Affinage

MYH10

Myosin-10 · UniProt P35580

Length
1976 aa
Mass
229.0 kDa
Annotated
2026-06-10
29 papers in source corpus 19 papers cited in narrative 19 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

MYH10 (non-muscle myosin IIB heavy chain) is an actin-based motor that generates and remodels actomyosin contractility to drive cell division, migration, epithelial-mesenchymal transition, and cytoskeletal architecture across developmental and disease contexts (PMID:24825879, PMID:29084269, PMID:33871354). Its motor activity is required not merely to contract but to disassemble actomyosin cross-links: a motor-dead knock-in mutant expressed at wild-type levels acts dominantly by prolonging actin cross-linking, disrupting body wall closure, midline fusion, and outflow tract myocardialization—phenotypes absent in null or hypomorphic animals (PMID:24825879). During mouse preimplantation development MYH10 provides contractility for cytokinesis that is redundant with the dominant paralog MYH9 (PMID:33871354), and the two heavy chains co-regulate one another's expression and act redundantly in tissue-specific contexts (PMID:39503257). The tail domain controls subcellular localization and actin network maintenance; patient tail-domain variants mislocalize the protein and disorganize actin in fibroblasts (PMID:40044823). MYH10 partners directly with MYH9 to recruit the deubiquitinase USP45, which stabilizes Snail to promote EMT, invasion, and chemoresistance (PMID:36929633), and both heavy chains complex with LAMC2 to regulate ER-mitochondria contacts and oxidative stress (PMID:37891404). MYH10 mediates polarized intracellular trafficking and organelle positioning: it is required with MYH9 for apical localization and transport of UMOD and NKCC2 in renal thick ascending limb epithelium (PMID:33001861, PMID:39500539), for GLUT4 translocation and adipogenesis (PMID:35216482), for centriole migration and IFT88 recruitment during ciliogenesis with downstream Hedgehog signaling (PMID:25881509, PMID:35980381), and for sperm flagellar assembly via interaction with CFAP57 (PMID:41466333). It also recruits ESCRT-III and autophagy receptors to drive autophagosome closure and mitophagy (PMID:36849436). MYH10 transcription is directly repressed by GATA1 during megakaryopoiesis through binding sites in the 3' UTR and intron 8, and pathogenic GATA1 variants elevate MYH10 with associated megakaryocyte polyploidization defects (PMID:34060193). Patient variants link MYH10 to neurodevelopmental disorders and to ocular coloboma with ptosis (PMID:35980381, PMID:40044823).

Mechanistic history

Synthesis pass · year-by-year structured walk · 19 steps
  1. 2014 High

    Established that MYH10 motor activity functions to disassemble actomyosin cross-links rather than only to contract, resolving why a motor-dead allele is more damaging than gene loss.

    Evidence Knock-in motor-deficient point mutant mice expressed at wild-type levels, compared to null and hypomorphic models with cardiac/body wall readouts

    PMID:24825879

    Open questions at the time
    • Does not define the molecular partners cross-linked at affected tissues
    • Mechanism of cross-link turnover at the filament level not resolved
  2. 2015 Medium

    Placed MYH10 upstream of centriole apical migration and ciliogenesis, linking it to cortical actin and IFT88 recruitment.

    Evidence siRNA knockdown in RPE1 cells with F-actin, EZRIN, centriole position, and IFT88 imaging

    PMID:25881509

    Open questions at the time
    • Direct biochemical interaction with IFT88 not shown
    • Single cell line, single lab
  3. 2017 High

    Demonstrated a developmental requirement for MYH10 in epicardial EMT and EPDC migration during coronary vessel formation.

    Evidence ENU splice-donor mutant mice with complementation, EMT and migration assays

    PMID:29084269

    Open questions at the time
    • Downstream signaling driving EMT not defined
    • Does not separate motor versus structural contributions
  4. 2018 High

    Extended MYH10 function to mesenchymal ECM remodeling, showing its loss alters Thrombospondin, MMP activity, and matrix deposition in the lung.

    Evidence Conditional mesenchymal KO mice plus cultured mutant fibroblasts with omics and ECM assays

    PMID:30389913

    Open questions at the time
    • Mechanism linking myosin activity to Thrombospondin/MMP regulation unresolved
  5. 2018 Medium

    Linked MYH10 to glioma migration/invasion and placed it upstream of EMT markers and Wnt/β-catenin signaling.

    Evidence siRNA/plasmid silencing in three glioma lines with migration assays, Western blot, qRT-PCR

    PMID:30552850

    Open questions at the time
    • No direct physical interaction with Wnt components shown
    • Pathway placement correlative
  6. 2020 High

    Identified a trafficking role for MYH9/MYH10 in renal epithelium, required for UMOD localization and apical NKCC2 placement.

    Evidence Inducible conditional Myh9/Myh10 KO mice with UMOD/NKCC2 localization and ER stress markers

    PMID:33001861

    Open questions at the time
    • MYH10-specific contribution not separated from MYH9
    • Step in the secretory/trafficking pathway not pinpointed
  7. 2021 High

    Defined the genetic hierarchy of non-muscle myosin II in early embryogenesis, showing MYH10 provides cytokinetic contractility redundant with the dominant MYH9.

    Evidence Single and double maternal-zygotic Myh9/Myh10 mutants with multiscale imaging

    PMID:33871354

    Open questions at the time
    • Molecular basis of the MYH9 dominance over MYH10 not defined
  8. 2021 High

    Showed MYH10 transcription is directly repressed by GATA1 during megakaryopoiesis via intron 8 and 3' UTR sites, connecting MYH10 dysregulation to polyploidization defects.

    Evidence Anti-GATA1 ChIP-seq, luciferase reporters with mutant GATA1, patient platelet measurements

    PMID:34060193

    Open questions at the time
    • Causal contribution of elevated MYH10 to the polyploidization defect is associative
  9. 2022 Medium

    Established a MYH10-GLUT4 trafficking complex required for insulin-responsive GLUT4 translocation and adipogenesis.

    Evidence siRNA KD in preadipocytes, MYH10-GLUT4 Co-IP, PKCζ interaction, co-culture rescue

    PMID:35216482

    Open questions at the time
    • Single lab
    • Direct versus indirect nature of MYH10-GLUT4 binding not fully resolved
  10. 2022 Medium

    Connected MYH10 to ciliary length control and Hedgehog signaling, and showed neurodevelopmental-disorder patient variants act dominant-negatively on cilia.

    Evidence CRISPR KO cells, ciliary length and Hedgehog reporter assays, patient-variant overexpression

    PMID:35980381

    Open questions at the time
    • Mechanism linking MYH10 to ciliary length not defined
    • Single lab
  11. 2023 High

    Defined the MYH10-MYH9-USP45-Snail axis, mechanistically linking the myosin heavy-chain complex to Snail deubiquitination and EMT/chemoresistance.

    Evidence Reciprocal Co-IP, GST pull-down, domain mapping, in vitro and in vivo functional studies in ovarian cancer

    PMID:36929633

    Open questions at the time
    • How the myosin complex recruits USP45 structurally not resolved
  12. 2023 Medium

    Implicated MYH10 in autophagosome closure and mitophagy via ESCRT-III and autophagy receptor recruitment, with knockdown rescuing FTD-associated neurodegeneration.

    Evidence Co-IP with ESCRT-III/autophagy receptors, Drosophila and iPSC-neuron rescue, autophagy induction assays

    PMID:36849436

    Open questions at the time
    • ESCRT-III recruitment mechanism inferred from correlative data
    • Direct binding interface not mapped
  13. 2023 High

    Demonstrated MYH10 can rescue actomyosin disorganization in arrhythmogenic cardiomyopathy from PKP2 deletion, with a dominant-negative mutant phenocopying disease.

    Evidence MYH10 overexpression and dominant-negative expression in mutant cardiomyocytes, 4-HAP pharmacology, cardiac function measures

    PMID:37833253

    Open questions at the time
    • Direct biochemical link between PKP2 and MYH10/actomyosin not established
  14. 2023 Medium

    Identified a LAMC2-MYH9/MYH10 complex regulating ER-mitochondria contacts, ROS, and apoptosis in cancer.

    Evidence Co-IP, LAMC2 overexpression/KD, mitochondrial/ER contact and ROS measures, in vivo tumor assay

    PMID:37891404

    Open questions at the time
    • MYH10-specific contribution not separated from MYH9
    • Single lab
  15. 2024 Low

    Identified an lncRNA (BlncAD1) that binds and stabilizes MYH10 protein against ubiquitin-mediated degradation to promote adipogenesis.

    Evidence RNA pull-down and ubiquitination Western blot in bovine model

    PMID:38661523

    Open questions at the time
    • Molecular link between lncRNA binding and ubiquitination protection not established
    • Single lab, bovine model only
  16. 2025 High

    Established a flagellar role: CFAP57 binds MYH10 and is required for its correct flagellar localization, with downstream IFT88 mislocalization and MMAF when lost.

    Evidence IP-MS, immunofluorescence/immunoEM, CRISPR Cfap57 KO mouse

    PMID:41466333

    Open questions at the time
    • Whether MYH10 motor activity is required for flagellar assembly not tested
    • Single lab
  17. 2025 High

    Confirmed and extended the cell-autonomous renal trafficking role of MYH9/MYH10 in maintaining apical NKCC2 and revealed compensatory transporter upregulation.

    Evidence TAL-specific conditional double KO mouse with segment-specific transporter immunofluorescence and renal function measures

    PMID:39500539

    Open questions at the time
    • MYH10-specific role not isolated from MYH9
    • Mechanism of compensatory NCC/ENaC induction not defined
  18. 2025 Medium

    Showed MYH9b and MYH10 reciprocally regulate one another's expression and act with tissue-specific redundancy in vertebrate development.

    Evidence CRISPR null mutants and double-mutant epistasis in zebrafish with expression analyses

    PMID:39503257

    Open questions at the time
    • Whether regulation is transcriptional or post-transcriptional unresolved
    • Single lab, ortholog study
  19. 2025 Medium

    Demonstrated the tail domain is essential for MYH10 subcellular localization and actin network integrity, linking tail-domain variants to ocular coloboma and ptosis.

    Evidence Patient sequencing, fibroblast localization/actin imaging, zebrafish model

    PMID:40044823

    Open questions at the time
    • Mechanism by which tail variants cause mislocalization not resolved
    • Single lab

Open questions

Synthesis pass · forward-looking unresolved questions
  • How MYH10 selectively engages distinct cargo and organelle systems (GLUT4, UMOD/NKCC2, IFT88, ESCRT-III) versus its bulk contractile role, and the structural basis of its many partner complexes, remains unresolved.
  • No structural model of partner-binding interfaces
  • MYH10-specific versus MYH9-redundant contributions rarely separated
  • Regulation of cargo-specific recruitment unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0003774 cytoskeletal motor activity 3 GO:0008092 cytoskeletal protein binding 3 GO:0140657 ATP-dependent activity 1
Localization
GO:0005856 cytoskeleton 3 GO:0005929 cilium 3 GO:0005886 plasma membrane 2 GO:0005815 microtubule organizing center 1
Pathway
R-HSA-1266738 Developmental Biology 3 R-HSA-9609507 Protein localization 3 R-HSA-1474244 Extracellular matrix organization 1 R-HSA-1640170 Cell Cycle 1 R-HSA-9612973 Autophagy 1
Partners
CFAP57GLUT4IFT88LAMC2MYH9PKCΖUSP45
Complex memberships
ESCRT-III (recruited)MYH9-MYH10 non-muscle myosin II complex

Evidence

Reading pass · 19 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2014 A motor-dead point mutation in NMII-B (MYH10) expressed at wild-type levels causes a dominant-negative effect by prolonging cross-linking of NMII-B to actin filaments, thereby interfering with actomyosin cytoskeletal dynamics. This gain-of-function (not loss-of-function) disrupts ventral body wall closure, midline fusion, and outflow tract myocardialization—phenotypes not seen in null or hypomorphic mice—demonstrating that NMII-B motor activity is required to disassemble actomyosin cross-links and drive myocyte cell-cell adhesion remodeling. Knock-in point mutant mice expressing motor-deficient NMII-B at wild-type levels; comparison with null and hypomorphic mouse phenotypes; histological and genetic analysis of cardiac outflow tract and body wall defects Circulation. Cardiovascular genetics High 24825879
2015 MYH10 is required for centriole migration to the apical plasma membrane at the onset of primary ciliogenesis. Knockdown of MYH10 in RPE1 cells reduces cortical filamentous actin (F-actin) and its binding protein EZRIN, impairs centriole migration, and blocks subsequent cilium assembly. MYH10 also influences centrosomal recruitment of IFT88 (required for intraflagellar transport), with IFT88 levels correlating with centriolar position along the apical-basal axis. siRNA knockdown of MYH10 in RPE1 cells; immunofluorescence of F-actin, EZRIN, centriole position, IFT88 recruitment; quantitative ciliogenesis assays Biochemical and biophysical research communications Medium 25881509
2018 Loss of MYH10 in lung mesenchymal cells results in decreased Thrombospondin expression, increased matrix metalloproteinase (MMP) activity, and disrupted extracellular matrix (ECM) remodeling, causing ECM deposition defects and alveolar simplification. These effects were demonstrated both in Myh10 mutant lungs in vivo and in cultured mutant fibroblasts. Conditional knockout of Myh10 in mesenchymal cells (mouse genetics); omics analyses; cultured mutant fibroblast assays for Thrombospondin expression, MMP activity, and ECM deposition Nature communications High 30389913
2018 MYH10 gene silencing in glioma cell lines reduces cell migration and invasion, accompanied by reduced expression of MTA-1, MMP-2, MMP-9, and vimentin, increased expression of TIMP-2, E-cadherin, and collagen 1, and inhibition of the Wnt/β-catenin pathway (reduced Wnt3a, β-catenin, cyclin D1 levels). siRNA/plasmid-mediated MYH10 silencing in U251, T98G, SHG44 glioma cell lines; scratch and transwell migration/invasion assays; Western blot and qRT-PCR for pathway components Medical science monitor Medium 30552850
2017 NMHC IIB (MYH10) is required for epicardial cell function: a point mutation in the Myh10 splice donor site causes abnormal epicardial cell morphology, reduced capacity for epithelial-mesenchymal transition (EMT), and impaired migration of epicardial-derived cells (EPDCs) into the myocardium, thereby disrupting coronary vessel formation. ENU mutagenesis screen; positional cloning; complementation testing; histological and cell morphology analysis of epicardium; EMT and EPDC migration assays in EHC mutant mice PLoS genetics High 29084269
2020 Conditional knockout of both Myh9 and Myh10 in adult renal tubular epithelium causes intracellular accumulation of the GPI-anchored protein uromodulin (UMOD) and loss of Na+K+2Cl- cotransporter (NKCC2) from the apical membrane of thick ascending limb epithelia. UMOD accumulation coincides with expansion of ER tubules and activation of ER stress/unfolded protein response pathways, establishing that MYH9 and MYH10 are required for localization and intracellular transport of UMOD. Inducible conditional knockout of Myh9 and Myh10 in adult mouse renal tubules; immunofluorescence and fractionation for UMOD and NKCC2 localization; ER stress marker analysis JCI insight High 33001861
2021 Maternal-zygotic loss of Myh10 (NMHC II-B) alone causes only mild preimplantation phenotypes, whereas double maternal-zygotic loss of both Myh9 and Myh10 causes near-complete cytokinesis failure, demonstrating that MYH9 is the dominant non-muscle myosin II during mouse preimplantation development but that MYH10 provides redundant contractility for cytokinesis. Generation of single and double maternal-zygotic mutants of Myh9 and Myh10; multiscale live and fixed imaging; quantification of cytokinesis, compaction, differentiation, and lumen formation eLife High 33871354
2021 GATA1 directly represses MYH10 transcription during megakaryopoiesis via two binding sites in the MYH10 gene (one in the 3' UTR and one in intron 8), as shown by chromatin immunoprecipitation sequencing and luciferase reporter assays. GATA1 pathogenic variants impair intron 8-driven MYH10 transcriptional silencing, leading to elevated MYH10 levels that are associated with a polyploidization defect in megakaryocytes. Anti-GATA1 ChIP-seq revealing binding sites in MYH10 3' UTR and intron 8; luciferase reporter assays with wild-type and mutant GATA1 variants; patient platelet MYH10 protein measurements Journal of thrombosis and haemostasis High 34060193
2022 MYH10 forms a complex with GLUT4 in adipocytes, an interaction regulated by insulin induction. MYH10 depletion in preadipocytes impairs adipogenesis and blocks GLUT4 translocation. PKCζ interacts with MYH10 to modify the localization and interaction of both GLUT4 and MYH10. Restoration of GLUT4 vesicle supply via co-culture rescues the adipogenic defect in MYH10 knockdown cells. siRNA knockdown of MYH10 in preadipocytes; co-immunoprecipitation of MYH10-GLUT4 complex; insulin stimulation assays; PKCζ interaction studies; co-culture rescue experiment International journal of molecular sciences Medium 35216482
2022 MYH10 knockout cells show defects in primary ciliogenesis (reduced ciliary length) and impaired Hedgehog signaling. Overexpression of MYH10 variants found in neurodevelopmental disorder patients exerts a dominant-negative effect on ciliary length, placing MYH10 in the pathway controlling primary cilia length and downstream Hedgehog signal transduction. CRISPR/Cas9 MYH10 knockout cell models; quantitative ciliogenesis assays (ciliary length measurement); Hedgehog signaling reporter assays; overexpression of patient-derived MYH10 variants in cells Genetics in medicine Medium 35980381
2023 MYH10 protein interacts directly with MYH9 (non-muscle myosin IIA) via its functional domain, and this complex recruits the deubiquitinating enzyme USP45, which deubiquitinates Snail to inhibit its proteasomal degradation. This MYH10-MYH9-USP45-Snail axis promotes EMT, migration, invasion, and cisplatin resistance in serous ovarian cancer cells. Co-immunoprecipitation; GST pull-down assays; confocal laser assays; knockdown and overexpression in vitro and in vivo; domain mapping of MYH10-MYH9 interaction Advanced science High 36929633
2023 MYH10 binds and recruits autophagy receptor proteins during autophagosome formation induced by mutant CHMP2B or nutrient starvation. MYH10 also interacts with ESCRT-III subunits to regulate phagophore closure by recruiting ESCRT-III to damaged mitochondria during PRKN/parkin-mediated mitophagy. Partial knockdown of MYH10 rescues neurodegeneration in Drosophila and human iPSC-derived cortical neurons expressing FTD-associated mutant CHMP2B. Co-immunoprecipitation of MYH10 with ESCRT-III and autophagy receptors; Drosophila genetic knockdown rescue assay; human iPSC-derived cortical neuron experiments; autophagy induction assays Autophagy Medium 36849436
2023 In arrhythmogenic cardiomyopathy caused by PKP2 C-terminal domain deletion mutations, PKP2 delocalization disrupts actomyosin network organization. Overexpression of MYH10 rescues actomyosin disorganization in mutant PKP2 cells, while expression of a dominant-negative MYH10 mutant mimics the pathogenic PKP2 CT-deletion phenotype (actin network abnormalities and right ventricle systolic dysfunction). The non-muscle myosin activator 4-hydroxyacetophenone (4-HAP) also restores normal contractility. Computational modeling of PKP2 variants; overexpression of MYH10 in mutant PKP2 cardiomyocytes; dominant-negative MYH10 mutant expression; pharmacological activation with 4-HAP; measurement of actomyosin organization and right ventricle systolic function Nature communications High 37833253
2023 LAMC2 forms protein complexes with both MYH9 and MYH10 to promote mitochondrial aggregation and increased ER-mitochondria interaction at the perinuclear region, attenuating ER stress and reducing reactive oxygen species and apoptosis in cancer cells. Co-immunoprecipitation identifying LAMC2-MYH9 and LAMC2-MYH10 complexes; LAMC2 overexpression/knockdown; measurement of mitochondrial membrane potential, ROS, ER-mitochondria contact sites; in vivo tumor growth assay Cancer gene therapy Medium 37891404
2025 CFAP57 interacts with MYH10 in sperm, as identified by immunoprecipitation-mass spectrometry. MYH10 localizes to the sperm flagella (confirmed by immunofluorescence and immunoelectron microscopy). In CFAP57 mutant sperm, MYH10 is mislocalized to the mid-piece region and absent from the principal and end pieces, causing downstream mislocalization of IFT88 and defective flagellar assembly (MMAF phenotype). Immunoprecipitation-mass spectrometry (IP-MS) identifying MYH10 as CFAP57 binding partner; immunofluorescence and immunoelectron microscopy of MYH10 and IFT88 localization in CFAP57 mutant sperm; CRISPR-Cas9 Cfap57 knockout mouse model Human genomics High 41466333
2024 LncRNA BlncAD1 binds MYH10 protein (identified by RNA pull-down) and protects MYH10 from ubiquitin-mediated degradation, thereby enhancing MYH10 protein stability and promoting bovine adipogenesis. RNA pull-down identifying MYH10 as BlncAD1 binding protein; BlncAD1 knockdown/overexpression with MYH10 ubiquitination measurement by Western blot Journal of agricultural and food chemistry Low 38661523
2025 In zebrafish, myh10 expression requires myh9b: myh9b null mutants show reduced myh10 expression, while myh10 null mutants show reduced myh9b expression, establishing reciprocal transcriptional or post-transcriptional regulatory interactions between myh9b and myh10 during development. Double myh9a/myh10 or myh9b/myh10 mutants display more severe phenotypes than single mutants at earlier time points, indicating tissue-specific genetic redundancy. CRISPR-Cas9 null mutants of myh9a, myh9b, and myh10 in zebrafish; qRT-PCR and protein analyses of expression levels in mutant backgrounds; double mutant epistasis analysis G3 (Bethesda, Md.) Medium 39503257
2025 TAL-specific conditional knockout of Myh9 and Myh10 impairs NKCC2 expression and trafficking in thick ascending limb cells, causing progressive kidney disease. Loss of TAL NM2 function triggers a compensatory mechanism involving sex-specific upregulation of NCC in the distal nephron (males) and ENaC in medullary collecting ducts (both sexes), demonstrating a cell-autonomous role for MYH9/MYH10 in maintaining apical NKCC2 expression. TAL-specific conditional double knockout mouse model; histology; immunofluorescence for NKCC2, ENaC, NCC; ER stress markers; blood urea nitrogen and creatinine measurements; sex-stratified analysis Function (Oxford, England) High 39500539
2025 Tail-domain variants of MYH10 found in patients with ocular coloboma and ptosis cause mislocalization of the MYH10 protein and abnormal actin networks in patient fibroblasts, demonstrating that the tail domain is required for proper subcellular localization and maintenance of normal actin cytoskeletal architecture. Exome/genome sequencing identifying tail-domain variants; immunofluorescence of MYH10 localization and actin networks in patient vs. control fibroblasts; zebrafish morpholino/mutant model for eye and muscle phenotypes European journal of human genetics Medium 40044823

Source papers

Stage 0 corpus · 29 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2018 Myh10 deficiency leads to defective extracellular matrix remodeling and pulmonary disease. Nature communications 43 30389913
2014 A point mutation in Myh10 causes major defects in heart development and body wall closure. Circulation. Cardiovascular genetics 40 24825879
2013 A human de novo mutation in MYH10 phenocopies the loss of function mutation in mice. Rare diseases (Austin, Tex.) 40 25003005
2015 Myosin heavy chain 10 (MYH10) is required for centriole migration during the biogenesis of primary cilia. Biochemical and biophysical research communications 36 25881509
2013 Nonmuscle myosin II-B (myh10) expression analysis during zebrafish embryonic development. Gene expression patterns : GEP 36 23665442
2018 Myosin Heavy Chain 10 (MYH10) Gene Silencing Reduces Cell Migration and Invasion in the Glioma Cell Lines U251, T98G, and SHG44 by Inhibiting the Wnt/β-Catenin Pathway. Medical science monitor : international medical journal of experimental and clinical research 33 30552850
2023 MYH10 Combines with MYH9 to Recruit USP45 by Deubiquitinating Snail and Promotes Serous Ovarian Cancer Carcinogenesis, Progression, and Cisplatin Resistance. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 28 36929633
2017 Non-muscle myosin IIB (Myh10) is required for epicardial function and coronary vessel formation during mammalian development. PLoS genetics 27 29084269
2021 Multiscale analysis of single and double maternal-zygotic Myh9 and Myh10 mutants during mouse preimplantation development. eLife 20 33871354
2022 MYH10 Governs Adipocyte Function and Adipogenesis through Its Interaction with GLUT4. International journal of molecular sciences 19 35216482
2020 Conditional Myh9 and Myh10 inactivation in adult mouse renal epithelium results in progressive kidney disease. JCI insight 18 33001861
2022 Heterozygous variants in MYH10 associated with neurodevelopmental disorders and congenital anomalies with evidence for primary cilia-dependent defects in Hedgehog signaling. Genetics in medicine : official journal of the American College of Medical Genetics 17 35980381
2017 Nonmuscle myosin 2 proteins encoded by Myh9, Myh10, and Myh14 are uniquely distributed in the tubular segments of murine kidney. Physiological reports 17 29208685
2021 Down-regulation of MYH10 driven by chromosome 17p13.1 deletion promotes hepatocellular carcinoma metastasis through activation of the EGFR pathway. Journal of cellular and molecular medicine 14 34738311
2020 MiR-200a Regulates Nasopharyngeal Carcinoma Cell Migration and Invasion by Targeting MYH10. Journal of Cancer 11 32226520
2023 LAMC2 mitigates ER stress by enhancing ER-mitochondria interaction via binding to MYH9 and MYH10. Cancer gene therapy 10 37891404
2023 Non-muscle MYH10/myosin IIB recruits ESCRT-III to participate in autophagosome closure to maintain neuronal homeostasis. Autophagy 7 36849436
2021 GATA1 pathogenic variants disrupt MYH10 silencing during megakaryopoiesis. Journal of thrombosis and haemostasis : JTH 7 34060193
2023 MYH10 activation rescues contractile defects in arrhythmogenic cardiomyopathy (ACM). Nature communications 6 37833253
2024 LncRNA BlncAD1 Modulates Bovine Adipogenesis by Binding to MYH10, PI3K/Akt Signaling Pathway, and miR-27a-5p/CDK6 Axis. Journal of agricultural and food chemistry 4 38661523
2025 myh9b is a critical non-muscle myosin II encoding gene that interacts with myh9a and myh10 during zebrafish development in both compensatory and redundant pathways. G3 (Bethesda, Md.) 3 39503257
2025 Novel MYH10 heterozygous variants associated to a syndrome combining mainly ptosis and ocular coloboma expand the MYH10 related phenotypes. European journal of human genetics : EJHG 3 40044823
2025 Thick Ascending Limb Specific Inactivation of Myh9 and Myh10 Myosin Motors Results in Progressive Kidney Disease and Drives Sex-specific Cellular Adaptation in the Distal Nephron and Collecting Duct. Function (Oxford, England) 2 39500539
2025 Disulfidptosis-related LncRNA signatures in gastric cancer: regulation of MYH10-driven cytoskeletal remodeling and therapeutic implications. Discover oncology 1 40694286
2025 Case Report: CD34-Negative, S100-Positive Spindle Cell Tumor With a MYH10-RET Fusion. Case reports in pathology 1 40873555
2026 CORT silencing impairs migration and invasion: validation of a glycosylation-based risk model (CORT/LPAR5/CEBPA/MYH10/MAGEA11) in osteosarcoma. European journal of medical research 0 41491534
2026 ECE1c promotes glioblastoma invasion via the ROCK2-MYH10 axis and interaction with ACTB. American journal of translational research 0 42007117
2025 Mutations in CFAP57 disrupt the localization of MYH10 and IFT88, leading to flagellogenesis failure in humans and mice. Human genomics 0 41466333
2021 Generation of heterozygous (MRli003-A-1) and homozygous (MRli003-A-2) MYH10 knockout human iPSC lines. Stem cell research 0 34864222

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