Affinage

Showing MYOD1 — MYOD is a alias.

MYOD1

Myoblast determination protein 1 · UniProt P15172

Length
320 aa
Mass
34.5 kDa
Annotated
2026-06-10
100 papers in source corpus 47 papers cited in narrative 47 extracted findings
Cross-family judge vs UniProt: tie faithfulness: 10/10 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

MYOD1 is a basic helix-loop-helix (bHLH) transcription factor that acts as a master regulator of skeletal myogenesis, capable of converting non-muscle cells into the myogenic lineage (PMID:3175662). Its function is partitioned into separable domains: a basic region (residues 102–135) directs nuclear localization, an N-terminal activation domain (within the first 53 residues) drives muscle-specific transcription but is normally masked, and a Myc-homology/HLH motif mediates lineage commitment and growth inhibition independently of differentiation (PMID:3175662, PMID:1651276, PMID:2359457). The HLH motif drives dimerization, and MyoD binds CANNTG E-box DNA preferentially as heterodimers with ubiquitous E proteins, with heterodimer selection driven by favorable DNA contacts rather than intrinsic protein affinity (PMID:1945842, PMID:9488706). MyoD specificity is sharpened by co-factors: PBX/MEIS-assisted binding at 'private' E-box sites is required for full myogenic identity over alternative neuronal fates (PMID:25801030, PMID:32231311). Through E-box recognition MyoD directly transactivates muscle structural and differentiation genes (e.g., the acetylcholine receptor α-subunit) and the fusogens Myomaker and Myomixer to drive myoblast fusion, while also inducing muscle-specific microRNAs (miR-206, miR-1) that silence non-muscle targets such as Fstl1, Utrn, and Pax3 and promote myoblast apoptosis (PMID:2342565, PMID:33355126, PMID:17030984, PMID:20956382). MyoD couples differentiation to cell-cycle exit by inducing p21 to enforce arrest during terminal differentiation (PMID:7791789). Genome-wide, MyoD assembles condition-specific muscle enhancers, recruiting the H3K4 monomethylase Set7 and organizing muscle-specific 3D chromatin loop architecture (PMID:23249738, PMID:35017543). MyoD activity is controlled at multiple post-translational levels — acetylation by CBP/p300 and PCAF enhances DNA binding and recruits the CBP/p300 bromodomain (PMID:10944526, PMID:11463815), cyclin B–Cdc2 phosphorylation at Ser5/Ser200 destabilizes it during G2/M (PMID:14749395), and N-terminal/lysine ubiquitination (including by HUWE1) and G9a methylation target it for proteasomal degradation (PMID:12397066, PMID:22277673, PMID:26149774) — and its own transcription is governed by an autoregulatory loop together with distal-enhancer inputs from FoxO3/Pax3, Six1, MASTR/MEF2, and CLOCK/BMAL1 (PMID:2546677, PMID:18854138, PMID:23840772, PMID:22279050, PMID:20956306). In quiescent muscle stem cells, Staufen1 represses MyoD mRNA translation to maintain quiescence despite abundant transcript (PMID:29073096). Note that timeline discovery (PMID:37590348) concerns MDFIC/MDFI, MyoD-family inhibitor proteins acting as PIEZO channel auxiliary subunits, and does not describe MYOD1 itself.

Mechanistic history

Synthesis pass · year-by-year structured walk · 26 steps
  1. 1988 High

    Established that MyoD1 is a modular nuclear protein in which distinct short domains independently confer nuclear localization and myogenic-inducing activity, defining it as a discrete master myogenic regulator.

    Evidence Deletional mutagenesis of MyoD1 cDNA with stable fibroblast transfection and antisera localization

    PMID:3175662

    Open questions at the time
    • Did not define the DNA sequence recognized or the dimerization requirement
    • Domain boundaries mapped functionally, not structurally
  2. 1989 High

    Answered how MyoD expression is sustained and amplified, showing a positive autoregulatory loop and a mutual cross-activation circuit with myogenin.

    Evidence cDNA transfection into fibroblast lines with endogenous mRNA induction readout

    PMID:2546677

    Open questions at the time
    • Did not identify the enhancer elements or co-factors mediating autoregulation
    • Direct versus indirect activation not distinguished
  3. 1990 High

    Demonstrated direct transactivation of a muscle structural gene via cognate E-boxes, and that MyoD growth-inhibitory and differentiation functions are genetically separable.

    Evidence E-box mutagenesis with myotube reporter assays; domain-swap microinjection DNA-synthesis assays in fibroblasts

    PMID:2342565 PMID:2359457

    Open questions at the time
    • Mechanism linking growth arrest to specific domains not molecularly defined
    • Did not identify the effectors of growth inhibition
  4. 1991 High

    Resolved the domain logic of transactivation and DNA binding, locating a normally masked N-terminal activation domain and showing the basic region requires a cell-type-specific recognition factor.

    Evidence Chimeric protein mutagenesis, reporter cotransfection, and VP16 domain-swap rescue

    PMID:1651276

    Open questions at the time
    • Identity of the cell-type-specific recognition factor not determined
    • Mechanism of activation-domain masking unknown
  5. 1991 High

    Defined the biochemical basis of MyoD DNA binding as obligate heterodimerization with E proteins, since myogenic homodimers cannot bind DNA.

    Evidence In vitro dimerization assays and EMSA with purified bHLH proteins

    PMID:1945842

    Open questions at the time
    • Did not explain what drives heterodimer selection in cells
  6. 1998 High

    Explained why MyoD–E47 heterodimers predominate, showing DNA contacts rather than protein–protein affinity drive heterodimer assembly.

    Evidence Fluorescence quenching, equilibrium binding, EMSA, and loop-swap mutagenesis of bHLH domains

    PMID:9488706

    Open questions at the time
    • In vitro biophysics; cellular partner competition not addressed
    • No structural model of the DNA-bound complex
  7. 1995 High

    Connected MyoD-driven differentiation to cell-cycle exit by showing MyoD induces p21 to enforce arrest, and identified MSX1 as a direct transcriptional repressor of MyoD.

    Evidence C2C12 differentiation with p21 immunodepletion and ectopic expression; somatic cell hybrids, EMSA, and antisense for MSX1

    PMID:7664340 PMID:7791789

    Open questions at the time
    • Mechanism of p21 promoter activation by MyoD not fully resolved here
    • MSX1 corepressor partners not identified
  8. 2000 High

    Identified acetylation as a positive regulatory mark, with CBP/p300 and PCAF acetylating MyoD near its DNA-binding domain to enhance activity.

    Evidence In vitro acetylation assays, acetylation-site mutagenesis, and microinjection functional assays

    PMID:10944526

    Open questions at the time
    • Did not establish the structural consequence of acetylation on DNA binding
  9. 2000 Medium

    Revealed two further regulatory inputs: p57(Kip2) directly binds and stabilizes MyoD beyond CDK inhibition, while EID-1 represses MyoD by inhibiting p300 HAT activity.

    Evidence Endogenous Co-IP and half-life assays for p57; yeast two-hybrid, Co-IP, and HAT assays for EID-1

    PMID:10764802 PMID:11073990

    Open questions at the time
    • EID-1 evidence is single-lab
    • p57 stabilization mechanism (which E3 it blocks) not defined
  10. 2001 High

    Mechanistically linked acetylation to coactivator recruitment, showing acetylated MyoD binds the CBP/p300 bromodomain with increased affinity.

    Evidence Endogenous reciprocal Co-IP, in vitro pull-down with acetylated MyoD, and bromodomain mutant analysis

    PMID:11463815

    Open questions at the time
    • Quantitative contribution of bromodomain binding to in vivo transcription not isolated
  11. 2002 High

    Defined the proteolytic control of MyoD, mapping N-terminus-dependent and lysine-dependent ubiquitination pathways compartmentalized by NLS/NES.

    Evidence NLS/NES mutagenesis, N-terminal tag blocking, and pulse-chase compartment-specific degradation assays

    PMID:12397066

    Open questions at the time
    • The responsible E3 ligases not identified in this study
  12. 2002 Medium

    Implicated Cdk9/cyclin T2a as a positive kinase partner that binds the bHLH region and enhances MyoD-dependent transcription and differentiation.

    Evidence Co-IP, in vitro kinase assay, and gain/dominant-negative expression in C2C12 cells

    PMID:12037670

    Open questions at the time
    • Single-lab; physiological phosphosites on MyoD not mapped
    • Relationship to transcription elongation not resolved
  13. 2003 Medium

    Established mutual antagonism between MyoD and STAT3, with STAT3 inhibiting MyoD DNA binding by competing for shared p300/CBP/PCAF coactivators.

    Evidence Co-IP, EMSA, and coactivator rescue reporter assays

    PMID:12947115

    Open questions at the time
    • Single-lab; in vivo relevance during signaling not established
  14. 2004 High

    Connected cell-cycle kinases to MyoD turnover, showing cyclin B–Cdc2 phosphorylation of Ser5/Ser200 destabilizes MyoD and downregulates p21 at G2/M.

    Evidence Phospho-site mutant inducible expression, kinase assays, and p21-null epistasis

    PMID:14749395

    Open questions at the time
    • Degradation machinery downstream of phosphorylation not identified here
  15. 2005 Medium

    Dissected how MyoD outperforms Myf5 at terminal differentiation through N/C-terminal inter-domain cooperation, and identified the MyoD–HEBβ heterodimer and a p73-dependent route to p57 induction.

    Evidence Domain-deletion microarray/PCR profiling; siRNA/Co-IP/ChIP for HEBβ; reporter and dominant-negative assays for p73/p57

    PMID:16275751 PMID:16405903 PMID:16847330

    Open questions at the time
    • Single-lab studies
    • Mechanism of inter-domain cooperation not structurally defined
    • p73-p57 link is indirect
  16. 2006 High

    Revealed that MyoD acts post-transcriptionally on the muscle program by directly activating miR-206, which silences Fstl1 and Utrn.

    Evidence ChIP at the miR-206 locus, 3'-UTR reporter assays, and MyoD gain-of-function

    PMID:17030984

    Open questions at the time
    • Full repertoire of miR-206 targets not enumerated
  17. 2007 High

    Showed co-factors shape MyoD target specificity in vivo, with Pbx required for fast-muscle gene induction, and FHL3 acting as a direct negative regulator.

    Evidence Zebrafish Pbx/Myod/Myf5 morpholino epistasis with in situ hybridization; GST pull-down, Co-IP, and siRNA for FHL3

    PMID:17389685 PMID:17699609

    Open questions at the time
    • Mechanism by which Pbx redirects MyoD binding not molecularly defined
    • FHL3 evidence single-lab
  18. 2008 High

    Defined the upstream transcriptional control of MyoD and additional repressors: codependent FoxO3/Pax3 activation, HP1α/β inhibition, and NFATc3 synergy at the myogenin promoter.

    Evidence ChIP, in vitro interactions, FoxO3-null regeneration assays; recombinant binding/Co-IP/ChIP for HP1; EMSA/ChIP and Myod/Nfatc3 double-null epistasis

    PMID:18599480 PMID:18676376 PMID:18854138

    Open questions at the time
    • How FoxO3/Pax3 recruit Pol II structurally not resolved
    • HP1 work single-lab
  19. 2010 High

    Linked MyoD to circadian and apoptotic control, with CLOCK/BMAL1 rhythmically driving MyoD transcription and MyoD driving myoblast apoptosis via miR-1/miR-206 repression of Pax3.

    Evidence ChIP with Clock/Bmal1 mutant mice and physiological phenotyping; reciprocal miRNA gain/loss-of-function and 3'-UTR reporter mutagenesis

    PMID:20956306 PMID:20956382

    Open questions at the time
    • Connection between circadian MyoD cycling and downstream physiology not fully mapped
  20. 2012 High

    Reframed MyoD as a genome-wide enhancer organizer that licenses muscle chromatin states, recruits Set7, and depends on upstream MASTR/MEF2 input; also identified HUWE1 as an N-terminal ubiquitin ligase.

    Evidence ChIP-seq with MyoD1-null and rescue myoblasts/myotubes; MASTR conditional KO with enhancer reporters; in vitro ubiquitination with site mapping

    PMID:22277673 PMID:22279050 PMID:23249738

    Open questions at the time
    • HUWE1 evidence single-lab
    • Why H3K27ac restoration requires the myotube context not explained
  21. 2013 Medium

    Demonstrated MyoD operates within feedback loops involving long-range chromatin contacts, binding the H19 CS9 enhancer (H19–Igf2–MyoD feedback) and synergizing with Ebf3/1 at the Atp2a1 promoter.

    Evidence ChIP and 3C with Myod/Igf2 double mutants; ChIP, reporter assays, and Ebf3 KO with transgenic rescue

    PMID:23406902 PMID:24786561

    Open questions at the time
    • H19 study single-lab
    • Direct mechanism of synergy with Ebf3 not structurally defined
  22. 2015 High

    Resolved how MyoD specifies myogenic versus alternative lineages and how a phospho-switchable scaffold gates its activity, via PBX/MEIS-assisted private-site binding, KAP1 corepressor/coactivator switching, and G9a-Jmjd2C methylation balance.

    Evidence ChIP-seq with chimeric factors and point mutagenesis; ChIP-seq/Co-IP/MSK1 kinase epistasis for KAP1; in vitro methylation/demethylation and Co-IP for G9a/Jmjd2C

    PMID:25737281 PMID:25801030 PMID:26149774

    Open questions at the time
    • G9a/Jmjd2C evidence single-lab
    • How PBX/MEIS sites are selected genome-wide not fully defined
  23. 2017 High

    Showed MyoD activity depends on enhancer-RNA-producing core enhancers (LSD1-licensed), a Linc-RAM-scaffolded Baf60c/Brg1 remodeling complex, and Staufen1-mediated translational repression that maintains stem-cell quiescence.

    Evidence ChIP with conditional Lsd1 KO and CEeRNA measurement; RNA pull-down/Co-IP/ChIP and Linc-RAM KO mice; RNA pulldown, smFISH, and Staufen1+/- mouse model

    PMID:28091529 PMID:28228264 PMID:29073096

    Open questions at the time
    • Mechanism by which the core-enhancer eRNA acts in cis not fully defined
  24. 2019 Medium

    Extended MyoD regulation to metabolite and RNA-mediated layers and quantified its context-dependent binding behavior, showing 2HG/IDH2 blocks myogenesis via H3K9 methylation, seRNA-1 recruits hnRNPL at the myoglobin super-enhancer, and weaker, motif-co-dependent binding makes MyoD more context dependent than Ascl1.

    Evidence MyoD-driven differentiation with IDH2-R172K, ATAC-seq, ChIP; CLIP/ChIP-seq/CAAA mutagenesis for seRNA-1; ChIP-seq/ATAC-seq and MyoD+Myt1l reprogramming

    PMID:31182575 PMID:31857580 PMID:32231311

    Open questions at the time
    • seRNA-1 study single-lab
    • Generalizability of super-enhancer eRNA mechanism to other loci untested
  25. 2020 High

    Established MyoD as the necessary and sufficient switch for myoblast fusion by directly activating Myomaker and Myomixer via E-box motifs.

    Evidence CRISPR mutagenesis of MyoD, E-box-mutant reporters, and forced expression in non-muscle cells

    PMID:33355126

    Open questions at the time
    • Co-factors required for fusogen induction not enumerated
  26. 2022 High

    Defined MyoD as a direct 3D-genome organizer that establishes muscle-specific chromatin loops independently of H3K27ac, and showed collaboration with the glucocorticoid receptor at myofiber enhancers anchored via Nrf1/CTCF loops.

    Evidence Hi-C in MyoD-null versus wild-type muscle cells with H3K27ac ChIP-seq; ChIP-seq/Hi-C/4C and GR conditional KO phenotyping

    PMID:33836079 PMID:35017543

    Open questions at the time
    • Mechanism by which MyoD nucleates loop formation not defined
    • Whether loop organization is direct or via recruited architectural proteins unresolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • How the many post-translational marks, co-factors, and architectural functions of MyoD are integrated dynamically to produce a single ordered differentiation trajectory remains unresolved.
  • No unified structural model of MyoD bound to chromatin with its co-factors
  • Temporal ordering of acetylation, phosphorylation, methylation, and ubiquitination across the cell cycle and differentiation not reconstructed
  • Quantitative rules distinguishing activated from bound-but-silent MyoD targets incompletely defined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140110 transcription regulator activity 6 GO:0003677 DNA binding 4
Localization
GO:0005634 nucleus 2 GO:0005654 nucleoplasm 2
Pathway
R-HSA-1266738 Developmental Biology 4 R-HSA-74160 Gene expression (Transcription) 4 R-HSA-1640170 Cell Cycle 3 R-HSA-4839726 Chromatin organization 3
Partners
EP300FOXO3HEB/TCF12PBX1PCAF/KAT2BSTAT3TCF3/E47TRIM28
Complex memberships
KAP1/TRIM28–MyoD–Mef2 scaffoldMyoD–Baf60c–Brg1 chromatin remodeling complexMyoD–E protein bHLH heterodimer

Evidence

Reading pass · 47 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1988 MyoD1 is a nuclear phosphoprotein; a basic region (residues 102–135) is required for nuclear localization, and a Myc-homology domain (residues 143–162) is required for induction of myogenesis but not nuclear localization. As few as 68 amino acids encompassing these two domains are sufficient to activate myogenesis in stably transfected 10T1/2 cells. Site-directed deletional mutagenesis of MyoD1 cDNA; stable transfection of fibroblasts; polyclonal antisera localization Science High 3175662
1991 MyoD transcriptional activation maps to an N-terminal activation domain (within the first 53 residues), which is normally masked. A specific alanine in the basic region increases DNA binding and a specific threonine is required for transcriptional activation. The basic region requires a cell-type-specific 'recognition factor' to function. Replacement of the MyoD basic region with that of E12 abolishes transactivation but not DNA binding in most cell types. Chimeric protein mutagenesis; reporter gene cotransfection; in vivo DNA binding assays; VP16 domain-swap rescue Genes & Development High 1651276
1989 MyoD1 activates its own transcription (positive autoregulation) in 10T1/2 and Swiss 3T6 cells. MyoD1 and myogenin engage in a mutual positive autoregulatory loop, each activating the other's expression. Transfection of MyoD1/myogenin cDNA expression vectors into fibroblast lines; measurement of endogenous mRNA induction Cell High 2546677
1990 Two adjacent MyoD1-binding sites (E-boxes) in the muscle-specific enhancer of the chicken acetylcholine receptor α-subunit gene are essential for full enhancer activity in transfected myotubes, demonstrating MyoD1 directly transactivates AChR gene expression. Site-directed mutagenesis of E-box elements; transient transfection reporter assays in myotubes Nature High 2342565
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's basic domain inhibits growth but fails to induce differentiation, indicating growth inhibition and differentiation are separable functions. Microinjection of MyoD1 constructs into NIH 3T3 cells; deletion and domain-swap mutagenesis; DNA synthesis assays Nature High 2359457
1991 The HLH motif of MyoD mediates dimerization, and dimerization partner determines MyoD activity. The four human muscle bHLH proteins (Myf3/MyoD, Myf4, Myf5, Myf6) form stable heterodimers with ubiquitous E proteins (E12, E2-2, E2-5) and bind CANNTG E-box sequences with similar efficiency; homodimers among Myf proteins do not bind DNA. In vitro dimerization assays; electrophoretic mobility shift assays (EMSA) with purified proteins Nucleic Acids Research High 1945842
1995 MyoD induces p21 expression at the mRNA and protein levels during terminal muscle differentiation. p21 forms a complex with cyclin-dependent kinases in myotubes and is sufficient for cell cycle arrest. MyoD-transformed 10T1/2 fibroblasts (but not parental cells) upregulate p21 upon serum withdrawal, linking p21 induction to myogenic commitment. C2C12 differentiation; immunodepletion of p21 from myotube extracts; ectopic p21 expression; MyoD-transformed 10T1/2 cells; Northern and Western blotting Molecular and Cellular Biology High 7791789
1995 MSX1 directly binds the MyoD enhancer and represses MyoD transcription. Human chromosome 4 (containing MSX1) inhibits myoD activation in fibroblast × 10T1/2 hybrids; forced MSX1 expression represses myoD enhancer activity; antisense MSX1 relieves repression. Somatic cell hybrid analysis; enhancer/promoter reporter assays; EMSA showing Msx1 binding to MyoD enhancer; antisense suppression Cell High 7664340
1998 In the absence of DNA, MyoD bHLH domain is unfolded and monomeric, whereas E47 forms a stable homodimer. MyoD does not dimerize with E47 under dilute conditions without DNA. In the presence of specific DNA, MyoD–E47 form almost exclusively heterodimeric complexes, driven by favorable DNA contacts rather than protein–protein interactions. Substituting the E47 loop into MyoD allows DNA-free dimerization. Fluorescence quenching; equilibrium binding assays; EMSA; loop-swap mutagenesis of bHLH domains The Journal of Biological Chemistry High 9488706
2000 MyoD is acetylated by both CBP/p300 and PCAF on two lysines at the boundary of the DNA-binding domain. Acetylation by CBP/p300 increases MyoD activity on muscle-specific promoters. MyoD mutants that cannot be acetylated in vitro are not activated in functional microinjection assays. MyoD is constitutively acetylated in muscle cells. In vitro acetylation assays; microinjection functional assays; site-directed mutagenesis of acetylation sites; Western blotting The Journal of Biological Chemistry High 10944526
2001 Acetylated MyoD interacts with the bromodomain of CBP/p300. In muscle cells, endogenous acetylated MyoD associates with CBP/p300. In vitro, acetylation increases the affinity and salt resistance of the MyoD–CBP interaction. MyoD mutants unable to be acetylated fail to associate with CBP/p300 in vivo and are strongly impaired in transcriptional cooperation with CBP. Co-immunoprecipitation of endogenous proteins; in vitro pull-down with acetylated/unacetylated MyoD; CBP bromodomain mutant analysis; reporter gene assays Molecular and Cellular Biology High 11463815
2000 p57(Kip2) directly binds MyoD via the NH2-terminal alpha-helix domain of p57 interacting with the bHLH domain of MyoD (basic region), stabilizing MyoD by increasing its half-life. This physical interaction was shown for both overexpressed and endogenous proteins. p57 increases MyoD transcriptional activity on muscle-specific genes through a mechanism distinct from CDK inhibition. Co-immunoprecipitation of endogenous proteins in C2C12 cells; site-directed mutagenesis; competition/association assays; half-life measurements The Journal of Biological Chemistry High 10764802
2002 MyoD is ubiquitinated preferentially at its N-terminus (N-terminus-dependent pathway) and degraded by the proteasome in the nucleus. The nuclear localization signal and nuclear export signal restrict ubiquitination and degradation to nuclear or cytoplasmic compartments. In the cytoplasm, lysine-dependent ubiquitination is more active; in the nucleus both pathways are active. Mutagenesis of NLS/NES; N-terminal 6×Myc tag blocking; pulse-chase half-life assays; compartment-restricted degradation assays The Journal of Biological Chemistry High 12397066
2002 Cdk9/cyclin T2a forms a multimeric complex with MyoD in C2C12 cells, with the minimal cdk9-binding region mapping within residues 101–161 (bHLH region) of MyoD. Cdk9 phosphorylates MyoD in vitro. Overexpression of cdk9/cyclinT2a enhances MyoD-dependent transcription and myogenic differentiation; dominant-negative cdk9 represses it. Co-immunoprecipitation; in vitro kinase assay; overexpression and dominant-negative expression in C2C12 and MyoD-converted fibroblasts Oncogene Medium 12037670
2004 MyoD is phosphorylated on Ser5 and Ser200 by cyclin B–Cdc2 during G2/M, destabilizing MyoD and downregulating p21. A non-phosphorylatable MyoD A5/A200 mutant sustains p21 expression, inhibits cyclin B–Cdc2 kinase activity, delays M-phase entry, and requires p21 for this G2 arrest (not observed in p21−/− cells). MyoD interaction with P/CAF coactivator is enhanced when Cdc2 phosphorylation is absent. Inducible expression of phospho-site mutants; cyclin B–Cdc2 kinase assays; luciferase reporter assays; p21−/− cell epistasis Molecular and Cellular Biology High 14749395
2005 MyoD NH2- and COOH-terminal regions cooperate to activate differentiation-phase target genes. MyoD is strikingly more effective than Myf5 at inducing terminal differentiation genes, a distinction arising from this novel inter-domain cooperation not present in Myf5. Microarray and PCR gene expression profiling; domain-deletion/chimeric constructs; in vitro myogenic conversion assays The Journal of Cell Biology Medium 16275751
2006 MyoD directly activates transcription of the muscle-specific microRNA miR-206, which in turn targets the 3′-UTR sequences of Fstl1 and Utrn mRNAs to suppress their expression during skeletal muscle differentiation. ChIP demonstrating MyoD binding to miR-206 locus; 3′-UTR reporter assays; MyoD gain-of-function in fibroblasts The Journal of Cell Biology High 17030984
2007 Pbx homeodomain proteins are required for MyoD to induce a subset of muscle genes including myogenin and fast-muscle genes in zebrafish somites. In the absence of Pbx function, Myod cannot induce fast-muscle but can still drive slow-muscle gene expression, demonstrating Pbx modulates MyoD target-gene specificity toward fast-fiber identity. Pbx loss-of-function (morpholino knockdown) in zebrafish embryos; combinatorial Pbx/Myod/Myf5 knockdown epistasis; in situ hybridization Development High 17699609
2007 FHL3 directly binds MyoD (demonstrated by GST pull-down and co-localization in the nucleus of myoblasts) and acts as a potent negative co-transcriptional regulator: overexpression of FHL3 impairs MyoD-mediated transcriptional activity and delays myotube formation, while siRNA-mediated FHL3 knockdown enhances both. GST pull-down; Co-IP; nuclear co-localization; reporter gene assays; siRNA knockdown in C2C12 cells Journal of Cell Science Medium 17389685
2008 FoxO3 and Pax3/7 act as codependent transcriptional activators of MyoD in myoblasts, requiring each other to cooperatively recruit RNA polymerase II and form a preinitiation complex at the MyoD promoter. FoxO3-null mice show impaired muscle regeneration with reduced MyoD expression. Cell-based reporter assays; in vitro pull-down; ChIP; FoxO3 knockout mouse muscle regeneration assays Developmental Cell High 18854138
2008 HP1α and HP1β (but not HP1γ) directly interact with MyoD in myoblasts, as shown with recombinant proteins in vitro and Co-IP. HP1α and HP1β inhibit MyoD transcriptional activity in a reporter assay. ChIP shows preferential recruitment of HP1 to MyoD target gene promoters in proliferating myoblasts, and modulation of HP1 levels alters MyoD target gene expression. In vitro binding with recombinant proteins; Co-immunoprecipitation; reporter gene assay; ChIP The Journal of Biological Chemistry Medium 18599480
2008 Calcineurin/NFATc2/c3 signaling cooperates synergistically with MyoD at the myogenin promoter. Two conserved NFAT binding sites in the myogenin promoter are occupied by NFATc3 upon differentiation, and combinatorial loss of myod and nfatc3 (but not either alone) severely impairs myogenin expression in vivo. Gel shift (EMSA) and ChIP for NFATc3 binding; genetic epistasis (double-null embryos); luciferase reporter assays The Journal of Biological Chemistry High 18676376
2010 CLOCK and BMAL1 directly bind the MyoD core enhancer in a rhythmic (circadian) manner and are required for normal MyoD mRNA and protein cycling. Clock and Bmal1 mutant mice show disrupted myofilament architecture and reduced maximal force, phenocopying aspects of MyoD-null muscle. ChIP demonstrating CLOCK/BMAL1 binding to MyoD promoter; Clock(Δ19) and Bmal1−/− mouse models; electron microscopy; force measurements; MyoD−/− comparison PNAS High 20956306
2010 MyoD drives apoptosis of myoblasts through transcriptional activation of miR-1 and miR-206, which target the Pax3 3′-UTR (two conserved miR-1/miR-206 binding sites required) to down-regulate Pax3 and suppress antiapoptotic Bcl-2 and Bcl-xL. MyoD knockdown increases cell survival of wild-type myoblasts. MyoD−/− myoblasts; forced MyoD expression; miRNA gain/loss-of-function; 3′-UTR reporter assays with site mutations; siRNA knockdown of MyoD The Journal of Cell Biology High 20956382
2012 MyoD1 is required for condition-specific muscle enhancer assembly genome-wide. MyoD1-null myoblasts show loss of transcription factor recruitment and reduction of H3K4me1 and H3K27ac at enhancers. Re-expression of MyoD1 in null myoblasts restores H3K4me1 but not H3K27ac; re-expression in null myotubes restores both. MyoD1 recruits Set7 (H3K4 monomethylase) to enhancers. ChIP-seq for histone modifications and TF binding; MyoD1-null myoblasts and myotubes; MyoD1 re-expression; genome-wide chromatin state mapping Genes & Development High 23249738
2012 MASTR activates a muscle-specific postnatal MyoD enhancer through associations with MEF2 and Myocardin family members, thereby regulating MyoD expression in satellite cells. MASTR deletion impairs skeletal muscle regeneration due to satellite cell differentiation defects, mimicking MyoD deficiency. Satellite cell-specific and global MASTR knockout mice; reporter assays with MyoD enhancer; Co-IP between MASTR and MEF2/myocardin family members Genes & Development Medium 22279050
2012 HUWE1 ubiquitinates MyoD at its N-terminal residue and targets it for proteasomal degradation. In vitro ubiquitination assay; co-expression studies; mapping of ubiquitination site to N-terminus Biochemical and Biophysical Research Communications Medium 22277673
2015 KAP1/TRIM28 is present with MyoD and Mef2 at muscle gene promoters in myoblasts, scaffolding both coactivators (p300, LSD1) and corepressors (G9a, HDAC1), resulting in net silencing. Upon differentiation, MSK1-mediated phosphorylation of KAP1 releases corepressors, enabling MyoD/Mef2 transcriptional activation. ChIP-seq; Co-IP of KAP1/MyoD/Mef2 complex; phospho-KAP1 analysis; MSK1 kinase and dominant-negative studies; reporter assays Genes & Development High 25737281
2015 MyoD DNA-binding specificity at 'private' E-box sites (CAGGTG) cooperates with PBX/MEIS co-factor binding motifs to determine myogenic lineage specification. Point mutations preventing MyoD interaction with PBX/MEIS convert a MyoD–NeuroD2 chimera from a mixed muscle/neuronal factor to a pure neurogenic factor, showing PBX/MEIS-assisted private-site binding is required for full myogenic identity. ChIP-seq; chimeric factor design with swapped DNA-binding domains; genome-wide binding analysis; point mutagenesis to disrupt PBX/MEIS interaction Cell Reports High 25801030
2015 G9a methylates MyoD, promoting its ubiquitination-dependent degradation via the Cul4/Ddb1/Dcaf1 pathway. Jmjd2C demethylase directly associates with MyoD in vitro and in vivo, demethylates it, and stabilizes it, thereby increasing MyoD transcriptional activity and myogenic differentiation. Co-IP; in vitro demethylation and methylation assays; half-life measurement; Jmjd2C overexpression/knockdown; ChIP for H3K9me3 Biochimica et Biophysica Acta Medium 26149774
2017 LSD1/KDM1a is recruited to the MyoD core enhancer upon muscle differentiation, removes H3K9 methylation, and enables RNA polymerase II recruitment to the core enhancer for transcription of a non-coding enhancer RNA (CEeRNA) required for MyoD expression. Lsd1 conditional inactivation delays MyoD expression in limb buds during embryogenesis. ChIP; siRNA knockdown in myoblasts; conditional Lsd1 KO in muscle progenitors during embryogenesis; measurement of CEeRNA Cell Reports High 28228264
2017 Staufen1 binds MyoD mRNA 3′-UTR in quiescent muscle stem cells and actively represses MyoD translation, maintaining quiescence despite high MyoD transcript levels. Staufen1+/− heterozygous muscle stem cells have increased MyoD protein, exit quiescence, and proliferate; blocking MyoD translation maintains quiescence. RNA pulldown; single-molecule FISH; single-cell co-staining; Staufen1+/− mouse model; translational repression rescue experiments PNAS High 29073096
2017 Linc-RAM directly binds MyoD and promotes assembly of the MyoD–Baf60c–Brg1 chromatin remodeling complex on regulatory elements of myogenic target genes. Linc-RAM knockout mice display impaired muscle regeneration and satellite cell differentiation defects. RNA pull-down and Co-IP for Linc-RAM/MyoD interaction; Linc-RAM KO mice; ChIP for complex assembly at target gene regulatory elements Nature Communications High 28091529
2019 MyoD activates enhancer RNA (seRNA-1) production at a super-enhancer. seRNA-1 binds hnRNPL via a CAAA tract and regulates RNA Pol II and H3K36me3 deposition at the myoglobin (Mb) locus, activating Mb transcription. Disruption of the seRNA-1/hnRNPL interaction attenuates this activation. ChIP-seq; RNA-seq; CLIP for seRNA-1/hnRNPL interaction; CAAA-tract mutagenesis; Pol II and H3K36me3 ChIP Nature Communications Medium 31857580
2019 2-Hydroxyglutarate (2HG) produced by oncogenic IDH2 blocks MyoD-driven myogenic differentiation through H3K9 hypermethylation and impaired chromatin accessibility at myogenic loci, while DNA 5mC hypermethylation is dispensable for this differentiation block. MyoD-driven fibroblast differentiation model; IDH2-R172K expression; ATAC-seq; H3K9 methylation ChIP; 5mC profiling PNAS Medium 31182575
2020 MyoD is the key molecular switch required and sufficient to initiate Myomixer and Myomaker expression for human myoblast fusion, binding E-box motifs on their promoters. CRISPR mutagenesis of MyoD abrogates fusion; forced MyoD expression in non-muscle cells induces Myomixer and Myomaker. CRISPR mutagenesis of MyoD; luciferase reporter assays with E-box mutants; forced MyoD expression; biochemical assays Science Advances High 33355126
2021 Myod1 collaborates with the glucocorticoid receptor (GR) at skeletal muscle enhancers to control gene expression; GR negatively controls muscle mass and strength by downregulating anabolic pathways. Myod1-bound enhancers contact gene promoters via CpG-bound Nrf1 and CTCF-anchored chromatin loops in a myofiber-specific manner. ChIP-seq for Myod1 and GR; ATAC-seq; Hi-C/4C chromatin conformation capture; GR conditional KO mouse model; muscle force/mass measurements Nucleic Acids Research High 33836079
2022 MyoD functions as a 3D genome organizer in muscle cells, establishing muscle-specific chromatin loop architecture. MyoD-null mouse muscle cells lack MyoD-induced chromatin loops; H3K27ac deposition is insufficient for establishing these loops, indicating MyoD is directly required for their formation. Hi-C in wild-type and MyoD-null mouse muscle cells; ChIP-seq for H3K27ac; chromatin loop analysis Nature Communications High 35017543
2023 MDFIC and MDFI (MyoD-family inhibitor proteins) are PIEZO1/2 interacting partners that bind PIEZO channels and regulate channel inactivation. Cryo-EM mapping shows MDFIC's lipidated C-terminal helix inserts laterally into the PIEZO1 pore module. These proteins function as auxiliary subunits of Piezo channels, explaining cell-type-specific differences in Piezo gating kinetics. Co-immunoprecipitation; single-particle cryo-EM structure determination; functional electrophysiology of channel inactivation Science High 37590348
2000 EID-1, a novel protein with an LXCXE Rb-binding motif, represses MyoD-dependent transcription by binding and inhibiting p300 histone acetyltransferase activity (an essential MyoD coactivator), independently of G1 cell cycle exit. Repression is potentiated by a mutation preventing EID-1 binding to Rb. Yeast two-hybrid; Co-IP; reporter gene assays; p300 HAT activity assay; domain mutant analysis Molecular and Cellular Biology Medium 11073990
2003 STAT3 directly interacts with MyoD, inhibiting both MyoD DNA-binding activity and transcriptional activity. STAT3-mediated inhibition of MyoD activity can be reversed by supplementing p300/CBP and PCAF, suggesting STAT3 competes for these coactivators. Reciprocally, MyoD inhibits STAT3 DNA binding activity. Co-immunoprecipitation; EMSA for DNA binding; reporter gene assays; p300/CBP/PCAF rescue experiments The Journal of Biological Chemistry Medium 12947115
2005 E-protein HEB beta is upregulated during early terminal differentiation. A MyoD–HEBβ heterodimer binds the E1 E-box of the myogenin promoter to activate transcription upon differentiation. Knockdown of HEBβ by siRNA in myoblasts blocks differentiation and inhibits myogenin induction. siRNA knockdown; Co-IP; ChIP; reporter gene assays; Western blotting during differentiation Molecular and Cellular Biology Medium 16847330
2005 p57 induction by MyoD during differentiation occurs through a p73-dependent, E-box-independent transcriptional mechanism requiring de novo protein synthesis. MyoD induces p73 alpha/beta/delta isoforms, which then activate p57 transcription; dominant-negative p73 interferes with p57 induction. Reporter assays with p57 promoter; p73 overexpression; dominant-negative p73; Western blotting Journal of Molecular Biology Medium 16405903
2013 MyoD binds directly to a mesodermal enhancer (CS9) of the H19 gene, and CS9 physically contacts the H19 promoter (demonstrated by chromatin conformation capture), increasing H19 expression. H19 RNA in turn represses Igf2, and Igf2 negatively regulates MyoD expression, forming a negative feedback loop. Loss of both MyoD and Igf2 causes severe diaphragm atrophy. ChIP for MyoD binding to CS9; 3C (chromatin conformation capture); double-mutant (Myod/Igf2) mouse model Development Medium 23406902
2013 Six1 binds the MyoD Core Enhancer Region (CER) in myoblasts and regenerating muscle, and is required for CER reporter activity and proper chromatin structure at the CER as well as for MyoD binding at its own enhancer (a positive autoregulatory loop involving Six1). ChIP for Six1 binding to MyoD CER; siRNA knockdown of Six1; reporter assays with CER constructs and mutated Six1-binding sites; assessment of chromatin structure PLOS ONE Medium 23840772
2014 Ebf3 (and the family member Ebf1 in skeletal muscle) binds directly to the Atp2a1 (Serca1) promoter and synergizes with MyoD to induce Atp2a1 transcription, controlling muscle relaxation by regulating Ca2+ efflux. ChIP demonstrating Ebf3 binding to Atp2a1 promoter; co-transfection reporter assays with MyoD and Ebf3/1; Ebf3 KO mouse model; transgenic rescue Nature Communications High 24786561
2019 Promiscuous binding of MyoD to neuronal target genes in fibroblasts results in neuronal reprogramming when the muscle program is inhibited by Myt1l. Quantitative differences in binding distinguish MyoD-activated from non-activated genes; strong MyoD-binding sites are co-enriched with non-bHLH motifs (unlike Ascl1), making MyoD more context dependent. ChIP-seq in fibroblasts; ATAC-seq; gain-of-function with MyoD+Myt1l; comparative binding analysis of MyoD vs Ascl1 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.) 1491 1846704
1989 A gene with homology to the myc similarity region of MyoD1 is expressed during myogenesis and is sufficient to activate the muscle differentiation program. Genes & development 755 2473006
1988 MyoD1: a nuclear phosphoprotein requiring a Myc homology region to convert fibroblasts to myoblasts. Science (New York, N.Y.) 741 3175662
2005 MyoD and the transcriptional control of myogenesis. Seminars in cell & developmental biology 637 16099183
1989 Expression of two myogenic regulatory factors myogenin and MyoD1 during mouse embryogenesis. Nature 597 2552320
1989 Positive autoregulation of the myogenic determination gene MyoD1. Cell 443 2546677
1995 MyoD-induced expression of p21 inhibits cyclin-dependent kinase activity upon myocyte terminal differentiation. Molecular and cellular biology 382 7791789
1995 The MyoD family of transcription factors and skeletal myogenesis. BioEssays : news and reviews in molecular, cellular and developmental biology 368 7748174
2010 CLOCK and BMAL1 regulate MyoD and are necessary for maintenance of skeletal muscle phenotype and function. Proceedings of the National Academy of Sciences of the United States of America 318 20956306
1991 Muscle-specific transcriptional activation by MyoD. Genes & development 303 1651276
2006 MyoD inhibits Fstl1 and Utrn expression by inducing transcription of miR-206. The Journal of cell biology 270 17030984
1990 Two adjacent MyoD1-binding sites regulate expression of the acetylcholine receptor alpha-subunit gene. Nature 242 2342565
1990 Cell proliferation inhibited by MyoD1 independently of myogenic differentiation. Nature 211 2359457
2000 MyoD(-/-) satellite cells in single-fiber culture are differentiation defective and MRF4 deficient. Developmental biology 208 10926754
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
2010 MyoD regulates apoptosis of myoblasts through microRNA-mediated down-regulation of Pax3. The Journal of cell biology 156 20956382
2017 Long non-coding RNA Linc-RAM enhances myogenic differentiation by interacting with MyoD. Nature communications 149 28091529
2012 Genome-wide identification of enhancers in skeletal muscle: the role of MyoD1. Genes & development 145 23249738
2005 MyoD induces myogenic differentiation through cooperation of its NH2- and COOH-terminal regions. The Journal of cell biology 136 16275751
1990 Myogenic programs of mouse muscle cell lines: expression of myosin heavy chain isoforms, MyoD1, and myogenin. The Journal of cell biology 130 2167895
1995 MSX1 inhibits myoD expression in fibroblast x 10T1/2 cell hybrids. Cell 126 7664340
2003 Myogenin and MyoD1 expression in paediatric rhabdomyosarcomas. Journal of clinical pathology 125 12783965
2008 Codependent activators direct myoblast-specific MyoD transcription. Developmental cell 123 18854138
2003 Myf5 and MyoD activation define independent myogenic compartments during embryonic development. Developmental biology 119 12798290
2014 Recurrent MYOD1 mutations in pediatric and adult sclerosing and spindle cell rhabdomyosarcomas: evidence for a common pathogenesis. Genes, chromosomes & cancer 116 24824843
1995 Expression of myogenic regulatory proteins (myogenin and MyoD1) in small blue round cell tumors of childhood. The American journal of pathology 112 7495304
2007 Pbx homeodomain proteins direct Myod activity to promote fast-muscle differentiation. Development (Cambridge, England) 111 17699609
2000 CREB-binding protein/p300 activates MyoD by acetylation. The Journal of biological chemistry 107 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
2022 MyoD is a 3D genome structure organizer for muscle cell identity. Nature communications 96 35017543
2015 Myomaker, Regulated by MYOD, MYOG and miR-140-3p, Promotes Chicken Myoblast Fusion. International journal of molecular sciences 96 26540045
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 91 27562493
2000 Stabilization of MyoD by direct binding to p57(Kip2). The Journal of biological chemistry 89 10764802
2001 Interaction between acetylated MyoD and the bromodomain of CBP and/or p300. Molecular and cellular biology 82 11463815
2020 Human myotube formation is determined by MyoD-Myomixer/Myomaker axis. Science advances 74 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
2008 Cooperative synergy between NFAT and MyoD regulates myogenin expression and myogenesis. The Journal of biological chemistry 70 18676376
2023 MyoD-family inhibitor proteins act as auxiliary subunits of Piezo channels. Science (New York, N.Y.) 69 37590348
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
1998 Myogenin, MyoD, and myosin expression after pharmacologically and surgically induced hypertrophy. Journal of applied physiology (Bethesda, Md. : 1985) 69 9516204
2014 FGF21 expression and release in muscle cells: involvement of MyoD and regulation by mitochondria-driven signalling. The Biochemical journal 61 25055037
2012 MASTR directs MyoD-dependent satellite cell differentiation during skeletal muscle regeneration. Genes & development 61 22279050
2002 MyoD1 and myogenin expression in human neoplasia: a review and update. Advances in anatomic pathology 60 11981115
1991 The four human muscle regulatory helix-loop-helix proteins Myf3-Myf6 exhibit similar hetero-dimerization and DNA binding properties. Nucleic acids research 59 1945842
2013 MyoD-expressing progenitors are essential for skeletal myogenesis and satellite cell development. Developmental biology 56 24055173
2002 Six and Eya expression during human somitogenesis and MyoD gene family activation. Journal of muscle research and cell motility 56 12500905
2013 The role of MyoD1 and histone modifications in the activation of muscle enhancers. Epigenetics 55 23880568
2008 Role of MyoD in denervated, disused, and exercised muscle. Muscle & nerve 55 18642380
2006 MyoD synergizes with the E-protein HEB beta to induce myogenic differentiation. Molecular and cellular biology 55 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 51 33782573
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
2013 Myod and H19-Igf2 locus interactions are required for diaphragm formation in the mouse. Development (Cambridge, England) 47 23406902
2011 Leucine limitation regulates myf5 and myoD expression and inhibits myoblast differentiation. Experimental cell research 46 22079119
2005 E12 and E47 modulate cellular localization and proteasome-mediated degradation of MyoD and Id1. Oncogene 46 16007194
1998 DNA-mediated folding and assembly of MyoD-E47 heterodimers. The Journal of biological chemistry 46 9488706
1998 Regeneration and myogenic cell proliferation correlate with taurine levels in dystrophin- and MyoD-deficient muscles. The Anatomical record 46 9776086
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
2003 Regulation of MyoD activity and muscle cell differentiation by MDM2, pRb, and Sp1. The Journal of biological chemistry 43 12702724
2000 Expression of MyoD and myogenin in dystrophic mice, mdx and dy, during regeneration. Acta neuropathologica 43 10867795
2017 LSD1 Controls Timely MyoD Expression via MyoD Core Enhancer Transcription. Cell reports 42 28228264
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
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 39 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 37 23840772
2017 HDAC11 Inhibits Myoblast Differentiation through Repression of MyoD-Dependent Transcription. Molecules and cells 35 28927261
2004 Mutant MyoD lacking Cdc2 phosphorylation sites delays M-phase entry. Molecular and cellular biology 35 14749395
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
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
2019 2-hydroxyglutarate inhibits MyoD-mediated differentiation by preventing H3K9 demethylation. Proceedings of the National Academy of Sciences of the United States of America 32 31182575
1998 Induced expression of myoD, myogenin and desmin during myoblast differentiation in embryonic mouse tongue development. Archives of oral biology 31 9681116
2019 β-Catenin is essential for differentiation of primary myoblasts via cooperation with MyoD and α-catenin. Development (Cambridge, England) 30 30683662
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
2021 Myod1 and GR coordinate myofiber-specific transcriptional enhancers. Nucleic acids research 27 33836079
1995 MyoD and myogenesis in C. elegans. BioEssays : news and reviews in molecular, cellular and developmental biology 27 7748176
2013 MyoD is a tumor suppressor gene in medulloblastoma. Cancer research 25 24092238
2022 Tcf12 is required to sustain myogenic genes synergism with MyoD by remodelling the chromatin landscape. Communications biology 24 36352000
2017 Incomplete MyoD-induced transdifferentiation is associated with chromatin remodeling deficiencies. Nucleic acids research 24 28977539
2009 Noggin producing, MyoD-positive cells are crucial for eye development. Developmental biology 23 19778533

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