Affinage

MEF2A

Myocyte-specific enhancer factor 2A · UniProt Q02078

Length
507 aa
Mass
54.8 kDa
Annotated
2026-06-10
100 papers in source corpus 46 papers cited in narrative 47 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 9/9 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

MEF2A is a MADS-box/MEF2-domain transcription factor that binds A+T-rich DNA and orchestrates muscle, cardiac, and neuronal gene programs through combinatorial cofactor recruitment and signal-dependent post-translational control (PMID:20132824, PMID:12379849). Its core MADS-box plus MEF2 domain functions as a single integrated module mediating both dimerization and DNA binding, contacting major and minor grooves to bend DNA ~15° and presenting a preformed cofactor-binding pocket; residues N-terminal to the MADS-box and position 154 dictate the binding-site specificity that distinguishes MEF2A from SRF (PMID:10835359, PMID:20132824, PMID:8095095). In muscle MEF2A predominantly acts as a MEF2A–MEF2D heterodimer, the species that occupies sites such as the GLUT4 promoter (PMID:10748204). MEF2A activity is gated by an opposing set of inputs: p38 MAPK and ERK5 dock on its transactivation domain and phosphorylate it to increase activity, while class IIa HDACs (HDAC4/HDAC5) bind the MADS-box/MEF2 domain to repress it—HDAC4 dimerizing via its glutamine-rich region to bridge two MEF2A–DNA complexes—and CaMK signaling promotes MEF2A nuclear translocation and promoter binding (PMID:12086621, PMID:38281192, PMID:10373581, PMID:10748098, PMID:15132737, PMID:16985263). A SUMOylation switch at K395, installed by PIAS1 and reversed by SENP2 (whose stability is in turn controlled by APC/C-Cdh1), converts MEF2A between repressive and active states in an activity-dependent manner (PMID:16563226, PMID:23224591, PMID:25483061). Functionally, MEF2A directly drives a costamere/Z-disc structural gene program (myomaxin, myospryn, Xirp2) required for cardiomyocyte cytoarchitecture and survival, and its loss in mice causes mitochondrial disorganization, myofibrillar fragmentation, and sudden cardiac death that MEF2D cannot rescue (PMID:12379849, PMID:17046827, PMID:16407236, PMID:21724844). In neurons, SUMOylated MEF2A represses synaptotagmin-1 to eliminate orphan presynaptic sites and MEF2A/D-dependent transcription drives activity-dependent synapse silencing and AMPAR trafficking (PMID:23486945, PMID:29588465, PMID:28901289). A loss-of-function variant (p.Gly240*) that abolishes MYH6/FHL2 transactivation and MEF2A–GATA4 synergy links MEF2A to dilated cardiomyopathy (PMID:33554560). MEF2A also sustains genome/transcriptional homeostasis, with its loss provoking R-loop accumulation and DDX41–cGAS–STING interferon activation (PMID:37467105).

Mechanistic history

Synthesis pass · year-by-year structured walk · 20 steps
  1. 1993 High

    Before MEF2A's DNA-recognition logic was known, it was unclear how a MADS-box factor achieves binding specificity distinct from SRF; swapping defined residues established that specificity is encoded by sequences N-terminal to the MADS-box and position 154 through an indirect mechanism.

    Evidence Site-directed mutagenesis converting SRF specificity to MEF2A, with EMSA and ternary complex assays

    PMID:8095095

    Open questions at the time
    • Did not resolve the atomic basis of the indirect specificity
    • Did not address dimer partner contributions to site selection
  2. 2000 High

    To explain how MEF2A engages DNA differently from related MADS-box proteins, structural studies showed the MEF2 domain adopts a fold distinct from SRF/MCM1, contacts both grooves, and bends DNA only ~15°.

    Evidence X-ray crystallography (1.5 Å) and NMR solution structure of MEF2A–DNA complexes

    PMID:10715212 PMID:10835359

    Open questions at the time
    • Did not capture cofactor-bound states
    • Limited to the DNA-binding core, not full-length protein
  3. 2000 High

    It was unknown which MEF2 species binds physiological promoters in muscle; isoform-specific antibody work showed MEF2A acts as a MEF2A–MEF2D heterodimer that occupies the GLUT4 promoter and is selectively lost in diabetic muscle.

    Evidence Co-IP with isoform-specific antibodies, EMSA, and immunodepletion from heart/muscle extracts

    PMID:10748204

    Open questions at the time
    • Did not establish heterodimer composition across non-muscle tissues
    • Mechanism of diabetes-specific MEF2A downregulation unresolved
  4. 1999 High

    To define activating signals, it was shown that p38 MAPK (and PKCδ/ε) but not ERK1/2 or JNK phosphorylates the MEF2A transactivation domain to increase its transcriptional output.

    Evidence Reporter assays, 32P metabolic labeling, phosphopeptide mapping

    PMID:10373581

    Open questions at the time
    • Did not map all phospho-sites to downstream gene programs
    • In vivo relevance of PKC inputs untested
  5. 2002 High

    The structural basis of MEF2A as a kinase substrate was resolved by showing p38 docks MEF2A and its activator MKK3b at the same C-terminal site outside the active site, coupling docking to active-site rearrangement.

    Evidence Crystal structures of p38–MEF2A and p38–MKK3b docking peptides with mutational analysis

    PMID:12086621

    Open questions at the time
    • Did not address how docking specificity is shared with ERK5
    • Full-length kinase–substrate complex not solved
  6. 2004 Medium

    A second MAPK input was defined: ERK5 uses a phi_A-X-phi_B docking motif in MEF2A—similar to p38 determinants—to phosphorylate and activate it.

    Evidence In vitro kinase assays and docking-domain mutagenesis with in vivo activation readouts

    PMID:15132737

    Open questions at the time
    • Target gene specificity of ERK5 versus p38 signaling unresolved
    • Structural docking model not directly determined
  7. 2000 High

    The repressive arm of MEF2A control was identified: HDAC5 binds the MADS-box/MEF2 domain via its N-terminal non-deacetylase region to repress activity independently of catalysis.

    Evidence Reciprocal Co-IP, in vitro binding, domain mapping, reporter assays

    PMID:10748098

    Open questions at the time
    • Did not define the stoichiometry of the repressive complex
    • Signals releasing HDAC5 not addressed here
  8. 2010 High

    Structural work clarified that the MADS-box/MEF2 domain folds the cofactor pocket intrinsically and acts as one DNA-binding/dimerization unit, explaining how HDAC and myocardin-family cofactors share a preformed binding surface.

    Evidence Crystal structure of the MADS-box/MEF2 domain on DNA with homology modeling and mutagenesis

    PMID:20132824

    Open questions at the time
    • Did not capture an actual cofactor in the pocket
    • Competition between activators and repressors not structurally resolved
  9. 2024 High

    The architecture of HDAC-mediated repression was solved, showing two HDAC4 molecules dimerize through their glutamine-rich domain to bridge two MEF2A–DNA dimers, and that this dimerization is required for repression.

    Evidence Crystal structure of HDAC4–MEF2A–DNA (2:4:2) with mutagenesis and luciferase assays

    PMID:38281192

    Open questions at the time
    • In vivo prevalence of the dumbbell complex unquantified
    • Whether HDAC5 adopts the same architecture not shown
  10. 2006 Medium

    A SUMO-based off-switch was identified: MEF2A is SUMOylated at K395 by PIAS1, and the K395R mutant has enhanced transcriptional activity.

    Evidence In vitro and in vivo SUMOylation assays, mutagenesis, reporter assays

    PMID:16563226

    Open questions at the time
    • Did not identify the de-SUMOylation enzyme
    • Gene-specific consequences of K395 SUMOylation not mapped
  11. 2012 Medium

    The reversal of the SUMO switch was assigned to SENP2, which de-SUMOylates MEF2A and accumulates after activity-dependent stimuli to drive activation.

    Evidence shRNA screen, in vivo SUMOylation assays, SENP2 knockout embryos, reporter assays

    PMID:23224591

    Open questions at the time
    • How activity stabilizes SENP2 was not yet explained
    • Direct neuronal target genes not enumerated
  12. 2014 Medium

    The upstream control of SENP2 was traced to APC/C-Cdh1, which ubiquitinates SENP2 via a D-box; activity-dependent signals block this degradation, allowing nuclear SENP2 to de-SUMOylate and de-repress MEF2A.

    Evidence Co-IP, ubiquitination assays, reporter and SUMOylation/acetylation assays

    PMID:25483061

    Open questions at the time
    • The signal coupling activity to APC/C inhibition not defined
    • Single-lab pathway without independent confirmation
  13. 2002 High

    The in vivo physiological requirement for MEF2A was established by knockout mice showing right ventricular dilation, mitochondrial disorganization, myofibrillar fragmentation, and sudden death not rescued by MEF2D.

    Evidence Mef2a knockout mouse with histology, EM, and MEF2-dependent transgene reporter

    PMID:12379849

    Open questions at the time
    • Did not identify the direct target genes responsible for the phenotype
    • Basis of MEF2D non-redundancy not molecularly defined
  14. 2006 Medium

    Direct cardiac structural targets were identified—myomaxin and myospryn—both downregulated in Mef2a-null hearts and localizing to the Z-disc/costamere via alpha-actinin-2.

    Evidence Mef2a knockout microarray, Co-IP with alpha-actinin-2, immunolocalization

    PMID:16407236 PMID:17046827

    Open questions at the time
    • Direct promoter occupancy not shown in these reports
    • Functional contribution of each target to phenotype untested
  15. 2011 Medium

    MEF2A was shown to directly bind a cohort of costamere gene promoters, and acute knockdown caused myofibril/focal-adhesion malformations and adhesion-dependent cell death, defining a survival role through costamere integrity.

    Evidence ChIP, Mef2a knockout, siRNA in primary cardiomyocytes, immunofluorescence, apoptosis assays

    PMID:21724844 PMID:33863999

    Open questions at the time
    • Which individual costamere targets are essential for survival not isolated
    • Mechanism linking costamere loss to apoptosis incomplete
  16. 2012 Medium

    A regeneration mechanism was defined whereby MEF2A drives the Gtl2-Dio3 miRNA cluster that represses sFRPs to sustain WNT signaling, with myogenic defects rescued by miR-410/433 or recombinant WNTs.

    Evidence Mef2a knockout muscle regeneration, miRNA profiling, miRNA and WNT rescue

    PMID:23154418

    Open questions at the time
    • Direct MEF2A occupancy at the Gtl2-Dio3 locus quantification limited
    • Generalizability beyond regeneration context untested
  17. 2013 Medium

    In neurons, SUMOylated MEF2A was shown to function as a repressor of synaptotagmin-1 to eliminate orphan presynaptic sites, linking the SUMO switch to synaptic refinement.

    Evidence In vivo knockdown in rat cerebellar cortex, target gene identification, reporter assays

    PMID:23486945

    Open questions at the time
    • Full repressive cofactor complex on Syt1 not defined
    • Single-lab in vivo result
  18. 2018 Medium

    MEF2A's role in postsynaptic plasticity was extended by showing MEF2A is required for Group I mGluR-mediated GluA2 AMPAR internalization, independent of Arc, and MEF2A/D transcription drives activity-dependent synapse silencing.

    Evidence siRNA/loss-of-function with GluA2 trafficking and electrophysiology, optogenetics

    PMID:28901289 PMID:29588465

    Open questions at the time
    • The MEF2A target genes mediating GluA2 internalization not identified
    • Distinction of MEF2A versus MEF2D contributions incomplete
  19. 2020 Medium

    A human disease link was established: the MEF2A p.Gly240* loss-of-function variant abolishes MYH6/FHL2 transactivation and MEF2A–GATA4 synergy, predisposing to dilated cardiomyopathy.

    Evidence Whole-exome/Sanger sequencing with dual-luciferase functional characterization

    PMID:33554560

    Open questions at the time
    • Causality in a model organism not demonstrated
    • Penetrance and mechanism in patient hearts not established
  20. 2023 Medium

    A genome-homeostasis function was revealed: MEF2A loss causes R-loop accumulation and ATR-dependent activation of the DDX41–cGAS–STING interferon pathway, positioning MEF2A as a suppressor of unscheduled interferon responses.

    Evidence Loss-of-function with R-loop detection, ATR-inhibition epistasis, STING/interferon reporters

    PMID:37467105

    Open questions at the time
    • Whether R-loops arise from direct MEF2A transcriptional targets unclear
    • Tissue contexts for this homeostatic role untested

Open questions

Synthesis pass · forward-looking unresolved questions
  • How the competing post-translational inputs (MAPK phosphorylation, SUMOylation, acetylation, ubiquitination, CMA-mediated turnover) are integrated at specific promoters to select repressor versus activator complexes in a given tissue remains unresolved.
  • No unified quantitative model of the modification code
  • Cell-type-specific cofactor selection rules undefined
  • Direct genome-wide MEF2A target maps not integrated with modification states

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140110 transcription regulator activity 7 GO:0003677 DNA binding 6 GO:0003723 RNA binding 1
Localization
GO:0005634 nucleus 3 GO:0005829 cytosol 2
Pathway
R-HSA-162582 Signal Transduction 4 R-HSA-397014 Muscle contraction 4 R-HSA-74160 Gene expression (Transcription) 4 R-HSA-112316 Neuronal System 3 R-HSA-1266738 Developmental Biology 2
Partners
GATA4HDAC1HDAC4HDAC5MEF2DP300PITX2SENP2
Complex memberships
HDAC4–MEF2A–DNA repressive complexMEF2A–MEF2D heterodimerTR–RxR–MEF2A–p300 complex

Evidence

Reading pass · 47 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2002 Crystal structures of p38 MAP kinase complexed with docking site peptides from MEF2A (substrate) and MKK3b (activator) revealed that both peptides bind the same site in the C-terminal domain of p38, outside the active site and distinct from the 'CD' domain, inducing conformational changes in the active site and phosphorylation lip. X-ray crystallography; mutational analysis of p38–MEF2A docking interaction Molecular cell High 12086621
2000 Crystal structure of MEF2A core (residues 2–78) bound to DNA at 1.5 Å resolution revealed how the absence of amino acids N-terminal to the MADS-box contributes to DNA-binding properties and that the MEF2 domain adopts a conformation considerably different from SRF and MCM1. X-ray crystallography Journal of molecular biology High 10715212
2000 NMR solution structure of the MEF2A–DNA complex showed that the MADS-box contacts both major and minor grooves, the MEF2S domain structure is entirely different from the SAM domain in SRF/MCM1, and critical protein–DNA contact differences explain the ~15° DNA bending by MEF2A versus ~70° by SRF/MCM1. NMR spectroscopy The EMBO journal High 10835359
2010 Crystal structure of the MADS-box/MEF2 domain of MEF2A bound to DNA showed that the MEF2 domain participates with the MADS-box in both dimerization and DNA binding as a single domain, and that the ligand-binding pocket (for cofactors such as HDACs/myocardin family) is preformed by intrinsic folding rather than induced by cofactor binding. X-ray crystallography; homology modeling; mutagenesis Journal of molecular biology High 20132824
2024 Crystal structure of an HDAC4–MEF2A–DNA complex revealed a 2:4:2 (HDAC4:MEF2A:DNA) dumbbell-shaped architecture in which two HDAC4 molecules dimerize via their glutamine-rich domain to bridge two MEF2A–DNA dimers; mutagenesis and luciferase assays confirmed that HDAC4 dimerization is required for its repression of MEF2A transcriptional activity. X-ray crystallography; biochemical mutagenesis assays; luciferase reporter assays Nucleic acids research High 38281192
1993 Mutational analysis (removal of N-terminal residues plus K154E substitution) demonstrated that DNA-binding specificity of SRF can be converted to that of MEF2A/RSRFC4, identifying that residues immediately N-terminal to the MADS box and position 154 determine binding-site specificity via an indirect mechanism not involving direct base recognition. Site-directed mutagenesis; DNA-binding assays (EMSA); ternary complex formation assays Nucleic acids research High 8095095
1999 p38 MAP kinase phosphorylates MEF2A on serine and threonine residues within its transactivation domain, causing decreased electrophoretic mobility and increased transcriptional activity; PKCδ and PKCε also enhance MEF2A transactivation, whereas ERK1/2 and JNK/SAPK do not. Transient transfection reporter assays; metabolic 32P-labeling; immunoprecipitation; phosphopeptide mapping; phosphoamino acid analysis Nucleic acids research High 10373581
2000 HDAC5 interacts with MEF2A in vivo and in vitro and strongly represses its transcriptional activity; repression is independent of the HDAC5 deacetylase domain and instead mediated by the N-terminal non-deacetylase domain; the MADS-box/MEF2 domain of MEF2A interacts with a limited region in the N-terminal part of HDAC5. Co-immunoprecipitation (in vivo); in vitro binding assays; domain-mapping experiments; transcriptional reporter assays The Journal of biological chemistry High 10748098
2003 A 7-amino-acid deletion in MEF2A disrupts nuclear localization of MEF2A, reduces MEF2A-mediated transcription activation, and abolishes synergistic activation by MEF2A and GATA-1 through a dominant-negative mechanism; MEF2A protein is strongly expressed in the endothelium of coronary arteries. Functional luciferase reporter assays; subcellular localization studies; dominant-negative analysis Science Medium 14645853
2006 MEF2A is sumoylated primarily at lysine K395 both in vitro and in vivo; the nuclear E3 ligase PIAS1 promotes this sumoylation; mutation K395R abolishes sumoylation and results in enhanced transcriptional activity of MEF2A. In vitro and in vivo SUMOylation assays; site-directed mutagenesis; transcriptional reporter assays Journal of cellular and molecular medicine Medium 16563226
2012 SENP2 is the de-SUMOylation enzyme for MEF2A; SENP2 knockdown or knockout increases detectable SUMOylated MEF2A; SENP2 accumulates in response to activity-dependent stimuli and thereby mediates activity-dependent MEF2A de-SUMOylation and transcriptional activation. shRNA screen; in vivo SUMOylation assays; SENP2 knockout embryos; transcriptional reporter assays Molecular biology reports Medium 23224591
2014 APC/C-Cdh1 interacts with and ubiquitinates SENP2 (recognizing a D-box motif) in the cytoplasm, targeting it for degradation; this controls MEF2A transcriptional activation in an activity-dependent manner, since activity-dependent stimuli prevent APC(Cdh1)-induced SENP2 ubiquitination, promote SENP2 nuclear accumulation, and cause MEF2A de-SUMOylation and acetylation. Co-immunoprecipitation; ubiquitination assays; luciferase reporter assays; SUMOylation/acetylation assays Cell cycle Medium 25483061
2002 MEF2A-deficient mice exhibit pronounced right ventricular dilation, myofibrillar fragmentation, mitochondrial disorganization, activation of a fetal cardiac gene program, and sudden cardiac death; MEF2D transcriptional activity is paradoxically enhanced in mutant hearts, showing that MEF2D cannot compensate for MEF2A-specific functions in maintaining mitochondrial content and cytoarchitectural integrity. Mef2a knockout mouse; histology; electron microscopy; MEF2-dependent transgene reporter Nature medicine High 12379849
2000 MEF2A forms a MEF2A–MEF2D heterodimer (with no detectable MEF2A homodimers or MEF2A–MEF2C dimers) in heart and skeletal muscle; this heterodimer is the species that binds the MEF2 site in the GLUT4 promoter; immunodepletion of MEF2A–MEF2D abolishes MEF2 site binding and addition of MEF2A to diabetic nuclear extracts restores it; MEF2A is specifically down-regulated in insulin-deficient diabetes without effect on MEF2D in muscle. Co-immunoprecipitation with isoform-specific antibodies; EMSA; immunodepletion assays The Journal of biological chemistry High 10748204
1997 The MEF2A 3′ UTR functions as a cis-acting translational repressor both in vivo and in vitro, with an internal conserved region responsible for inhibition; this repression is independent of mRNA steady-state levels and is relaxed during muscle cell differentiation. CAT reporter gene fusion assays in vivo; in vitro translation in rabbit reticulocyte lysates; RNase protection assays Molecular and cellular biology High 9111346
2004 ERK5 uses a docking domain (phi_A-X-phi_B motif) in MEF2A to promote both in vitro phosphorylation and in vivo transcriptional activation of MEF2A; the specificity determinants for ERK5 at the MEF2A docking domain are similar to those for p38; the catalytic domain of ERK5 recognizes the docking domain. In vitro kinase assays; mutational analysis of MEF2A docking domain; in vivo transcriptional activation assays The Biochemical journal Medium 15132737
2013 Sumoylated MEF2A acts as a transcriptional repressor to eliminate orphan presynaptic sites in neurons; knockdown of MEF2A in rat cerebellar cortex in vivo increases orphan presynaptic site density; sumoylated MEF2A directly represses the synaptotagmin 1 (Syt1) gene, and Syt1 repression mediates MEF2A-dependent elimination of orphan presynaptic sites, which promotes accumulation of presynaptic material at maturing boutons. In vivo knockdown (rat cerebellar cortex); direct target gene identification; reporter assays; neuronal culture experiments The Journal of neuroscience Medium 23486945
2014 MEF2A undergoes chaperone-mediated autophagy (CMA)-dependent degradation by lysosomes under basal conditions; mild oxidative stress enhances MEF2A degradation and activity, whereas excessive oxidative stress disrupts lysosomal integrity causing accumulation of non-functional MEF2A and production of an HDAC4 N-terminal cleavage product (HDAC4-NT) by lysosomal serine proteases, which acts as a MEF2 repressor. Lysosomal fractionation; CMA pathway inhibition; oxidative stress treatments; western blot; DNA-binding and transcriptional activity assays Autophagy Medium 24879151
2012 MEF2A ubiquitination in dopaminergic neurons is isoform-specific (MEF2A but not MEF2C or MEF2D); ubiquitination occurs at the N-terminus, first detectable in the nuclear compartment then in the cytoplasm; ubiquitinated MEF2A has reduced DNA-binding and transcriptional activity; neurotoxins that cause proteasome pathway disruption lead to accumulation of ubiquitinated MEF2A and impaired neuronal viability. Ubiquitination assays in neuronal SN4741 cells; subcellular fractionation; DNA-binding activity assays; proteasome inhibitor treatments Journal of neurochemistry Medium 22764880
2003 p300/CBP binds the N-terminal domain of both TR and MEF2A via the same C-terminal portion of p300; TR, MEF2A, and p300 form a ternary complex in vivo; p300/CBP modulates transactivation of the TR-RxR-MEF2A complex at a thyroid hormone response element; adenovirus E1A inhibits TR-RxR-MEF2A-p300 activation but not TR-RxR-MEF2A alone, indicating p300 recruits an inhibitor. GST pull-down; co-immunoprecipitation; domain mapping; CAT reporter assays in U2OS cells The Biochemical journal Medium 12371907
2004 PITX2a directly interacts with MEF2A (demonstrated by yeast two-hybrid and GST pull-down); coexpression of MEF2A and PITX2a/Pitx2c results in strong synergistic activation of the ANF promoter in a cell-type- and promoter-context-specific manner (LS8 cells but not NIH/3T3, CHO, or C2C12); synergism requires MEF2 binding sites and DNA binding by MEF2A. Yeast two-hybrid; GST pull-down; luciferase reporter assays; cell-type specificity analysis The Journal of biological chemistry Medium 15466416
2008 GLUT4 enhancer factor (GEF) dimerizes with hypophosphorylated MEF2A with increased affinity; MEF2A binding to its cognate site increases the DNA binding activity of GEF to Domain I of the GLUT4 promoter; HDAC5 interacts with GEF and specifically inhibits GLUT4 promoter activity. Co-immunoprecipitation; EMSA; luciferase reporter assays; domain mapping The Journal of biological chemistry Medium 18216015
2006 Myomaxin (a Xin-related protein) is a direct downstream transcriptional target of MEF2A; it is markedly down-regulated in Mef2a knockout hearts; myomaxin localizes to the Z-disc/costameric region and interacts with the sarcomeric Z-disc protein alpha-actinin-2. Mef2a knockout mouse; microarray expression analysis; co-immunoprecipitation (myomaxin–alpha-actinin-2); immunolocalization The Journal of biological chemistry Medium 17046827
2006 Myospryn is a direct downstream transcriptional target of MEF2A, identified by microarray in Mef2a knockout mice; myospryn localizes to the costamere and interacts with alpha-actinin-2. Mef2a knockout mouse; microarray expression analysis; co-immunoprecipitation (myospryn–alpha-actinin-2); immunolocalization The Journal of biological chemistry Medium 16407236
2011 MEF2A directly regulates a cohort of costamere genes in cardiac muscle; acute knockdown of Mef2a in primary neonatal cardiomyocytes causes profound myofibril and focal adhesion malformations and adhesion-dependent programmed cell death, identifying a role for MEF2A in cardiomyocyte survival through regulation of costamere integrity. Mef2a knockout mouse; expression analysis; Mef2a siRNA knockdown in primary cardiomyocytes; immunofluorescence; apoptosis assays The Journal of biological chemistry Medium 21724844
2012 MEF2A directly regulates the Gtl2-Dio3 miRNA mega-cluster; Gtl2-Dio3-encoded miRNAs repress secreted Frizzled-related proteins (sFRPs), inhibitors of WNT signaling; in Mef2a knockout regenerating muscle these miRNAs are downregulated, sFRP expression is upregulated, and WNT activity is attenuated; myogenic differentiation in MEF2A-deficient myoblasts is rescued by miR-410/miR-433 overexpression or recombinant WNT3A/WNT5A treatment. Mef2a knockout mouse; muscle regeneration assays; miRNA expression profiling; rescue with miRNA overexpression and recombinant WNTs Development Medium 23154418
2010 MEF2A activates Xirp2 expression in response to angiotensin II by directly stimulating MEF2A transcriptional activity at the Xirp2 promoter; Xirp2 (an actin-binding protein) functions downstream of MEF2A to modulate Ang II-mediated pathological cardiac remodeling. Xirp2 promoter characterization; MEF2A binding assays; Xirp2 hypomorphic mouse with Ang II infusion Circulation research Medium 20093629
2009 TGF-β transcriptionally induces MMP-10 through MEF2A; TGF-β promotes proteasome-dependent degradation of class IIa HDACs, resulting in increased histone acetylation around the MEF2 site on the MMP-10 promoter and increased MEF2A binding; knockdown of MEF2A reduces and overexpression increases TGF-β-induced MMP-10 expression. MEF2A knockdown/overexpression; ChIP assay; luciferase reporter assays; HDAC knockdown/overexpression Oncogene Medium 19935709
2008 CaMK II activation during exercise is required for histone H3 hyperacetylation at the GLUT4 MEF2 site and for increased MEF2A binding to this site in vivo; inhibition of CaMK II with KN93 prior to exercise abolishes these increases and attenuates exercise-induced GLUT4 mRNA and protein increases. In vivo exercise model; chromatin immunoprecipitation (ChIP); Western blot; RT-PCR; CaMK II inhibitor (KN93) American journal of physiology. Endocrinology and metabolism Medium 18647882
2006 Exercise increases MEF2A binding to the GLUT4 promoter in vivo; CaMK signaling mediates MEF2A/DNA associations, as constitutively active CaMK IV increases MEF2A binding by ~75% compared to dominant-negative CaMK IV in C2C12 myotubes. In vivo exercise model; ChIP assay; constitutively active and dominant-negative CaMK IV overexpression American journal of physiology. Endocrinology and metabolism Medium 16985263
2010 MEF2A is present on the c-Jun promoter in macrophages; MEF2A/MEF2D heterodimers strongly interact with HDAC1 (and to a lesser extent HDAC7) in macrophages; endogenous p300 associates with MEF2A only in differentiated macrophages (not undifferentiated cells or monocytes), indicating a switch from repressor to activator complex during differentiation. Chromatin immunoprecipitation (ChIP); co-immunoprecipitation; trichostatin A treatment The Biochemical journal Medium 20590529
2022 HDAC5 interacts with MEF2A and suppresses MEF2A binding to the Smad7 promoter, resulting in Smad7 promoter activity repression; luciferase reporter and ChIP-qPCR assays confirmed this interaction; HDAC5 deficiency increases Smad7 expression, which in turn decreases TGF-β1-induced Smad2/3 phosphorylation. Luciferase reporter assays; ChIP-qPCR; HDAC5 knockdown; in vivo scar model International journal of biological sciences Medium 36263180
2004 MEF2A nuclear translocation is regulated by p38 and calcineurin in a biphasic, time-dependent manner in response to static stretch; stretch produces increased p38 phosphorylation preceding MEF2A nuclear translocation; inhibition of p38 (SB-203580) or calcineurin (cyclosporine A) blocks MEF2A phosphorylation and nuclear translocation. Pharmacological inhibition (SB-203580, cyclosporine A); Western blot; subcellular fractionation/nuclear translocation assays; static stretch application in C2C12 myocytes American journal of physiology. Cell physiology Medium 15483225
2011 MEF2A directly binds MEF2A-binding sites in the promoter region of Xirp2 (Myomaxin/Myospryn network) and a cohort of costamere genes, establishing MEF2A as a direct transcriptional regulator of a costamere gene program in cardiac muscle. ChIP assay; Mef2a knockout mouse; luciferase reporter assays The Journal of biological chemistry Medium 21724844
2014 MEF2A binds the Cpt1b promoter in skeletal muscle; exercise training elevates MEF2A binding and reduces HDAC5 binding at the Cpt1b promoter; exercise induces MEF2A hyperacetylation which correlates with enhanced DNA-binding; HDAC5 and HDAC3 binding to MEF2A decreases with exercise; MEF2A overexpression increases Cpt1b mRNA expression suppressed by HDAC5. ChIP assay; co-immunoprecipitation; MEF2A overexpression; luciferase reporter assays; exercise treadmill model Acta physiologica Medium 25213552
2011 MEF2A directly binds the promoter region of ZEB2 and CTNNB1 to initiate their transcription in colorectal cancer cells, promoting EMT and WNT/β-catenin signaling; demonstrated by direct promoter binding assays. ChIP assay; luciferase reporter assays; MEF2A overexpression/knockdown Oncogene Medium 33863999
2011 AMPKα2 regulates MEF2A nuclear translocation and MEF2A binding to the Glut4 promoter; overexpression of AMPKα2 increases nuclear MEF2A content and promoter-bound MEF2A, while knockout attenuates these effects; however, AMPKα2 does not regulate HDAC5 nuclear export after 28 days of training. AMPKα2 OE and KO mice; treadmill training; ChIP assay; Western blot; co-immunoprecipitation Medicine and science in sports and exercise Medium 21233771
2018 MEF2A is required for Group I mGluR-mediated GluA2 AMPA receptor internalization in neurons; knockdown of MEF2A specifically abolishes mGluR-dependent GluA2 internalisation without affecting basal AMPAR expression or trafficking; this process is independent of Arc/Arg3.1 expression. MEF2A knockdown in primary neuronal culture; GluA2 trafficking assays; Arc/Arg3.1 expression analysis Scientific reports Medium 29588465
2017 MEF2A/D-dependent transcription (specifically MEF2A/D) is required for synapse silencing (depression of AMPAR transmission) induced by 1-hour theta-frequency burst firing in CA1 neurons; MEF2A/D-induced Arc expression contributes to synapse silencing and elimination; more prolonged (24-hr) firing-induced spine elimination did not require MEF2A/D. Optogenetics; MEF2A/D loss-of-function; Arc expression measurement; electrophysiology (AMPAR and NMDAR EPSCs); de novo transcription inhibition eLife Medium 28901289
2018 MEF2A directly binds the Calpain 3 (Capn3) promoter and positively regulates Capn3 expression; demonstrated by luciferase reporter assay, EMSA, and ChIP in rat denervated gastrocnemius muscle; MEF2A siRNA knockdown in L6 myoblasts reduces Capn3 protein. Luciferase reporter assay; EMSA; ChIP; siRNA knockdown; Western blot Gene Medium 29783071
2020 MEF2A loss-of-function variant (p.Gly240*) abolishes transactivation on target genes MYH6 and FHL2 and nullifies synergistic activation between MEF2A and GATA4, establishing MEF2A loss-of-function as predisposing to dilated cardiomyopathy. Whole-exome sequencing; Sanger sequencing; dual-luciferase assay; functional characterization of variant Clinical chemistry and laboratory medicine Medium 33554560
2017 MEF2A immunoprecipitation followed by RNA isolation confirmed direct binding of MEF2A protein to pri-miR-494 RNA, suggesting a novel post-transcriptional function of MEF2A as an RNA-binding protein regulating processing of 14q32 microRNAs miR-329 and miR-494. MEF2A immunoprecipitation followed by RNA isolation and RT-qPCR; in vivo hind-limb ischemia model with MEF2A gene silencing Molecular therapy. Nucleic acids Low 28624225
2023 MEF2A loss leads to R-loop accumulation and activates the DDX41–cGAS–STING interferon pathway; MEF2A-deficient cells show ATR kinase activation, which is necessary for STING activation; MEF2A thus sustains transcriptional homeostasis and suppresses unscheduled interferon responses. MEF2A loss-of-function; R-loop detection assays; ATR inhibition experiments; STING pathway activation measurements; interferon reporter assays Cell reports Medium 37467105
2017 MEF2A transcriptional activation in response to oxytocin (OT) involves reduced phosphorylation of MEF2A at Serine 408, under control of the OTR-coupled MAPK (MEK1/2) pathway; MEK1/2 inhibition (U0126) blocks MEF2A activation; siRNA-mediated MEF2A knockdown prevents OT-induced neurite retraction in hypothalamic neurons. Pharmacological inhibition (U0126); siRNA knockdown of MEF2A; Western blot for pSer408-MEF2A; neurite morphology measurements Molecular and cellular endocrinology Medium 29928931
2018 MEF2A and MEF2D function as scaffold proteins interacting with HDAC1 (in undifferentiated THP-1 cells) or p300 (in TPA-differentiated THP-1 cells) at the SOD3 promoter region, mediating switches between repression and activation of SOD3 gene expression. ChIP assay; co-immunoprecipitation; MEF2A/MEF2D knockdown; Western blot Free radical research Medium 29842805
2024 MEF2A directly activates transcription of PGC1α and inhibits transcription of KEAP1, thereby promoting mitochondrial biogenesis and activating the KEAP1/NRF2 pathway to modulate reactive oxygen species levels and confer cisplatin resistance in gastric cancer cells. MEF2A overexpression/knockdown; luciferase reporter assays for PGC1α and KEAP1 promoters; in vitro and in vivo cisplatin sensitivity assays Biochimica et biophysica acta. Molecular basis of disease Medium 39237047
2024 MEF2A directly modulates CYP7A1 transcription as confirmed by dual luciferase reporter assays; MEF2A knockdown in HepG2 cells leads to CYP7A1 downregulation and lipid accumulation, while overexpression reverses these effects; reduced MEF2A expression in offspring of HFD-fed dams is attributable to DNA hypermethylation in the MEF2A promoter region. Dual luciferase reporter assays; MEF2A knockdown/overexpression; MassARRAY EpiTYPER methylation analysis; 5-azacitidine treatment Cellular & molecular biology letters Medium 39695937

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2009 MicroRNA-1 negatively regulates expression of the hypertrophy-associated calmodulin and Mef2a genes. Molecular and cellular biology 334 19188439
2002 Crystal structures of MAP kinase p38 complexed to the docking sites on its nuclear substrate MEF2A and activator MKK3b. Molecular cell 271 12086621
2002 Mitochondrial deficiency and cardiac sudden death in mice lacking the MEF2A transcription factor. Nature medicine 270 12379849
2003 Mutation of MEF2A in an inherited disorder with features of coronary artery disease. Science (New York, N.Y.) 264 14645853
2014 Requirement of MEF2A, C, and D for skeletal muscle regeneration. Proceedings of the National Academy of Sciences of the United States of America 180 24591619
2000 mHDA1/HDAC5 histone deacetylase interacts with and represses MEF2A transcriptional activity. The Journal of biological chemistry 175 10748098
2011 The cardiac transcription network modulated by Gata4, Mef2a, Nkx2.5, Srf, histone modifications, and microRNAs. PLoS genetics 170 21379568
2012 MEF2A regulates the Gtl2-Dio3 microRNA mega-cluster to modulate WNT signaling in skeletal muscle regeneration. Development (Cambridge, England) 100 23154418
2000 The MEF2A isoform is required for striated muscle-specific expression of the insulin-responsive GLUT4 glucose transporter. The Journal of biological chemistry 94 10748204
1999 Post-translational control of the MEF2A transcriptional regulatory protein. Nucleic acids research 91 10373581
2000 Crystal structure of MEF2A core bound to DNA at 1.5 A resolution. Journal of molecular biology 89 10715212
2008 CaMK activation during exercise is required for histone hyperacetylation and MEF2A binding at the MEF2 site on the Glut4 gene. American journal of physiology. Endocrinology and metabolism 86 18647882
2011 miR-155 inhibits expression of the MEF2A protein to repress skeletal muscle differentiation. The Journal of biological chemistry 82 21868385
2005 Lack of MEF2A mutations in coronary artery disease. The Journal of clinical investigation 80 15841183
2000 Solution structure of the MEF2A-DNA complex: structural basis for the modulation of DNA bending and specificity by MADS-box transcription factors. The EMBO journal 79 10835359
2012 Variants in exon 11 of MEF2A gene and coronary artery disease: evidence from a case-control study, systematic review, and meta-analysis. PloS one 71 22363637
2004 Transcription factor MEF2A mutations in patients with coronary artery disease. Human molecular genetics 71 15496429
2010 Modulation of angiotensin II-mediated cardiac remodeling by the MEF2A target gene Xirp2. Circulation research 61 20093629
2008 Caffeine induces hyperacetylation of histones at the MEF2 site on the Glut4 promoter and increases MEF2A binding to the site via a CaMK-dependent mechanism. American journal of physiology. Endocrinology and metabolism 56 18198354
2006 Exercise and CaMK activation both increase the binding of MEF2A to the Glut4 promoter in skeletal muscle in vivo. American journal of physiology. Endocrinology and metabolism 53 16985263
2022 HDAC5-mediated Smad7 silencing through MEF2A is critical for fibroblast activation and hypertrophic scar formation. International journal of biological sciences 50 36263180
2014 Disruption of chaperone-mediated autophagy-dependent degradation of MEF2A by oxidative stress-induced lysosome destabilization. Autophagy 50 24879151
2006 Myomaxin is a novel transcriptional target of MEF2A that encodes a Xin-related alpha-actinin-interacting protein. The Journal of biological chemistry 50 17046827
2010 Dual roles for MEF2A and MEF2D during human macrophage terminal differentiation and c-Jun expression. The Biochemical journal 49 20590529
1993 The identification of elements determining the different DNA binding specificities of the MADS box proteins p67SRF and RSRFC4. Nucleic acids research 48 8095095
2021 MEF2A transcriptionally upregulates the expression of ZEB2 and CTNNB1 in colorectal cancer to promote tumor progression. Oncogene 47 33863999
2005 The Pro279Leu variant in the transcription factor MEF2A is associated with myocardial infarction. Journal of medical genetics 47 15958500
2020 Long Noncoding RNA Ahit Protects Against Cardiac Hypertrophy Through SUZ12 (Suppressor of Zeste 12 Protein Homolog)-Mediated Downregulation of MEF2A (Myocyte Enhancer Factor 2A). Circulation. Heart failure 46 31957467
1997 The MEF2A 3' untranslated region functions as a cis-acting translational repressor. Molecular and cellular biology 46 9111346
2006 Myospryn is a direct transcriptional target for MEF2A that encodes a striated muscle, alpha-actinin-interacting, costamere-localized protein. The Journal of biological chemistry 44 16407236
2006 SUMO-1 modification of MEF2A regulates its transcriptional activity. Journal of cellular and molecular medicine 43 16563226
1997 Influence of PDGF-BB on proliferation and transition through the MyoD-myogenin-MEF2A expression program during myogenesis in mouse C2 myoblasts. Growth factors (Chur, Switzerland) 43 9401815
2009 Transcriptional induction of MMP-10 by TGF-beta, mediated by activation of MEF2A and downregulation of class IIa HDACs. Oncogene 41 19935709
2016 Houttuynia cordata Thunb Promotes Activation of HIF-1A-FOXO3 and MEF2A Pathways to Induce Apoptosis in Human HepG2 Hepatocellular Carcinoma Cells. Integrative cancer therapies 39 27698266
2010 Structure of the MADS-box/MEF2 domain of MEF2A bound to DNA and its implication for myocardin recruitment. Journal of molecular biology 39 20132824
2008 GLUT4 enhancer factor (GEF) interacts with MEF2A and HDAC5 to regulate the GLUT4 promoter in adipocytes. The Journal of biological chemistry 38 18216015
1995 MEF2 proteins, including MEF2A, are expressed in both muscle and non-muscle cells. Nucleic acids research 36 7501445
2015 Inhibition of MEF2A prevents hyperglycemia-induced extracellular matrix accumulation by blocking Akt and TGF-β1/Smad activation in cardiac fibroblasts. The international journal of biochemistry & cell biology 34 26482596
2004 Static stretch promotes MEF2A nuclear translocation and expression of neonatal myosin heavy chain in C2C12 myocytes in a calcineurin- and p38-dependent manner. American journal of physiology. Cell physiology 34 15483225
2011 The Mef2A transcription factor coordinately regulates a costamere gene program in cardiac muscle. The Journal of biological chemistry 33 21724844
2013 Sumoylated MEF2A coordinately eliminates orphan presynaptic sites and promotes maturation of presynaptic boutons. The Journal of neuroscience : the official journal of the Society for Neuroscience 31 23486945
2004 ERK5 is targeted to myocyte enhancer factor 2A (MEF2A) through a MAPK docking motif. The Biochemical journal 31 15132737
2003 p300/cAMP-response-element-binding-protein ('CREB')-binding protein (CBP) modulates co-operation between myocyte enhancer factor 2A (MEF2A) and thyroid hormone receptor-retinoid X receptor. The Biochemical journal 31 12371907
2014 Exercise increases the binding of MEF2A to the Cpt1b promoter in mouse skeletal muscle. Acta physiologica (Oxford, England) 30 25213552
2007 Lack of association between the MEF2A gene and myocardial infarction. Circulation 30 18086930
2001 The MEF2A and MEF2D isoforms are differentially regulated in muscle and adipose tissue during states of insulin deficiency. Endocrinology 30 11316766
2005 MEF2A sequence variants and coronary artery disease: a change of heart? The Journal of clinical investigation 29 15841171
2023 Evolutionary conserved circular MEF2A RNAs regulate myogenic differentiation and skeletal muscle development. PLoS genetics 27 37676887
2021 MEF2A-mediated lncRNA HCP5 Inhibits Gastric Cancer Progression via MiR-106b-5p/p21 Axis. International journal of biological sciences 27 33613117
2015 Inducible knockout of Mef2a, -c, and -d from nestin-expressing stem/progenitor cells and their progeny unexpectedly uncouples neurogenesis and dendritogenesis in vivo. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 27 26286136
2014 The novel regulations of MEF2A, CAMKK2, CALM3, and TNNI3 in ventricular hypertrophy induced by arsenic exposure in rats. Toxicology 27 25089838
2011 MEF2A binding to the Glut4 promoter occurs via an AMPKα2-dependent mechanism. Medicine and science in sports and exercise 27 21233771
2011 HB-EGF induces cardiomyocyte hypertrophy via an ERK5-MEF2A-COX2 signaling pathway. Cellular signalling 26 21244855
2006 Prediction of MEF2A-DNA interface by rigid body docking: a tool for fast estimation of protein mutational effects on DNA binding. Journal of structural biology 26 16427316
2017 Exercise increases hyper-acetylation of histones on the Cis-element of NRF-1 binding to the Mef2a promoter: Implications on type 2 diabetes. Biochemical and biophysical research communications 25 28263745
2015 Co-activator binding protein PIMT mediates TNF-α induced insulin resistance in skeletal muscle via the transcriptional down-regulation of MEF2A and GLUT4. Scientific reports 25 26468734
2021 Dexmedetomidine and Netrin-1 Combination Therapy Inhibits Endoplasmic Reticulum Stress by Regulating the ERK5/MEF2A Pathway to Attenuate Cerebral Ischemia Injury. Frontiers in neuroscience 24 33584197
2009 Association and functional analyses of MEF2A as a susceptibility gene for premature myocardial infarction and coronary artery disease. Circulation. Cardiovascular genetics 24 20031581
2005 Assessment of MEF2A mutations in myocardial infarction in Japanese patients. Circulation journal : official journal of the Japanese Circulation Society 24 16195615
2021 Decreased MEF2A Expression Regulated by Its Enhancer Methylation Inhibits Autophagy and May Play an Important Role in the Progression of Alzheimer's Disease. Frontiers in neuroscience 22 34220439
2019 MEF2A Regulates the MEG3-DIO3 miRNA Mega Cluster-Targeted PP2A Signaling in Bovine Skeletal Myoblast Differentiation. International journal of molecular sciences 22 31167510
2004 Cell-specific activation of the atrial natriuretic factor promoter by PITX2 and MEF2A. The Journal of biological chemistry 22 15466416
2021 The lncRNA MALAT1 participates in regulating coronary slow flow endothelial dysfunction through the miR-181b-5p-MEF2A-ET-1 axis. Vascular pharmacology 19 33545365
2021 lncRNA MIR155HG Accelerates the Progression of Sepsis via Upregulating MEF2A by Sponging miR-194-5p. DNA and cell biology 19 34030477
2018 MALAT1 promoted cell proliferation and migration via MALAT1/miR-155/MEF2A pathway in hypoxia of cardiac stem cells. Journal of cellular biochemistry 19 30362213
2017 Distinct stages of synapse elimination are induced by burst firing of CA1 neurons and differentially require MEF2A/D. eLife 19 28901289
2022 Histone methyltransferase KMT2D cooperates with MEF2A to promote the stem-like properties of oral squamous cell carcinoma. Cell & bioscience 18 35477537
2007 Relationship of the CAG repeat polymorphism of the MEF2A gene and coronary artery disease in a Chinese population. Clinical chemistry and laboratory medicine 18 17579569
2023 MEF2A suppresses stress responses that trigger DDX41-dependent IFN production. Cell reports 17 37467105
2018 Oxytocin alters the morphology of hypothalamic neurons via the transcription factor myocyte enhancer factor 2A (MEF-2A). Molecular and cellular endocrinology 17 29928931
2017 Inhibition of Mef2a Enhances Neovascularization via Post-transcriptional Regulation of 14q32 MicroRNAs miR-329 and miR-494. Molecular therapy. Nucleic acids 16 28624225
2012 Neurotoxin-induced selective ubiquitination and regulation of MEF2A isoform in neuronal stress response. Journal of neurochemistry 16 22764880
2006 Myocyte enhancing factor-2A in Alzheimer's disease: genetic analysis and association with MEF2A-polymorphisms. Neuroscience letters 16 17112666
2017 AKT2 deficiency induces retardation of myocyte development through EndoG-MEF2A signaling in mouse heart. Biochemical and biophysical research communications 14 28965945
1996 Structures and chromosome locations of the human MEF2A gene and a pseudogene MEF2AP. Cytogenetics and cell genetics 14 8697817
2006 Lack of MEF2A Delta7aa mutation in Irish families with early onset ischaemic heart disease, a family based study. BMC medical genetics 13 16872533
2024 Maternal high-fat diet orchestrates offspring hepatic cholesterol metabolism via MEF2A hypermethylation-mediated CYP7A1 suppression. Cellular & molecular biology letters 12 39695937
2015 Linkage and whole genome sequencing identify a locus on 6q25-26 for formal thought disorder and implicate MEF2A regulation. Schizophrenia research 12 26421691
2012 SENP2 regulates MEF2A de-SUMOylation in an activity dependent manner. Molecular biology reports 12 23224591
2010 Structural changes in exon 11 of MEF2A are not related to sporadic coronary artery disease in Han Chinese population. European journal of clinical investigation 12 20546016
2024 Structural insights into the HDAC4-MEF2A-DNA complex and its implication in long-range transcriptional regulation. Nucleic acids research 11 38281192
2018 MEF2A regulates mGluR-dependent AMPA receptor trafficking independently of Arc/Arg3.1. Scientific reports 11 29588465
2024 MEF2A is a transcription factor for circPVT1 and contributes to the malignancy of acute myeloid leukemia. International journal of oncology 10 39329212
2022 MEF2A Is the Trigger of Resveratrol Exerting Protection on Vascular Endothelial Cell. Frontiers in cardiovascular medicine 10 35047575
2018 The MEF2A and MEF2D function as scaffold proteins that interact with HDAC1 or p300 in SOD3 expression in THP-1 cells. Free radical research 10 29842805
2012 Promoter variant-dependent mRNA expression of the MEF2A in longissimus dorsi muscle in cattle. DNA and cell biology 10 22320864
2020 Detection and functional characterization of a novel MEF2A variation responsible for familial dilated cardiomyopathy. Clinical chemistry and laboratory medicine 9 33554560
2018 MEF2A regulates Calpain 3 expression in L6 myoblasts. Gene 9 29783071
2013 Analysis of MEF2A mutations in a Chinese population with premature coronary artery disease. Genetic testing and molecular biomarkers 9 23461724
2016 Novel 6-bp deletion in MEF2A linked to premature coronary artery disease in a large Chinese family. Molecular medicine reports 8 27221044
2016 Novel regulations of MEF2-A, MEF2-D, and CACNA1S in the functional incompetence of adipose-derived mesenchymal stem cells by induced indoxyl sulfate in chronic kidney disease. Cytotechnology 8 27550174
2014 Association of MEF2A gene polymorphisms with coronary artery disease. Iranian Red Crescent medical journal 8 25389475
2024 The MEF2A/SNHG16/miR-425-5p/NOTCH2 axis induces gemcitabine resistance by inhibiting ferroptosis in the starving bladder tumor microenvironment. Cellular signalling 7 39121977
2024 MEF2A, a gene associated with mitochondrial biogenesis, promotes drug resistance in gastric cancer. Biochimica et biophysica acta. Molecular basis of disease 7 39237047
2022 MiRNA-615-3p Alleviates Oxidative Stress Injury of Human Cardiomyocytes Via PI3K/Akt Signaling by Targeting MEF2A. Anatolian journal of cardiology 7 35552173
2015 Association of MEF2A gene 3'UTR mutations with coronary artery disease. Genetics and molecular research : GMR 7 26400337
2014 The E3 ligase APC/C-Cdh1 regulates MEF2A-dependent transcription by targeting SUMO-specific protease 2 for ubiquitination and degradation. Cell cycle (Georgetown, Tex.) 7 25483061
2013 Mef2A, a homologue of animal Mef2 transcription factors, regulates cell differentiation in Dictyostelium discoideum. BMC developmental biology 7 23577638
1998 MyoD and MEF2A mediate activation and repression of the p75NGFR gene during muscle development. Biochemical and biophysical research communications 7 9588207
2023 Brusatol enhances MEF2A expression to inhibit RCC progression through the Wnt signalling pathway in renal cell carcinoma. Journal of cellular and molecular medicine 6 37859585

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