Affinage

SMYD1

Histone-lysine N-methyltransferase SMYD1 · UniProt Q8NB12

Length
490 aa
Mass
56.6 kDa
Annotated
2026-06-10
46 papers in source corpus 23 papers cited in narrative 23 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

SMYD1 is a striated muscle-specific lysine methyltransferase that couples sarcomere assembly to the transcriptional and epigenetic control of cardiac and skeletal muscle gene programs (PMID:16477022, PMID:21852424). Its catalytic core is built on a 'split' SET domain with an associated MYND zinc-finger protein-interaction module and a C-terminal domain, an architecture that imposes autoinhibition and uses the MYND domain primarily for partner binding (PMID:20943667). SMYD1 operates in two compartments. At the sarcomeric M-line it binds the N-terminal region of myosin heavy chain and mono-methylates MyHC at lysine 35; this modification is required for correct incorporation into thick filaments and protects MyHC from ubiquitin-proteasome degradation, and this sarcomere-assembly function depends on myosin binding rather than histone methyltransferase activity (PMID:21852424, PMID:40972758). In the nucleus SMYD1 trimethylates H3K4 to activate target genes and partners with skNAC, its major cardiac binding partner, to execute a transcriptional program governing ventricular development (PMID:21071677, PMID:26688546). Through H3K4me3-dependent activation of PGC-1α and Perm1 it controls cardiac mitochondrial energetics, while its association with ASH2L drives gene activation (e.g., Isl1) and its recruitment of HDAC and CHD4/NuRD complexes represses other loci to restrain pathological cardiomyocyte growth (PMID:30061404, PMID:32574189, PMID:33869215, PMID:38619323, PMID:27663768). SMYD1 expression is driven by SRF and myogenin, its activity feeds back through methylation of TRB3, and its stability and nuclear/cytoplasmic distribution are governed by PML-dependent SUMOylation (PMID:19783823, PMID:25803368, PMID:33241844).

Mechanistic history

Synthesis pass · year-by-year structured walk · 16 steps
  1. 2006 High

    Established that SMYD1 is a histone methyltransferase essential for myofibril organization and sarcomere assembly, defining its core developmental role in muscle.

    Evidence Morpholino knockdown of both splice isoforms in zebrafish embryos with HMT assay

    PMID:16477022

    Open questions at the time
    • Did not resolve whether the assembly defect required catalytic activity or a separate function
    • Mammalian relevance not yet tested
    • Histone substrate specificity not mapped
  2. 2009 High

    Identified the upstream transcriptional control of SMYD1, placing it downstream of the SRF/myogenin myogenic program.

    Evidence EMSA, ChIP, promoter deletion, SRF-null rescue, and C2C12 overexpression

    PMID:19783823

    Open questions at the time
    • Did not address downstream SMYD1 targets
    • Relative contribution of SRF vs myogenin in different muscle types unresolved
  3. 2010 High

    Solved the structural basis of SMYD1 activity, revealing a split-SET wrench architecture and an autoinhibition mechanism, and assigned the MYND domain a protein-interaction role.

    Evidence X-ray crystallography at 2.3 Å with sinefungin plus structural mutagenesis and activity assays

    PMID:20943667

    Open questions at the time
    • No substrate-bound structure
    • Trigger that relieves autoinhibition in vivo unknown
  4. 2010 High

    Defined skNAC as SMYD1's major cardiac binding partner and placed both in a common transcriptional pathway controlling ventricular development.

    Evidence Co-IP plus skNAC conditional knockout mouse and genetic epistasis (Irx4)

    PMID:21071677

    Open questions at the time
    • Mechanism by which the skNAC–SMYD1 complex selects target promoters unresolved
    • Why skNAC loss is less severe than SMYD1 loss not explained
  5. 2011 High

    Separated SMYD1's two functions, showing sarcomere assembly requires myosin binding while histone methyltransferase activity is dispensable for sarcomerogenesis.

    Evidence Zebrafish flatline positional cloning, SMYD1–myosin Co-IP, and domain-specific rescue with two mutant constructs

    PMID:21852424

    Open questions at the time
    • The myosin residue and modification involved were not yet identified
    • How M-line localization is achieved unresolved
  6. 2014 Medium

    Showed SUMOylation governs the nuclear/cytoplasmic balance of the skNAC–SMYD1 complex, linking post-translational modification to its dual-compartment function.

    Evidence Co-IP, sumoylation assay, Nse2/Mms21 knockdown, and localization with sarcomere readout in muscle cells

    PMID:25002400

    Open questions at the time
    • Single lab; SUMO sites on SMYD1 not definitively mapped here
    • Physiological signal triggering translocation unclear
  7. 2015 Medium

    Extended SMYD1 function to mammalian myoblast differentiation and identified TRB3 as a non-histone substrate forming a transcriptional feedback loop.

    Evidence Myf5-Cre and Nkx2.5-Cre conditional knockouts, in vitro TRB3 methylation assay, and transcriptomics

    PMID:25803368 PMID:26688546

    Open questions at the time
    • TRB3 methylation site not defined
    • Direct vs indirect contribution of TRB3 methylation to phenotype unresolved
    • Single in vitro methylation demonstration
  8. 2015 Medium

    Demonstrated that the skNAC–SMYD1 complex shapes H3K4 di-/trimethylation and acetylation at promoters controlling metabolism, inflammation, and migration.

    Evidence siRNA knockdown, microarray, and ChIP in differentiating C2C12 cells

    PMID:26162853

    Open questions at the time
    • Direct vs indirect promoter occupancy not fully separated
    • Single lab
  9. 2016 Medium

    Revealed SMYD1 as a chromatin-binding repressor restraining adult cardiomyocyte hypertrophy, establishing a protective role in the adult heart.

    Evidence Inducible adult cardiac conditional KO with quantitative proteomics and cardiac phenotyping

    PMID:27663768

    Open questions at the time
    • Repressive partner complexes not identified in this study
    • Direct target genes of repression not pinpointed
  10. 2016 Medium

    Showed fiber-type-selective requirement for SMYD1 in mature skeletal muscle and a role beyond the heart in endothelial SRF-driven angiogenesis.

    Evidence Myf6-Cre conditional KO with histopathology/EM; endothelial Co-IP, GST pull-down, EMSA, and tube formation assays

    PMID:26799706 PMID:26935107

    Open questions at the time
    • Basis of fast-twitch preference unexplained
    • SMYD1–SRF complex not validated in vivo for angiogenesis
  11. 2018 High

    Linked SMYD1 catalytic activity to cardiac energetics through H3K4me3-dependent activation of PGC-1α.

    Evidence Adult cardiac KO, H3K4me3 ChIP-seq, luciferase, Seahorse respirometry, and PGC-1α rescue

    PMID:29499397 PMID:30061404

    Open questions at the time
    • Whether PGC-1α regulation is direct or via cofactor recruitment beyond H3K4me3 unresolved
  12. 2021 High

    Defined SMYD1 as a bifunctional regulator using ASH2L for H3K4me3 activation and HDAC/CHD4-NuRD complexes for repression of distinct cardiac gene sets.

    Evidence ChIP-PCR, Co-IP, luciferase, TSA treatment (Isl1/ANF); Co-IP-MS, RNA-seq, ATAC-seq in Smyd1- and Chd4-null hearts

    PMID:33869215 PMID:38619323

    Open questions at the time
    • How SMYD1 switches between activating and repressive complexes at given loci unresolved
    • Stoichiometry within NuRD not defined
  13. 2021 Medium

    Established PML-dependent SUMOylation as a stability switch targeting SMYD1 for proteasomal degradation under cytokine signaling, and showed methyltransferase-dependent pro-inflammatory IL-6 induction.

    Evidence Endothelial transfection of PML/SUMO/UBC9 constructs, cycloheximide chase, MG132; catalytically inactive mutant with IL-6 ChIP and reporter assays

    PMID:33241844 PMID:34944023

    Open questions at the time
    • Endothelial findings not yet reconciled with muscle-specific role
    • In vivo relevance of cytokine-driven degradation untested
  14. 2023 Medium

    Identified additional regulatory inputs and outputs: MSI2 destabilizes Smyd1 mRNA, and SMYD1 H3K4me2 represses P2RX7 to influence myoblast survival.

    Evidence AAV9 Msi2 overexpression with RNA-IP and rescue; adenoviral Smyd1 modulation with P2rx7 ChIP in C2C12

    PMID:37385529 PMID:37923788

    Open questions at the time
    • Single-lab studies
    • Whether MSI2 and P2RX7 axes operate in the same physiological context unknown
  15. 2024 Medium

    Connected SMYD1 to cardiac progenitor fate via H3K4me3 activation of GSK3β, controlling β-catenin/ERK signaling balance during differentiation.

    Evidence CRISPR SMYD1-KO hESCs with inducible re-expression, ChIP, dual-luciferase, and inhibitor intervention

    PMID:39380045

    Open questions at the time
    • Single lab
    • Whether GSK3β is the dominant effector among many SMYD1 targets unresolved
  16. 2025 High

    Resolved the long-standing question of how SMYD1 drives sarcomere assembly by identifying mono-methylation of myosin heavy chain at K35 as the protective modification preventing UPS degradation.

    Evidence SMYD1–MyHC Co-IP, in vitro methylation assay, Smyd1-null zebrafish, MG132 rescue, K35 mutagenesis, and human iPSC-CM validation

    PMID:40972758

    Open questions at the time
    • Reader/effector that recognizes K35me1 during thick filament assembly unknown
    • Whether other sarcomeric substrates are methylated unresolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • How SMYD1 dynamically partitions between its nuclear epigenetic role and its cytoplasmic sarcomeric substrate methylation, and how it switches between activating (ASH2L) and repressive (HDAC/NuRD) complexes at specific loci, remains unresolved.
  • No unified model linking SUMO-regulated localization to substrate choice
  • Locus-level determinants of activation vs repression undefined
  • Full non-histone substrate repertoire beyond MyHC and TRB3 unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0016740 transferase activity 4 GO:0042393 histone binding 3 GO:0008092 cytoskeletal protein binding 2 GO:0140096 catalytic activity, acting on a protein 2 GO:0140110 transcription regulator activity 2
Localization
GO:0005634 nucleus 3 GO:0005856 cytoskeleton 3 GO:0005829 cytosol 1
Pathway
R-HSA-1266738 Developmental Biology 3 R-HSA-397014 Muscle contraction 3 R-HSA-4839726 Chromatin organization 3 R-HSA-74160 Gene expression (Transcription) 3 R-HSA-1430728 Metabolism 2
Partners
ASH2LCHD4MYH (MYOSIN HEAVY CHAIN)PMLSKNACSRFTRB3
Complex memberships
NuRD (CHD4)skNAC-SMYD1 complex

Evidence

Reading pass · 23 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2006 SmyD1a and SmyD1b, generated by alternative splicing of the SmyD1 gene, possess histone methyltransferase activity and are required for myofibril organization and sarcomere assembly during myofiber maturation in skeletal and cardiac muscles of zebrafish embryos; morpholino knockdown of both isoforms disrupts myofibril organization and results in immature myofibers with centrally located nuclei. Morpholino antisense knockdown in zebrafish embryos; histone methyltransferase assay; whole-mount in situ hybridization Proceedings of the National Academy of Sciences of the United States of America High 16477022
2010 Crystal structure of full-length SmyD1 in complex with the cofactor analog sinefungin at 2.3 Å resolution reveals a wrench-shaped architecture with a 'split' SET domain, MYND zinc finger, and C-terminal domain (CTD); structural and functional analysis indicates SmyD1 is regulated by an autoinhibition mechanism, with the spacious target lysine-access channel and CTD domain both negatively contributing to its methyltransferase activity; the MYND domain serves primarily as a protein-interaction module. X-ray crystallography (2.3 Å); functional methyltransferase activity assays; structural mutagenesis analysis The Journal of biological chemistry High 20943667
2011 SMYD1 localizes to both the sarcomeric M-line (where it physically associates with myosin) and the nucleus in heart and fast-twitch skeletal muscle cells; the SMYD1–myosin interaction is essential for thick filament assembly, as ectopic expression of myosin-binding-deficient SMYD1 fails to rescue sarcomere assembly in smyd1 mutant (flatline) zebrafish, whereas histone methyltransferase-deficient SMYD1 does rescue, indicating that histone methyltransferase activity is dispensable for sarcomerogenesis. Positional cloning of zebrafish flatline mutant; co-immunoprecipitation (SMYD1–myosin); rescue experiments with methyltransferase-deficient and myosin-binding-deficient SMYD1 constructs; immunofluorescence/subcellular fractionation Journal of cell science High 21852424
2010 The muscle-specific transcription factor skNAC is the major binding partner for Smyd1 in the developing heart; genetic deletion of skNAC in mice phenocopies (but is less severe than) Smyd1 mutants, with ventricular hypoplasia and decreased cardiomyocyte proliferation, and skNAC deletion reduces expression of Irx4, a ventricle-specific transcription factor that is also down-regulated when Smyd1 is absent, placing skNAC and Smyd1 in the same transcriptional pathway. Co-immunoprecipitation; conditional knockout mouse (skNAC−/−); genetic epistasis analysis; cardiac phenotyping Proceedings of the National Academy of Sciences of the United States of America High 21071677
2009 SMYD1 expression in heart and skeletal muscle is directly regulated by serum response factor (SRF) binding to CArG sites and by myogenin binding to E-box elements in the SMYD1 promoter; SRF deletion in mouse embryonic hearts dramatically reduces Smyd1 mRNA, and forced expression of SMYD1 accelerates myoblast differentiation and myotube formation in C2C12 cells. EMSA; ChIP assay; promoter deletion analysis; SRF-null ES cell rescue; C2C12 overexpression Nucleic acids research High 19783823
2015 Smyd1 directly methylates the stress-response factor Tribbles3/TRB3, and when methylated TRB3 acts as a co-repressor of Smyd1-mediated transcription, constituting a feedback mechanism; conditional ablation of Smyd1 in cardiomyocytes leads to impaired proliferation and dysregulation of ER stress transcripts, with mid-gestational lethality also associated with impaired oxidative stress defense. Conditional knockout (Nkx2.5-Cre); in vitro methylation assay of TRB3 by Smyd1; transcriptomic analysis; proliferation assays PloS one Medium 25803368
2014 Smyd1 contains a sumoylation motif and is sumoylated in muscle cells; the E3 SUMO ligase Nse2/Mms21 interacts with skNAC and is required for sumoylation of Smyd1; knockdown of Nse2 blocks nuclear-to-cytoplasmic translocation of the skNAC–Smyd1 complex, retains it in PML-like nuclear bodies, and disrupts sarcomerogenesis, establishing sumoylation as a regulator of the nuclear/cytosolic balance of Smyd1 function. Co-immunoprecipitation; siRNA knockdown; sumoylation assay; immunofluorescence (subcellular localization); electron microscopy Journal of cell science Medium 25002400
2018 Cardiac-specific deletion of Smyd1 in adult mice leads to a significant reduction in H3K4me3 enrichment at the PGC-1α locus (a mark of gene activation), reduced PGC-1α expression, and impaired mitochondrial energetics; overexpression of Smyd1 increases mitochondrial respiration capacity in an effect abolished by PGC-1α knockdown, demonstrating that Smyd1 regulates cardiac energetics via H3K4 trimethylation at the PGC-1α promoter. Cardiac-specific conditional KO mouse; ChIP-seq (H3K4me3); siRNA knockdown; luciferase reporter assay; Seahorse XF respirometry; PGC-1α rescue experiment Proceedings of the National Academy of Sciences of the United States of America High 30061404
2015 Smyd1 methylates histone H3K4 and its loss-of-function specifically impairs myoblast differentiation (second wave of myogenesis) in mammals; conditional knockout of Smyd1 at the myoblast stage (Myf5-Cre) results in fewer myofibers and decreased expression of muscle-specific genes, with Smyd1 shuttling from nucleus to cytosol during myoblast differentiation. Conditional knockout mouse (Myf5-Cre); immunofluorescence subcellular localization; gene expression analysis; myofiber counting Developmental biology Medium 26688546
2016 Smyd1 acts as a chromatin-binding repressor to restrict adult cardiomyocyte growth; inducible loss of Smyd1 in adult mouse heart leads to cellular hypertrophy, organ remodeling, and heart failure, while activation of Smyd1 prevents pathological cell growth; Smyd1 modulates expression of gene isoforms associated with cardiac pathology. Inducible loss-of-function conditional KO in adult mice; quantitative proteomics; gene expression analysis; cardiac phenotyping American journal of physiology. Heart and circulatory physiology Medium 27663768
2016 Ablation of SMYD1 specifically in post-differentiation skeletal myocytes (Myf6-Cre) causes a non-degenerative myopathy characterized by myofiber hypotrophy, predominance of oxidative fibers, reduced triad numbers, regional myofibrillar disorganization, and centralized nuclei; the phenotype preferentially affects fast-twitch muscle despite equivalent SMYD1 expression across fiber types. Conditional KO mouse (Myf6-Cre); histopathology; electron microscopy; fiber-type analysis; gene expression profiling Disease models & mechanisms Medium 26935107
2015 The skNAC–Smyd1 complex regulates transcription by affecting histone H3K4 di- and trimethylation and potentially histone acetylation at target gene promoters involved in inflammation, cellular metabolism, and cell migration, as demonstrated by ChIP analysis in differentiating C2C12 cells. siRNA knockdown; cDNA microarray; Western blot; ELISA; ChIP analysis Experimental cell research Medium 26162853
2021 Smyd1 activates transcription of Isl1 by interacting with ASH2L and trimethylating H3K4 at the Isl1 promoter; Smyd1 also associates with HDAC to repress ANF expression, demonstrating that Smyd1 regulates early heart development through both positive (H3K4me3-mediated) and negative (HDAC-mediated) gene regulation. ChIP-PCR; co-immunoprecipitation; pGL3 luciferase reporter assay; TSA deacetylase inhibitor treatment Frontiers in cell and developmental biology Medium 33869215
2021 CHD4 (catalytic core of the NuRD complex) physically interacts with SMYD1 in cardiomyocytes; both proteins co-repress a common set of genes involved in glycolysis, response to hypoxia, and angiogenesis, as determined by combined transcriptomic and chromatin accessibility studies in Smyd1- and Chd4-null embryonic mouse hearts. Quantitative proteomics (Co-IP-MS); transcriptomics (RNA-seq); ATAC-seq (chromatin accessibility); null mouse embryo hearts Development (Cambridge, England) High 38619323
2016 SMYD1 physically associates with SRF (Serum Response Factor) and enhances SRF DNA-binding activity; knockdown of SMYD1 in endothelial cells impairs EC migration and tube formation, indicating a role for SMYD1 in angiogenesis via the SMYD1–SRF complex. Co-IP; GST pull-down; EMSA; siRNA knockdown; tube formation and migration assays PloS one Medium 26799706
2020 Smyd1 directly binds the Perm1 gene promoter (shown by ChIP) and activates its transcription; Perm1 in turn activates ERRα and its mitochondrial targets (e.g., Ndufv1/Complex I), and Perm1 overexpression rescues hypertrophic stress-induced loss of ERRα and mitochondrial function, placing Perm1 downstream of Smyd1 in a cardiac energetics regulatory network. RNA-seq; ChIP; luciferase reporter assay; siRNA knockdown; Seahorse XF respirometry; adenoviral overexpression PloS one Medium 32574189
2021 Smyd1 is expressed in endothelial cells and contributes to LPS-triggered IL-6 expression via two mechanisms: activation of NF-κB signaling and H3K4me3 trimethylation at the IL-6 promoter; catalytically inactive Smyd1 mutant fails to drive this response, confirming dependence on methyltransferase activity. Transfection with WT and catalytically inactive Smyd1 mutant; siRNA; ChIP-RT-qPCR; IL-6 promoter luciferase reporter; ELISA Cells Medium 34944023
2021 In endothelial cells, Smyd1 localizes predominantly to PML nuclear bodies and is SUMOylated in a PML-dependent manner; SUMOylation addresses Smyd1 for proteasomal degradation; cytokines (TNF-α, IFN-γ) modulate Smyd1 protein stability through this PML-dependent SUMOylation mechanism, constituting a negative feedback loop. Transfection of Smyd1, PML, SUMO1, active/mutant SuPr1, UBC9 constructs; cycloheximide chase; proteasome inhibitor (MG132); siRNA knockdown; computational modeling; immunofluorescence The Biochemical journal Medium 33241844
2018 siRNA knockdown of Smyd1 in C2C12 cells prevents myofibrillogenesis and sarcomere formation as determined by immunofluorescence and electron microscopy, resulting in a disorganized array of myofilaments beneath the plasma membrane, consistent with a direct role for Smyd1 in cytoplasmic sarcomere assembly. siRNA knockdown; immunofluorescence; electron microscopy Micron (Oxford, England : 1993) Medium 29499397
2024 SMYD1 activates the GSK3β promoter through H3K4me3 modification; loss of SMYD1 in pluripotent stem cells reduces GSK3β transcription (confirmed by ChIP and dual-luciferase assay), leading to enhanced β-catenin/ERK signaling and excess cardiac progenitor cell proliferation at the expense of cardiomyocyte differentiation. CRISPR-Cas9 SMYD1 KO hESC; doxycycline-inducible SMYD1 re-expression; ChIP; dual-luciferase reporter; small molecule inhibitor intervention; RNA-seq Stem cell research & therapy Medium 39380045
2025 SMYD1 physically associates with the N-terminal region of multiple myosin heavy chain (MyHC) isoforms and specifically catalyzes mono-methylation of MyHC at lysine 35 (K35); methylated MyHC is correctly incorporated into sarcomeres, whereas unmethylated MyHC in Smyd1-deficient zebrafish is degraded via the ubiquitin-proteasome system (UPS); UPS inhibition with MG132 restores MyHC protein levels but not proper thick filament assembly due to absence of K35 methylation, indicating K35 mono-methylation is required for sarcomere assembly and homeostasis. Co-immunoprecipitation (SMYD1–MyHC); in vitro methylation assay; Smyd1-deficient zebrafish; MG132 UPS inhibition; human iPSC-derived cardiomyocytes; site-directed mutagenesis (K35) Journal of molecular and cellular cardiology High 40972758
2023 MSI2 (Musashi-2) RNA-binding protein destabilizes Smyd1 mRNA, leading to reduced Smyd1 protein; Cluh and Smyd1 are identified as direct downstream targets of Msi2, and overexpression of Smyd1 inhibits Msi2-induced cardiac malfunction and mitochondrial dysfunction. AAV9-mediated Msi2 overexpression in mice; global proteomics; RNA-IP; Smyd1 overexpression rescue; Seahorse respirometry; transmission electron microscopy Basic research in cardiology Medium 37923788
2023 Smyd1-mediated H3K4me2 modification at the P2rx7 promoter represses P2RX7 expression in myoblasts; CSE exposure reduces H3K4me2 and increases P2RX7-mediated apoptosis/pyroptosis; Smyd1 overexpression partially rescues CSE-impaired myoblast differentiation via the Smyd1–H3K4me2–P2RX7 axis. Adenoviral Smyd1 overexpression/knockdown in C2C12; ChIP (H3K4me2 at P2rx7 promoter); flow cytometry; Western blot Toxicology letters Medium 37385529

Source papers

Stage 0 corpus · 46 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2006 SmyD1, a histone methyltransferase, is required for myofibril organization and muscle contraction in zebrafish embryos. Proceedings of the National Academy of Sciences of the United States of America 178 16477022
2011 The myosin-interacting protein SMYD1 is essential for sarcomere organization. Journal of cell science 90 21852424
2018 Histone methyltransferase Smyd1 regulates mitochondrial energetics in the heart. Proceedings of the National Academy of Sciences of the United States of America 88 30061404
2010 skNAC, a Smyd1-interacting transcription factor, is involved in cardiac development and skeletal muscle growth and regeneration. Proceedings of the National Academy of Sciences of the United States of America 74 21071677
2010 Crystal structure of cardiac-specific histone methyltransferase SmyD1 reveals unusual active site architecture. The Journal of biological chemistry 72 20943667
2016 The chromatin-binding protein Smyd1 restricts adult mammalian heart growth. American journal of physiology. Heart and circulatory physiology 54 27663768
2015 Smyd1 facilitates heart development by antagonizing oxidative and ER stress responses. PloS one 52 25803368
2009 SMYD1, the myogenic activator, is a direct target of serum response factor and myogenin. Nucleic acids research 52 19783823
2015 SMYD1 and G6PD modulation are critical events for miR-206-mediated differentiation of rhabdomyosarcoma. Cell cycle (Georgetown, Tex.) 40 25644430
2016 Mouse myofibers lacking the SMYD1 methyltransferase are susceptible to atrophy, internalization of nuclei and myofibrillar disarray. Disease models & mechanisms 34 26935107
2015 Defective myogenesis in the absence of the muscle-specific lysine methyltransferase SMYD1. Developmental biology 34 26688546
2020 Perm1 regulates cardiac energetics as a downstream target of the histone methyltransferase Smyd1. PloS one 29 32574189
2020 Role of Muscle-Specific Histone Methyltransferase (Smyd1) in Exercise-Induced Cardioprotection against Pathological Remodeling after Myocardial Infarction. International journal of molecular sciences 27 32977624
2014 The E3 SUMO ligase Nse2 regulates sumoylation and nuclear-to-cytoplasmic translocation of skNAC-Smyd1 in myogenesis. Journal of cell science 25 25002400
2019 A de novo mutation of SMYD1 (p.F272L) is responsible for hypertrophic cardiomyopathy in a Chinese patient. Clinical chemistry and laboratory medicine 23 30205637
2006 Muscle-specific expression of the smyd1 gene is controlled by its 5.3-kb promoter and 5'-flanking sequence in zebrafish embryos. Developmental dynamics : an official publication of the American Association of Anatomists 23 17048253
2021 Smyd1 Orchestrates Early Heart Development Through Positive and Negative Gene Regulation. Frontiers in cell and developmental biology 21 33869215
2015 skNAC and Smyd1 in transcriptional control. Experimental cell research 21 26162853
2008 smyd1 and smyd2 are expressed in muscle tissue in Xenopus laevis. Cytotechnology 20 19003161
2017 Proteomic and microRNA Transcriptome Analysis revealed the microRNA-SmyD1 network regulation in Skeletal Muscle Fibers performance of Chinese perch. Scientific reports 17 29184116
2024 CHD4 and SMYD1 repress common transcriptional programs in the developing heart. Development (Cambridge, England) 13 38619323
2021 The Methyltransferase Smyd1 Mediates LPS-Triggered Up-Regulation of IL-6 in Endothelial Cells. Cells 13 34944023
2016 SMYD1, an SRF-Interacting Partner, Is Involved in Angiogenesis. PloS one 12 26799706
2023 Musashi-2 causes cardiac hypertrophy and heart failure by inducing mitochondrial dysfunction through destabilizing Cluh and Smyd1 mRNA. Basic research in cardiology 11 37923788
2021 Smyd1 is essential for myosin expression and sarcomere organization in craniofacial, extraocular, and cardiac muscles. Journal of genetics and genomics = Yi chuan xue bao 11 33958316
2018 Domain swapping and SMYD1 interactions with the PWWP domain of human hepatoma-derived growth factor. Scientific reports 11 29321480
2021 Stability of Smyd1 in endothelial cells is controlled by PML-dependent SUMOylation upon cytokine stimulation. The Biochemical journal 10 33241844
2019 Modulation of chromatin remodeling proteins SMYD1 and SMARCD1 promotes contractile function of human pluripotent stem cell-derived ventricular cardiomyocyte in 3D-engineered cardiac tissues. Scientific reports 10 31097748
2018 siRNA-mediated inhibition of skNAC and Smyd1 expression disrupts myofibril organization: Immunofluorescence and electron microscopy study in C2C12 cells. Micron (Oxford, England : 1993) 10 29499397
2018 SMYD1 is the underlying gene for the AnWj-negative blood group phenotype. European journal of haematology 10 29956848
2015 Master redox regulator Trx1 upregulates SMYD1 & modulates lysine methylation. Biochimica et biophysica acta 10 26410624
2023 Resistance training up-regulates Smyd1 expression and inhibits oxidative stress and endoplasmic reticulum stress in the heart of middle-aged mice. Free radical biology & medicine 9 38042222
2020 The SMYD1 and skNAC transcription factors contribute to neurodegenerative diseases. Brain, behavior, & immunity - health 9 34589886
2019 Heart Transplantation from Biventricular Support in Infant with Novel SMYD1 Mutation. Pediatric cardiology 9 31278431
2018 Loss of SMYD1 Results in Perinatal Lethality via Selective Defects within Myotonic Muscle Descendants. Diseases (Basel, Switzerland) 9 30577454
2024 The histone methyltransferase SMYD1 is induced by thermogenic stimuli in adipose tissue. Epigenomics 6 38440863
2021 SMYD1 alleviates septic myocardial injury by inhibiting endoplasmic reticulum stress. Bioscience, biotechnology, and biochemistry 6 34601561
2024 SMYD1 modulates the proliferation of multipotent cardiac progenitor cells derived from human pluripotent stem cells during myocardial differentiation through GSK3β/β-catenin&ERK signaling. Stem cell research & therapy 5 39380045
2023 Down-regulated Smyd1 participated in the inhibition of myoblast differentiation induced by cigarette smoke extract. Toxicology letters 4 37385529
2023 Identification of Two Homozygous Variants in MYBPC3 and SMYD1 Genes Associated with Severe Infantile Cardiomyopathy. Genes 2 36980931
2025 SMYD1-mediated mono-methylation of lysine K35 of sarcomeric myosin heavy chain (MHC) regulates sarcomere assembly and homeostasis in zebrafish and human iPSC-derived cardiomyocytes. Journal of molecular and cellular cardiology 1 40972758
2023 Smyd1: Implications for novel approaches in rhabdomyosarcoma therapy. Experimental cell research 1 38097153
2026 Histone methyltransferase SMYD1: playing a crucial role in disease progression. Frontiers in molecular biosciences 0 41737831
2026 Sirt1 Promotes Cardiomyocyte Differentiation Through the XR_951230.1/miR-3663-3p/SMYD1 Axis. Genes 0 41898814
2025 Cinobufagin induced myocardial cell toxicity in H9c2 cells via inhibiting histone methyltransferase SMYD1 expression. Toxicology mechanisms and methods 0 40536054
2024 Binding Behavior of Human Hepatoma-Derived Growth Factor on SMYD1. The journal of physical chemistry. B 0 39091133

Missed literature

Know a paper Affinage missed for SMYD1? Flag it for the maintainers and the community.

No submissions yet.