatin remodelers for enhancer establishment not resolved
    • Relative contributions of MyoD versus Myf5 to enhancer assembly in vivo not separated
  18. 2012 Medium

    Identifying HUWE1 as the E3 ubiquitin ligase that ubiquitinates MyoD at its N-terminal residue resolved the molecular identity of the enzyme responsible for the N-terminal degradation pathway discovered a decade earlier.

    Evidence In vitro ubiquitination assay, co-immunoprecipitation, proteasome inhibitor treatment

    PMID:22277673

    Open questions at the time
    • Single study without independent confirmation
    • In vivo validation of HUWE1-dependent MyoD degradation during differentiation not shown
    • Whether HUWE1 acts on MyoD at specific cell cycle phases not addressed
  19. 2015 High

    Demonstrating that KAP1 scaffolds both coactivators and corepressors at MyoD/MEF2 targets, with MSK1 phosphorylation releasing corepressors to permit activation, defined a kinase-triggered chromatin switch governing the proliferation-to-differentiation transition.

    Evidence ChIP-seq, co-immunoprecipitation, MSK1 kinase assay, myoblast differentiation

    PMID:25737281

    Open questions at the time
    • Upstream signals activating MSK1 at differentiation onset not fully mapped
    • Whether KAP1 phosphorylation is sufficient or only necessary for corepressor release not tested
  20. 2015 High

    Showing that G9a methylates MyoD to trigger Cul4/Ddb1/Dcaf1-mediated ubiquitination and degradation, while Jmjd2C demethylase reverses this mark to stabilize MyoD, established a methylation-dependent degradation pathway distinct from the N-terminal ubiquitination mechanism.

    Evidence In vitro demethylation and ubiquitination assays, co-IP, half-life measurements, ChIP, myogenic conversion assay

    PMID:26149774

    Open questions at the time
    • Specific methylation site(s) on MyoD not identified
    • How the G9a and HUWE1 degradation pathways are coordinated or prioritized unknown
  21. 2015 High

    Converting MyoD from a myogenic to a neurogenic master regulator by altering its private-site DNA-binding specificity and disrupting PBX/MEIS interaction definitively established that lineage identity is encoded in the combination of E-box preference and co-factor interactions.

    Evidence Chimeric MyoD-NeuroD2 DNA-binding domain mutations, ChIP-seq, gene expression, fibroblast lineage conversion

    PMID:25801030

    Open questions at the time
    • Structural basis for private-site selectivity not resolved at atomic level
    • Whether lineage conversion is complete or partial at single-cell resolution not examined
  22. 2017 High

    Multiple studies converged to show that noncoding RNAs (Linc-RAM, Malat1, eRNAs) serve as scaffolds and switches at MyoD target loci: Linc-RAM promotes MyoD-Baf60c-Brg1 remodeling complex assembly, while Malat1 recruits Suv39h1 for H3K9me3 silencing until degraded by miR-181a.

    Evidence RNA pulldown/RIP, co-IP, ChIP-seq, Linc-RAM knockout mice, Malat1 knockout mice with muscle regeneration phenotypes

    PMID:28091529 PMID:28326190

    Open questions at the time
    • Whether Linc-RAM and Malat1 act at overlapping or distinct genomic loci not compared
    • Quantitative stoichiometry of lncRNA-MyoD interactions in vivo unknown
  23. 2017 High

    Demonstrating that Staufen1 binds MyoD mRNA 3'UTR to repress its translation in quiescent satellite cells, with Staufen1 haploinsufficiency causing premature exit from quiescence, established translational control as a critical layer of MyoD regulation in stem cells.

    Evidence Single-molecule FISH, RNA pulldown, in vivo Staufen1+/- mice with MyoD protein/mRNA quantification

    PMID:29073096

    Open questions at the time
    • RNA-binding specificity of Staufen1 on MyoD mRNA (exact binding site/structure) not mapped
    • What signal releases Staufen1 from MyoD mRNA upon activation unknown
  24. 2020 High

    Showing that MyoD directly activates Myomaker and Myomixer expression via E-box binding in human myoblasts connected MyoD transcriptional activity to the cell fusion machinery essential for multinucleation.

    Evidence CRISPR MyoD knockout, ChIP at E-box motifs, promoter assays, fusion assays in human primary myoblasts

    PMID:33355126

    Open questions at the time
    • Whether MyoD is sufficient for fusion gene expression without additional MRFs not fully resolved
    • Regulation of fusion gene timing relative to other MyoD targets not examined
  25. 2022 High

    Hi-C analysis in MyoD-null mice revealed that MyoD organizes muscle-specific three-dimensional chromatin loops that cannot be established by H3K27ac alone, extending MyoD's role from enhancer assembly to higher-order genome architecture.

    Evidence Hi-C, ChIP-seq for H3K27ac, ChIA-PET in MyoD-knockout versus wild-type muscle cells

    PMID:35017543

    Open questions at the time
    • Whether MyoD directly mediates loop formation or recruits architectural factors such as cohesin/CTCF not determined
    • Temporal dynamics of loop formation relative to gene activation unknown

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include how the multiple degradation pathways (HUWE1 N-terminal ubiquitination versus G9a methylation-Cul4 ubiquitination) are coordinated during the cell cycle and differentiation, the identity of the cellular factor required for MyoD-E47 heterodimer DNA binding, and the structural basis of MyoD pioneer activity at nucleosome-occupied enhancers.
  • Structural mechanism of nucleosome engagement and enhancer opening by MyoD unknown
  • Integration of multiple PTM-mediated degradation pathways not modeled
  • Identity of the reconstitution-defined DNA-binding co-factor from 1993 remains unresolved

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140110 transcription regulator activity 10 GO:0003677 DNA binding 7
Localization
GO:0005634 nucleus 2 GO:0005654 nucleoplasm 1
Pathway
R-HSA-74160 Gene expression (Transcription) 11 R-HSA-1266738 Developmental Biology 6 R-HSA-4839726 Chromatin organization 6 R-HSA-392499 Metabolism of proteins 5
Partners
CTNNB1EP300HUWE1KAT2BMYOGTCF12TCF3TRIM28
Complex memberships
KAP1-MyoD/MEF2 scaffold complexMyoD-Baf60c-Brg1 remodeling complexMyoD-E47/HEB heterodimer

Evidence

Reading pass · 50 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1991 MyoD contains a basic-helix-loop-helix (bHLH) domain of 68 amino acids that is necessary and sufficient for myogenic conversion; the helix-loop-helix motif mediates dimerization, while the basic region mediates DNA binding to muscle-specific enhancers, and MyoD activates its own transcription through positive autoregulation. Deletion/chimeric mutagenesis, transient transfection, DNA-binding assays, cell conversion assays Science High 1846704
1989 MyoD1 positively autoregulates its own transcription and engages in a mutual positive feedback loop with myogenin; MyoD1 activates endogenous MyoD1 mRNA and myogenin expression, and myogenin reciprocally activates MyoD1 expression upon transfection. cDNA transfection into 10T1/2 and Swiss 3T6 cells, Northern blot analysis of endogenous gene activation Cell High 2546677
1991 MyoD transcriptional activation requires a specific alanine in the basic region for increased DNA binding and a specific threonine for transcriptional activation; the activation domain maps to the amino-terminal 53 residues and is normally masked by the rest of the molecule, requiring a basic-region-recognizing 'recognition factor' for activity. Back-mutation of MyoD-E12Basic chimera, reporter gene assays, VP16 domain swap, cotransfection in multiple cell lines Genes & development High 1651276
1992 c-Jun physically interacts with MyoD both in vivo and in vitro, with the leucine zipper domain of Jun contacting the helix-loop-helix region of MyoD; this interaction mediates mutual transcriptional antagonism — Jun inhibits MyoD transactivation of muscle genes and MyoD inhibits Jun transactivation of AP-1 target genes. Co-immunoprecipitation (in vivo), in vitro binding assays, transient transfection reporter assays, mutational analysis Cell High 1310896
1992 c-Fos, c-Jun, and JunB (but not JunD) repress MyoD- and myogenin-mediated transactivation of muscle creatine kinase enhancer by targeting the basic-HLH region of myogenic factors; repression can be mediated through the amino terminus of c-Jun and is specific to myogenic HLH proteins, not the widely expressed E47. Transient transfection reporter assays, myogenin deletion mutant analysis, comparison of Jun family members Genes & development High 1313772
1990 MyoD1 inhibits cell proliferation independently of myogenic differentiation; deletion of the myc-like domain eliminates inhibition of DNA synthesis, while substitution of the basic domain with E12 basic domain inhibits growth but fails to induce differentiation, demonstrating that cell cycle arrest and differentiation are controlled by separable MyoD domains. Microinjection of MyoD1 expression constructs into NIH 3T3 cells, deletion/chimeric mutagenesis, DNA synthesis measurement Nature High 2359457
1989 Activated Ras inhibits myogenic differentiation by suppressing expression of MyoD1 and myogenin; forced retroviral expression of MyoD1 in ras-transformed myoblasts restores both terminal differentiation markers and lineage markers, placing Ras upstream of MyoD1. Retroviral transformation, retroviral MyoD1 re-expression, Northern blot, epistasis analysis Cell High 2548731
2006 MyoD directly activates transcription of the muscle-specific microRNA miR-206, which then targets the 3'UTR sequences of Fstl1 and Utrn mRNAs to suppress their expression during skeletal muscle differentiation, revealing an indirect suppression mechanism for MyoD. Chromatin immunoprecipitation, reporter assays with 3'UTR constructs, fibroblast-to-muscle conversion by MyoD The Journal of cell biology High 17030984
2012 MyoD1 is required for assembly of condition-specific muscle enhancers genome-wide; MyoD1-null myoblasts show loss of H3K4me1, H3K27ac, and recruitment of Set7 (H3K4 monomethylase) and other transcription factors at enhancers, and MyoD1 re-expression restores H3K4me1 (and H3K27ac in myotubes), defining MyoD1 as a genome-wide enhancer organizer. Chromatin state mapping (ChIP-seq for histone modifications), MyoD1-null myoblasts, re-expression of MyoD1, genome-wide analysis Genes & development High 23249738
2005 MyoD is functionally distinct from Myf5 in inducing differentiation-phase target genes; a novel cooperation between MyoD NH2- and COOH-terminal regions (absent in Myf5) underlies this distinction, as revealed by microarray-based gene expression analysis with domain-swap mutants. Microarray gene expression profiling, PCR, in vitro myoblast differentiation model with MyoD/Myf5 domain mutants The Journal of cell biology High 16275751
2000 MyoD is acetylated by both CBP/p300 and PCAF on two lysines at the boundary of the DNA-binding domain; acetylation by either enzyme increases MyoD transcriptional activity on muscle-specific promoters, and MyoD mutants that cannot be acetylated in vitro are not activated in functional assays. In vitro acetylation assays, microinjection functional assays, site-directed mutagenesis of acetylation sites The Journal of biological chemistry High 10944526
2001 MyoD is degraded by the ubiquitin-proteasome system in the nucleus; nuclear HeLa nucleoplasm supports MyoD ubiquitination and proteasomal degradation in vitro, and leptomycin B treatment (blocking nuclear export) confirms nuclear degradation in vivo. In vitro degradation assay using purified HeLa nucleoplasm, proteasome inhibitors, leptomycin B nuclear export blockade The Journal of biological chemistry High 11309375
2002 MyoD is preferentially ubiquitinated on its N-terminus for proteasomal degradation (N-terminus-dependent pathway); nuclear localization signal and nuclear export signal modifications restrict ubiquitination to specific compartments, revealing that the lysine-dependent pathway predominates in the cytoplasm while both pathways are active in the nucleus. In vitro ubiquitination assays, site-directed mutagenesis of N-terminus and NLS/NES, subcellular fractionation The Journal of biological chemistry High 12397066
2012 HUWE1 E3 ubiquitin ligase ubiquitinates MyoD at its N-terminal residue, targeting it for proteasomal degradation. In vitro ubiquitination assay, co-immunoprecipitation, proteasome inhibitor treatment Biochemical and biophysical research communications Medium 22277673
2000 p57(Kip2) directly binds MyoD through its NH2-terminal intermediate alpha-helix domain interacting with the basic helix-loop-helix region of MyoD; this interaction (independent of Cdk-inhibitory activity) stabilizes MyoD protein by increasing its half-life and enhancing its transcriptional activity on muscle-specific genes. Cross-immunoprecipitation of endogenous proteins, competition/association assays, site-directed mutagenesis, half-life measurement by pulse-chase, transactivation assays The Journal of biological chemistry High 10764802
2002 Cdk9/cyclin T2 complex directly interacts with MyoD (mapping to amino acids 101-161 in the bHLH region), can phosphorylate MyoD in vitro, and activates MyoD-dependent transcription and myogenic differentiation; cdk9 dominant-negative represses the myogenic program. Co-immunoprecipitation, in vitro kinase assay, overexpression/dominant-negative experiments, reporter gene assays Oncogene High 12037670
1993 Phosphorylated MyoD homodimers fail to bind DNA whereas MyoD-E12 heterodimers are unaffected by phosphorylation; cellular phosphorylation shifts the homodimer-heterodimer equilibrium, modulating binding site competition in muscle cells. Baculovirus expression of MyoD, in vitro dephosphorylation, gel mobility shift/EMSA, comparison with immunoaffinity-purified native protein The Journal of biological chemistry High 8226992
1998 MyoD bHLH domain is intrinsically unfolded and monomeric in solution without DNA; E47 forms stable homodimers off DNA. In the presence of specific DNA, MyoD and E47 form almost exclusively heterodimers, driven by favorable DNA contacts rather than protein-protein affinity, revealing a DNA-mediated folding and assembly mechanism for bHLH heterodimer formation. Fluorescence quenching, equilibrium sedimentation, gel shift/EMSA, loop-swap mutagenesis between MyoD and E47 The Journal of biological chemistry High 9488706
2015 KAP1/TRIM28 acts as a scaffold at MyoD/Mef2 target muscle gene promoters in myoblasts, recruiting both coactivators (p300, LSD1) and corepressors (G9a, HDAC1) to maintain gene silencing; upon differentiation cue, MSK1-mediated phosphorylation of KAP1 releases corepressors, unleashing MyoD/Mef2 transcriptional activation. ChIP-seq, co-immunoprecipitation, MSK1 kinase assay, myoblast differentiation assays Genes & development High 25737281
2008 FoxO3 and Pax3/7 form a codependent transcriptional partnership to directly activate MyoD transcription in myoblasts; in vitro studies show they cooperate to recruit RNA polymerase II and form a preinitiation complex at the MyoD locus, and FoxO3-null mice display impaired muscle regeneration with reduced MyoD. Cell-based transcriptional assays, in vitro preinitiation complex assembly, FoxO3 knockout mouse analysis, chromatin immunoprecipitation Developmental cell High 18854138
1995 MSX1 homeobox protein directly binds the MyoD enhancer and represses MyoD transcription; chromosome 4-mediated inhibition of MyoD activation in fibroblast hybrids is attributed to MSX1, and antisense MSX1 relieves this repression. Somatic cell hybrid analysis, enhancer/promoter reporter assays, gel shift/EMSA showing MSX1 binding to MyoD enhancer, antisense MSX1 rescue Cell High 7664340
2017 Linc-RAM lncRNA directly binds MyoD protein and promotes assembly of the MyoD-Baf60c-Brg1 chromatin remodeling complex on regulatory elements of myogenic target genes to activate their expression; Linc-RAM knockout mice show impaired satellite cell differentiation and muscle regeneration. RNA pulldown/RIP, co-immunoprecipitation, Linc-RAM knockout mice, muscle regeneration assays Nature communications High 28091529
2017 In proliferating myoblasts, Malat1 lncRNA recruits the histone methyltransferase Suv39h1 to MyoD-binding loci, causing H3K9me3 trimethylation and repressing target gene expression; upon differentiation, miR-181a-mediated degradation of Malat1 destabilizes the Suv39h1/HP1β/HDAC1 repressive complex and allows a Set7-containing activating complex to displace it, permitting MyoD transactivation. RNA pulldown, ChIP-seq, knockdown/knockout models, miRNA overexpression, Malat1 KO mice, mdx dystrophic mice Cell discovery High 28326190
2004 Prohibitin 2 (PHB2) directly interacts with MyoD and MEF2 through its central region (aa 120-232), recruits HDAC1, and represses MyoD- and MEF2-dependent transcription; Akt binds PHB2 and partially reduces PHB2-MyoD binding, relieving transcriptional repression and promoting muscle differentiation. Yeast two-hybrid, co-immunoprecipitation, GST pulldown, reporter assays, stable cell line overexpression Journal of cell science High 15173318
2010 TAZ (transcriptional coactivator with PDZ-binding motif) physically interacts with MyoD through its WW domain, enhances MyoD binding to the myogenin gene promoter, and activates MyoD-dependent transcription to promote myogenic differentiation. Co-immunoprecipitation, reporter assays, chromatin immunoprecipitation, overexpression/knockdown in myoblasts and fibroblasts FASEB journal High 20466877
2003 STAT3 directly interacts with MyoD, inhibiting its DNA-binding and transcriptional activities; reciprocally, MyoD inhibits STAT3 DNA-binding activity. The STAT3-mediated inhibition of MyoD transcriptional activity can be restored by excess p300/CBP and PCAF, suggesting STAT3 competes for these coactivators. Co-immunoprecipitation, EMSA (DNA-binding assay), reporter assays, C2C12 cell differentiation assays The Journal of biological chemistry High 12947115
2008 Beta-catenin directly interacts with MyoD and enhances its binding to E-box elements and transcriptional activity; beta-catenin deficiency inhibits MyoD-mediated transactivation in muscle cells, identifying MyoD as a direct effector in the Wnt canonical pathway independent of TCF/LEF. Co-immunoprecipitation, EMSA, reporter assays, beta-catenin knockdown in muscle cells Molecular and cellular biology High 18316399
2007 FHL3 directly binds MyoD (shown by GST pulldown and co-localization in myoblast nuclei) and functions as a potent negative co-transcriptional regulator; FHL3 overexpression impairs MyoD transcriptional activity and myotube formation, while FHL3 siRNA knockdown enhances MyoD transcriptional activity and differentiation. GST pulldown, confocal co-localization, siRNA knockdown, reporter assays, C2C12 differentiation Journal of cell science High 17389685
2017 Staufen1 interacts with the 3'UTR of MyoD mRNA and represses its translation in quiescent muscle stem cells (MuSCs); Staufen1+/- mice show elevated MyoD protein (without increased mRNA), exit quiescence, and proliferate; conversely, blocking MyoD translation maintains quiescence. Single-molecule FISH, RNA pulldown, co-staining in vivo, Staufen1 heterozygous mouse model, MyoD protein/mRNA quantification Proceedings of the National Academy of Sciences High 29073096
2017 Mettl3 (m6A RNA methyltransferase) is required for MyoD mRNA stability in proliferating myoblasts; Mettl3 knockdown specifically downregulates processed (but not pre-) MyoD mRNA, and m6A modification sites are identified in the 5'UTR of MyoD mRNA which is required for proper mRNA processing. m6A-seq, siRNA knockdown, RT-qPCR of processed vs. unprocessed MyoD mRNA, 5'UTR deletion analysis Open biology Medium 28878038
2023 MyoD-family inhibitor proteins MDFIC and MDFI physically interact with PIEZO1/2 mechanosensitive channels as auxiliary subunits; cryo-EM mapping shows that a lipidated C-terminal helix of MDFIC inserts laterally into the PIEZO1 pore module, regulating channel inactivation kinetics. Co-immunoprecipitation, single-particle cryo-EM structure, electrophysiology (channel inactivation assay) Science High 37590348
2015 Conversion of MyoD's DNA-binding specificity toward NeuroD2 private sites (CAGATG) plus elimination of MyoD interaction with PBX/MEIS co-factors (via point mutations) is sufficient to convert MyoD from a master myogenic regulator to a master neurogenic regulator, demonstrating that private-site binding specificity and PBX/MEIS cooperative binding together determine muscle lineage specification. Chimeric MyoD-NeuroD2 DNA-binding domain mutations, ChIP-seq, gene expression analysis, cell conversion assays in fibroblasts Cell reports High 25801030
1993 A cellular factor (heat- and protease-sensitive, non-ATP-dependent) specifically enables DNA binding of MyoD-E47 heterodimers, which fail to bind DNA when reconstituted from purified components; this factor also stimulates MyoD and E47 homodimer DNA binding in a sequence-context-dependent manner. In vitro reconstitution with purified proteins, cell extract fractionation, gel mobility shift/EMSA, heat/protease sensitivity tests Proceedings of the National Academy of Sciences High 8393567
2010 HIRA (replication-independent histone chaperone) and Asf1a mediate H3.3 incorporation at the MyoD gene promoter and upstream regulatory regions; this replication-independent histone deposition is required for epigenetic transition to permissive chromatin enabling RNA pol II recruitment for MyoD activation during myogenic differentiation. ChIP for HIRA, Asf1a, and H3.3; siRNA knockdown of HIRA; muscle differentiation assays Proceedings of the National Academy of Sciences High 21173268
2017 LSD1/KDM1a histone demethylase is recruited to the MyoD core enhancer upon differentiation, removes H3K9 methylation, and enables RNA polymerase II recruitment for transcription of the core enhancer non-coding RNA (CEeRNA), which is required for MyoD expression; Lsd1 conditional inactivation in muscle progenitors delays MyoD expression during embryogenesis. ChIP, Lsd1 conditional knockout mice, enhancer RNA detection, myoblast siRNA knockdown Cell reports High 28228264
2015 G9a methyltransferase methylates MyoD and targets it for ubiquitin-mediated degradation via the Cul4/Ddb1/Dcaf1 E3 ligase pathway; Jmjd2C demethylase directly associates with MyoD in vitro and in vivo to remove this methyl mark and stabilize MyoD, increasing its transcriptional activity and promoting muscle differentiation. Co-immunoprecipitation, in vitro demethylation assay, ubiquitination assay, half-life measurement, myogenic conversion assay, ChIP Biochimica et biophysica acta High 26149774
2022 MyoD functions as a 3D genome organizer in muscle cells; MyoD-null mice show loss of muscle-specific chromatin loops, and H3K27ac alone is insufficient to establish MyoD-induced chromatin loops, establishing MyoD as a lineage-specific regulator of 3D genome architecture. Hi-C (3D genome mapping), ChIP-seq (H3K27ac), MyoD-knockout mouse cells, ChIA-PET analysis Nature communications High 35017543
2008 HP1alpha and HP1beta (but not HP1gamma) directly interact with MyoD protein in myoblasts, inhibit MyoD transcriptional activity, and are preferentially recruited to MyoD target gene promoters in proliferating myoblasts to maintain their silenced state; modulation of HP1 levels impairs MyoD target gene expression and terminal differentiation. In vitro binding with recombinant proteins, co-immunoprecipitation, reporter assays, ChIP, HP1 overexpression/knockdown The Journal of biological chemistry High 18599480
2007 Pbx homeodomain proteins are required for MyoD to induce fast-muscle gene expression (including myogenin and fast-muscle markers) in zebrafish somites; Pbx marks promoters of a subset of MyoD target genes and Pbx loss selectively prevents MyoD-driven fast-muscle but not slow-muscle gene expression, demonstrating that homeodomain co-factors direct bHLH lineage specification. Morpholino knockdown in zebrafish, genetic epistasis (Pbx+Myod double knockdown vs. Myf5+Pbx), in situ hybridization for muscle markers Development High 17699609
2020 MyoD is the key molecular switch required for Myomixer and Myomaker expression in human myoblasts; MyoD directly binds E-box motifs on the Myomixer and Myomaker promoters to induce their expression, which is required and sufficient to initiate myoblast fusion and multinucleation. CRISPR mutagenesis of MyoD, biochemical promoter assays (E-box identification), ChIP, fusion assays in human primary myoblasts Science advances High 33355126
2000 EID-1 (E1A-like inhibitor of differentiation 1) binds p300 and inhibits its histone acetyltransferase activity, thereby blocking MyoD transactivation independently of G1 exit; EID-1 also binds Rb through its LXCXE motif, and this interaction is separable from its MyoD repression function. Yeast two-hybrid, co-immunoprecipitation, HAT activity assay, reporter assays in skeletal muscle cells, dominant-negative constructs Molecular and cellular biology High 11073990
2003 MyoD associates with CREB and p300 in a multiprotein complex in differentiating myoblasts, targeting this complex to the CRE element of the RB promoter to stimulate RB transcription; MyoD stimulation of RB promoter is independent of direct MyoD-DNA binding and requires the CRE and CREB phosphorylation at Ser-133. Co-immunoprecipitation, ChIP, reporter assays with CRE mutations, Western blot for CREB phosphorylation Molecular and cellular biology High 12665587
2017 Loss of MyoD in myoblasts downregulates miR-133, leading to upregulation of the miR-133 target Igf1r and amplification of PI3K-Akt signaling, which drives adipogenic transdifferentiation; forced MyoD expression in brown preadipocytes upregulates miR-133 to block adipogenesis, establishing MyoD as a negative regulator of brown adipocyte fate through miR-133-Akt-Prdm16 axis. CRISPR/Cas9 MyoD deletion in C2C12, miRNA profiling, PI3K/Akt inhibition, miR-133 knockout, forced MyoD expression in preadipocytes EBioMedicine High 28117277
2019 MyoD-induced super-enhancer-derived eRNA (seRNA-1) binds heterogeneous nuclear ribonucleoprotein L (hnRNPL) through a CAAA tract; this seRNA-1/hnRNPL interaction is required for Pol II and H3K36me3 deposition at the myoglobin (Mb) locus and its transcriptional activation. ChIP-seq, RNA pulldown/RIP, CAAA motif mutagenesis in seRNA-1, hnRNPL CLIP-seq, knockdown experiments Nature communications High 31857580
2012 MASTR transcription factor activates MyoD expression through a muscle-specific postnatal MyoD enhancer via association with MEF2 and Myocardin family members; MASTR deletion impairs satellite cell differentiation and muscle regeneration, mimicking MyoD loss-of-function. Global and satellite cell-specific knockout mice, ChIP, reporter assays for MyoD enhancer, genetic epistasis with MRTF-A deletion Genes & development High 22279050
2013 Six1 transcription factor binds the Core Enhancer Region (CER) of MyoD directly and is required for MyoD expression in satellite cells; Six1 knockdown reduces MyoD expression in myoblasts, and Six1 binding sites in the CER are required for reporter activity in myoblasts and regenerating muscle; Six1 is also required for proper chromatin structure at the CER and for MyoD binding at its own enhancer. ChIP, reporter assays (with Six1 binding site mutations), siRNA knockdown, muscle regeneration model PLoS one High 23840772
2014 Ebf3 (and Ebf1 in skeletal muscle) cooperates with MyoD by directly binding the Atp2a1 (Serca1) promoter and synergizing with MyoD for its induction; loss of Ebf3 leads to impaired Ca2+ efflux in diaphragm (due to reduced Serca1), and transgenic Serca1 rescues the hypercontractile phenotype. ChIP at Atp2a1 promoter, reporter assays (Ebf3+MyoD co-transfection), Ebf3 knockout mice, transgenic rescue Nature communications High 24786561
2006 HEB-beta (alternative splice isoform of the E-protein HEB) is upregulated during early myoblast differentiation and forms a MyoD-HEB-beta complex that binds the E1 E-box of the myogenin promoter to activate transcription; HEB-beta knockdown by siRNA blocks differentiation and myogenin induction. Co-immunoprecipitation, ChIP at myogenin promoter, siRNA knockdown, reporter assays, forced HEB-beta expression in myoblasts Molecular and cellular biology High 16847330
2019 2-hydroxyglutarate (2HG) produced by oncogenic IDH2 blocks MyoD-driven myogenic differentiation by causing H3K9 hypermethylation (not DNA 5mC hypermethylation) at myogenic chromatin regions, impairing chromatin accessibility and preventing MyoD-mediated transcriptional activation. IDH2-R172K mutant expression in fibroblasts with MyoD, ATAC-seq, H3K9 methylation ChIP, 5mC analysis, MyoD-inducible differentiation model Proceedings of the National Academy of Sciences High 31182575
2020 Promiscuous binding of MyoD to neuronal target loci occurs in fibroblasts, and when the muscle program is inhibited by Myt1l, this promiscuous binding is sufficient to drive neuronal reprogramming; strong MyoD binding at muscle sites correlates with non-bHLH co-factor motifs (unlike Ascl1), indicating that MyoD lineage fidelity requires active silencing by Myt1l. ChIP-seq in fibroblasts comparing Ascl1 vs. MyoD, ATAC-seq, RNA-seq, gain-of-function in fibroblasts with Myt1l co-expression Nature cell biology High 32231311

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1991 The myoD gene family: nodal point during specification of the muscle cell lineage. Science (New York, N.Y.) 1488 1846704
1989 Expression of two myogenic regulatory factors myogenin and MyoD1 during mouse embryogenesis. Nature 596 2552320
1989 Positive autoregulation of the myogenic determination gene MyoD1. Cell 443 2546677
1992 Functional antagonism between c-Jun and MyoD proteins: a direct physical association. Cell 414 1310896
1995 The MyoD family of transcription factors and skeletal myogenesis. BioEssays : news and reviews in molecular, cellular and developmental biology 367 7748174
1991 Muscle-specific transcriptional activation by MyoD. Genes & development 303 1651276
1991 Myogenin and MyoD join a family of skeletal muscle genes regulated by electrical activity. Proceedings of the National Academy of Sciences of the United States of America 300 1705035
1989 Transformation by activated ras or fos prevents myogenesis by inhibiting expression of MyoD1. Cell 290 2548731
2006 MyoD inhibits Fstl1 and Utrn expression by inducing transcription of miR-206. The Journal of cell biology 270 17030984
1987 The human tumour-associated epithelial mucins are coded by an expressed hypervariable gene locus PUM. Nature 260 3600778
1992 Fos and Jun repress transcriptional activation by myogenin and MyoD: the amino terminus of Jun can mediate repression. Genes & development 238 1313772
1990 Cell proliferation inhibited by MyoD1 independently of myogenic differentiation. Nature 211 2359457
1995 Determination versus differentiation and the MyoD family of transcription factors. Biochemistry and cell biology = Biochimie et biologie cellulaire 195 8714693
1991 c-myc inhibition of MyoD and myogenin-initiated myogenic differentiation. Molecular and cellular biology 179 1850105
1993 Regulation of muscle transcription by the MyoD family. The heart of the matter. Circulation research 164 8380257
1991 Developmental patterns in the expression of Myf5, MyoD, myogenin, and MRF4 during myogenesis. The New biologist 157 1911647
2017 Long non-coding RNA Linc-RAM enhances myogenic differentiation by interacting with MyoD. Nature communications 148 28091529
2012 Genome-wide identification of enhancers in skeletal muscle: the role of MyoD1. Genes & development 142 23249738
2005 MyoD induces myogenic differentiation through cooperation of its NH2- and COOH-terminal regions. The Journal of cell biology 135 16275751
1990 Myogenic regulatory protein (MyoD1) expression in childhood solid tumors: diagnostic utility in rhabdomyosarcoma. The American journal of pathology 132 2260621
1995 MSX1 inhibits myoD expression in fibroblast x 10T1/2 cell hybrids. Cell 126 7664340
1989 5-bromo-2'-deoxyuridine blocks myogenesis by extinguishing expression of MyoD1. Science (New York, N.Y.) 126 2547249
2003 Myogenin and MyoD1 expression in paediatric rhabdomyosarcomas. Journal of clinical pathology 125 12783965
1987 The hypervariable gene locus PUM, which codes for the tumour associated epithelial mucins, is located on chromosome 1, within the region 1q21-24. Annals of human genetics 124 3447512
2008 Codependent activators direct myoblast-specific MyoD transcription. Developmental cell 122 18854138
2000 Wnt signaling regulates the function of MyoD and myogenin. The Journal of biological chemistry 122 10915791
2003 Myf5 and MyoD activation define independent myogenic compartments during embryonic development. Developmental biology 119 12798290
2007 Pbx homeodomain proteins direct Myod activity to promote fast-muscle differentiation. Development (Cambridge, England) 109 17699609
2017 Malat1 regulates myogenic differentiation and muscle regeneration through modulating MyoD transcriptional activity. Cell discovery 108 28326190
2000 CREB-binding protein/p300 activates MyoD by acetylation. The Journal of biological chemistry 106 10944526
2000 A novel Rb- and p300-binding protein inhibits transactivation by MyoD. Molecular and cellular biology 105 11073990
2002 Activation of MyoD-dependent transcription by cdk9/cyclin T2. Oncogene 104 12037670
2001 Regulation of MyoD function in the dividing myoblast. FEBS letters 98 11223032
2015 Myomaker, Regulated by MYOD, MYOG and miR-140-3p, Promotes Chicken Myoblast Fusion. International journal of molecular sciences 95 26540045
2010 TAZ as a novel enhancer of MyoD-mediated myogenic differentiation. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 94 20466877
2022 MyoD is a 3D genome structure organizer for muscle cell identity. Nature communications 93 35017543
2004 Akt binds prohibitin 2 and relieves its repression of MyoD and muscle differentiation. Journal of cell science 92 15173318
2016 MYOD1 (L122R) mutations are associated with spindle cell and sclerosing rhabdomyosarcomas with aggressive clinical outcomes. Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc 89 27562493
2000 Stabilization of MyoD by direct binding to p57(Kip2). The Journal of biological chemistry 89 10764802
2017 The requirement of Mettl3-promoted MyoD mRNA maintenance in proliferative myoblasts for skeletal muscle differentiation. Open biology 80 28878038
1995 Regulation of vertebrate muscle differentiation by thyroid hormone: the role of the myoD gene family. BioEssays : news and reviews in molecular, cellular and developmental biology 79 7748175
2010 Myogenic transcriptional activation of MyoD mediated by replication-independent histone deposition. Proceedings of the National Academy of Sciences of the United States of America 74 21173268
2020 Human myotube formation is determined by MyoD-Myomixer/Myomaker axis. Science advances 73 33355126
2019 MyoD induced enhancer RNA interacts with hnRNPL to activate target gene transcription during myogenic differentiation. Nature communications 73 31857580
2015 A KAP1 phosphorylation switch controls MyoD function during skeletal muscle differentiation. Genes & development 72 25737281
1996 Casein kinase II increases the transcriptional activities of MRF4 and MyoD independently of their direct phosphorylation. Molecular and cellular biology 72 8657135
2017 Staufen1 inhibits MyoD translation to actively maintain muscle stem cell quiescence. Proceedings of the National Academy of Sciences of the United States of America 69 29073096
2010 Structure and functions of powerful transactivators: VP16, MyoD and FoxA. The International journal of developmental biology 69 21404180
2008 Beta-catenin interacts with MyoD and regulates its transcription activity. Molecular and cellular biology 68 18316399
2003 MyoD stimulates RB promoter activity via the CREB/p300 nuclear transduction pathway. Molecular and cellular biology 66 12665587
2023 MyoD-family inhibitor proteins act as auxiliary subunits of Piezo channels. Science (New York, N.Y.) 65 37590348
2017 Loss of MyoD Promotes Fate Transdifferentiation of Myoblasts Into Brown Adipocytes. EBioMedicine 65 28117277
2001 The nuclear ubiquitin-proteasome system degrades MyoD. The Journal of biological chemistry 65 11309375
2012 MASTR directs MyoD-dependent satellite cell differentiation during skeletal muscle regeneration. Genes & development 59 22279050
1991 The four human muscle regulatory helix-loop-helix proteins Myf3-Myf6 exhibit similar hetero-dimerization and DNA binding properties. Nucleic acids research 58 1945842
1994 Jun, Fos, MyoD1, and myogenin proteins are increased in skeletal muscle fiber nuclei after denervation. Acta neuropathologica 57 8140895
2013 MyoD-expressing progenitors are essential for skeletal myogenesis and satellite cell development. Developmental biology 56 24055173
2008 Role of MyoD in denervated, disused, and exercised muscle. Muscle & nerve 55 18642380
2013 The role of MyoD1 and histone modifications in the activation of muscle enhancers. Epigenetics 54 23880568
2006 MyoD synergizes with the E-protein HEB beta to induce myogenic differentiation. Molecular and cellular biology 54 16847330
1990 Rhabdomyosarcoma-associated locus and MYOD1 are syntenic but separate loci on the short arm of human chromosome 11. Proceedings of the National Academy of Sciences of the United States of America 54 2315312
2021 Humanized skeletal muscle in MYF5/MYOD/MYF6-null pig embryos. Nature biomedical engineering 50 33782573
2010 S100B protein in myoblasts modulates myogenic differentiation via NF-kappaB-dependent inhibition of MyoD expression. Journal of cellular physiology 49 20069545
2003 Reciprocal inhibition between MyoD and STAT3 in the regulation of growth and differentiation of myoblasts. The Journal of biological chemistry 49 12947115
2002 Determinants of nuclear and cytoplasmic ubiquitin-mediated degradation of MyoD. The Journal of biological chemistry 49 12397066
2015 Conversion of MyoD to a neurogenic factor: binding site specificity determines lineage. Cell reports 48 25801030
2019 Master control: transcriptional regulation of mammalian Myod. Journal of muscle research and cell motility 47 31301002
1992 Inhibition of protein phosphatases blocks myogenesis by first altering MyoD binding activity. The Journal of biological chemistry 47 1321827
1998 DNA-mediated folding and assembly of MyoD-E47 heterodimers. The Journal of biological chemistry 46 9488706
2014 Ebf factors and MyoD cooperate to regulate muscle relaxation via Atp2a1. Nature communications 45 24786561
2020 CASZ1 induces skeletal muscle and rhabdomyosarcoma differentiation through a feed-forward loop with MYOD and MYOG. Nature communications 44 32060262
2012 Hedgehog signaling regulates MyoD expression and activity. The Journal of biological chemistry 44 23266826
2002 Identification of novel MyoD gene targets in proliferating myogenic stem cells. Molecular and cellular biology 44 12167713
2020 Pro-neuronal activity of Myod1 due to promiscuous binding to neuronal genes. Nature cell biology 43 32231311
1997 Inactivation of MyoD-mediated expression of p21 in tumor cell lines. Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research 42 9372238
2017 LSD1 Controls Timely MyoD Expression via MyoD Core Enhancer Transcription. Cell reports 41 28228264
2007 FHL3 binds MyoD and negatively regulates myotube formation. Journal of cell science 40 17389685
2005 p57Kip2 is induced by MyoD through a p73-dependent pathway. Journal of molecular biology 40 16405903
2021 Interaction between SNAI2 and MYOD enhances oncogenesis and suppresses differentiation in Fusion Negative Rhabdomyosarcoma. Nature communications 38 33420019
2008 PAX3/7 expression coincides with MyoD during chronic skeletal muscle overload. Muscle & nerve 38 18508329
1989 Expression of the MyoD1 muscle determination gene defines differentiation capability but not tumorigenicity of human rhabdomyosarcomas. Molecular and cellular biology 38 2601695
2013 Six1 regulates MyoD expression in adult muscle progenitor cells. PloS one 36 23840772
1998 Temporal restriction of MyoD induction and autocatalysis during Xenopus mesoderm formation. Developmental biology 36 9769179
2017 HDAC11 Inhibits Myoblast Differentiation through Repression of MyoD-Dependent Transcription. Molecules and cells 35 28927261
1993 A cellular factor stimulates the DNA-binding activity of MyoD and E47. Proceedings of the National Academy of Sciences of the United States of America 35 8393567
2019 Twist2 amplification in rhabdomyosarcoma represses myogenesis and promotes oncogenesis by redirecting MyoD DNA binding. Genes & development 34 30975722
2012 HUWE1 ubiquitinates MyoD and targets it for proteasomal degradation. Biochemical and biophysical research communications 34 22277673
1993 Phosphorylation inhibits the DNA-binding activity of MyoD homodimers but not MyoD-E12 heterodimers. The Journal of biological chemistry 34 8226992
2015 Jmjd2C increases MyoD transcriptional activity through inhibiting G9a-dependent MyoD degradation. Biochimica et biophysica acta 33 26149774
2012 miR-203b: a novel regulator of MyoD expression in tilapia skeletal muscle. The Journal of experimental biology 33 23038733
2021 Dissecting dual roles of MyoD during lineage conversion to mature myocytes and myogenic stem cells. Genes & development 32 34413137
2013 Stepwise acetyltransferase association and histone acetylation at the Myod1 locus during myogenic differentiation. Scientific reports 32 23928680
2019 β-Catenin is essential for differentiation of primary myoblasts via cooperation with MyoD and α-catenin. Development (Cambridge, England) 30 30683662
2019 2-hydroxyglutarate inhibits MyoD-mediated differentiation by preventing H3K9 demethylation. Proceedings of the National Academy of Sciences of the United States of America 30 31182575
2018 Antagonistic and cooperative AGO2-PUM interactions in regulating mRNAs. Scientific reports 29 30333515
2014 Contrasting roles for MyoD in organizing myogenic promoter structures during embryonic skeletal muscle development. Developmental dynamics : an official publication of the American Association of Anatomists 29 25329411
2015 FHL3 differentially regulates the expression of MyHC isoforms through interactions with MyoD and pCREB. Cellular signalling 28 26499038
2008 Differential cooperation between heterochromatin protein HP1 isoforms and MyoD in myoblasts. The Journal of biological chemistry 28 18599480
2002 Diaphragm contractile dysfunction in MyoD gene-inactivated mice. American journal of physiology. Regulatory, integrative and comparative physiology 27 12184991
2003 Expression of muscle-related genes and two MyoD genes during amphioxus notochord development. Evolution & development 26 12950624