Affinage

MYO1C

Unconventional myosin-Ic · UniProt O00159

Length
1063 aa
Mass
121.7 kDa
Annotated
2026-06-10
48 papers in source corpus 31 papers cited in narrative 31 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 8/8 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

MYO1C is an unconventional class I myosin motor that couples ATP hydrolysis and actin binding to the targeted delivery, tethering, and surface display of membrane cargo across diverse cell types (PMID:12490950, PMID:22918957). Its best-characterized role is in insulin-stimulated GLUT4 trafficking, where it operates in a PI3K-independent branch: motor activity is required for GLUT4 vesicle movement, plasma-membrane tethering on submembrane actin, and fusion-dependent surface display (PMID:12490950, PMID:15169906, PMID:22918957), and is licensed by CaMKIIδ phosphorylation at S701, which enhances 14-3-3 binding, reduces calmodulin binding, and elevates ATPase activity (PMID:19046570). RalA serves as a cargo receptor linking the motor to the exocyst, while calmodulin acts as its regulatory light chain (PMID:17765682). Both motor activity (abolished by the ATPase-dead K111A mutant) and actin binding are essential for stimulated glucose uptake in skeletal muscle in vivo (PMID:21127070, PMID:22918957). Beyond GLUT4, MYO1C drives recycling of lipid-raft/GPI-anchored cargo from the perinuclear recycling compartment to the surface (PMID:22328521), delivers slit-diaphragm proteins Neph1 and nephrin in podocytes (PMID:21402783, PMID:23715127, PMID:27044863), targets VEGFR2 to the endothelial surface (PMID:23262137), traffics rhodopsin in photoreceptors (PMID:34073294), stabilizes F-actin at the Golgi to sustain transport-carrier arrival (PMID:30872458), and facilitates autophagosome-lysosome fusion through F-actin remodeling and lipid distribution (PMID:25551774, PMID:31699152). As nuclear myosin 1, MYO1C directly binds the GDF-15 promoter to control TGF-β-responsive transcription in podocytes (PMID:31097328). Its mechanochemistry is tuned by calcium-dependent calmodulin binding to IQ motifs (PMID:17910470), alternative N-terminal splicing that sets actomyosin state occupancy (PMID:28893906), and cryo-EM-resolved features including a unique actin interface, skewed lever-arm trajectory, and force sensing through ATP-binding isomerization rather than ADP release [PMID:bio_10.1101_2025.01.10.632429]. Disease-associated mutations (R156W, V252A, T380M) that disrupt nucleotide handling, actin affinity, or ATPase-motility coupling are linked to hearing loss (PMID:21265502, PMID:20640478).

Mechanistic history

Synthesis pass · year-by-year structured walk · 13 steps
  1. 2002 High

    Established that an unconventional myosin operates in the insulin-to-glucose axis, identifying MYO1C as a motor controlling GLUT4 vesicle movement to the plasma membrane independently of PI3K.

    Evidence GLUT4 vesicle purification, dominant-negative cargo domain, siRNA, and 2-deoxyglucose uptake in adipocytes

    PMID:12490950

    Open questions at the time
    • Did not define the molecular step (transport vs tethering vs fusion) the motor acts on
    • Cargo receptor linking motor to GLUT4 vesicle unknown
  2. 2006 Medium

    Showed MYO1C also functions as a cargo motor in inflammatory signaling, trafficking NEMO to membrane ruffles to promote TNF-α-induced IRS-1 Ser307 phosphorylation.

    Evidence Co-IP, dominant-negative/overexpression constructs, IRS-1 phosphorylation and glucose uptake assays

    PMID:16754954

    Open questions at the time
    • Single lab, no reciprocal structural validation of NEMO binding interface
    • Physiological significance relative to GLUT4 role unclear
  3. 2008 High

    Defined the regulatory switch for the GLUT4 function, showing CaMKIIδ phosphorylation at S701 (not just calmodulin) gates motor activity and is required for insulin-stimulated translocation.

    Evidence In vitro kinase assay, S701A and K111A mutants, CaMKIIδ knockdown, GLUT4 translocation and ATPase assays

    PMID:17765682 PMID:18426911 PMID:19046570

    Open questions at the time
    • How 14-3-3 binding mechanistically alters cargo transport not resolved
    • Distinct Rictor-MYO1C complex function separate from mTORC2 incompletely defined
  4. 2007 High

    Resolved how calcium tunes the motor, showing calmodulin dissociation from IQ1 inhibits actin gliding while raising ATPase, and that CaBP1/CIB1 can compete for the IQ motifs.

    Evidence ATPase, stopped-flow kinetics, actin gliding assays, pull-downs and colocalization

    PMID:17910470 PMID:17994197

    Open questions at the time
    • In vivo relevance of CaBP1/CIB1 substitution for calmodulin not established
    • Link between calcium regulation and specific trafficking events unclear
  5. 2010 High

    Demonstrated physiological requirement in vivo, showing motor activity (ATPase-dead K111A) is needed for both contraction- and insulin-stimulated glucose uptake in skeletal muscle.

    Evidence In vivo electroporation of K111A and WT MYO1C, in vivo glucose uptake, in situ contraction; plus hearing-loss mutant biochemistry

    PMID:20640478 PMID:21127070

    Open questions at the time
    • Whether muscle and adipocyte mechanisms are identical not shown
    • Disease mutations characterized biochemically but not in an in vivo hearing model here
  6. 2012 High

    Broadened MYO1C function beyond GLUT4, establishing it as a motor for perinuclear recycling of raft/GPI cargo, submembrane actin-dependent vesicle tethering, and vectorial G-actin transport to the leading edge.

    Evidence TIRF vesicle tracking, actin-binding-deficient mutant, RNAi, live-cell GPI-cargo and photoactivatable G-actin imaging, VEGFR2 fractionation

    PMID:22328521 PMID:22778278 PMID:22918957 PMID:23262137

    Open questions at the time
    • Cargo-selectivity determinants (raft vs non-raft) not defined
    • Whether G-actin transport and vesicle tethering use the same molecular mode unclear
  7. 2013 High

    Identified MYO1C as the motor delivering slit-diaphragm proteins, directly binding Neph1 and nephrin to drive their membrane targeting and podocyte morphogenesis.

    Evidence Co-IP and direct binding, dominant-negative, RNAi, zebrafish morpholino with mRNA rescue, ultrastructure

    PMID:21402783 PMID:23715127

    Open questions at the time
    • Cargo handoff mechanism at the membrane not defined
    • Structural basis of Neph1/nephrin binding to tail not yet resolved here
  8. 2016 High

    Refined the cargo-binding architecture and motile-component roles, showing an extended S-shaped conformation with Neph1 docking on the C-terminal tail, and structural participation in a SHIP2/filamin A lamellipodial complex governing migration.

    Evidence SAXS, mutagenesis, FRAP, live-cell imaging; co-IP and FAK phosphorylation/migration assays

    PMID:27044863 PMID:27246739

    Open questions at the time
    • Atomic-resolution tail-cargo interface absent
    • Whether SHIP2-complex role is motor-dependent or scaffolding unclear
  9. 2017 High

    Explained isoform diversity by showing the three N-terminally spliced variants set distinct actomyosin state occupancy and that full-length motors undergo a pre-ADP-release isomerization absent in truncated constructs.

    Evidence Recombinant purification of all three isoforms, ATPase kinetics, global modeling, NTR peptide and R21G mutagenesis

    PMID:28893906

    Open questions at the time
    • Cell-type-specific functional consequences of each isoform not mapped
    • Link between NTR-set kinetics and specific cargo trafficking unresolved
  10. 2019 High

    Expanded MYO1C into Golgi integrity, autophagy, and a distinct nuclear transcriptional role, including direct GDF-15 promoter binding controlling TGF-β signaling and fibrosis resistance.

    Evidence siRNA Golgi/transport assays; LC3/LAMP1 colocalization and EM; podocyte-specific knockout mouse and ChIP for GDF-15 promoter

    PMID:30872458 PMID:31097328 PMID:31699152

    Open questions at the time
    • How a single motor partitions between cytoplasmic trafficking and nuclear chromatin roles unclear
    • Mechanism of promoter recognition by a myosin not defined
  11. 2021 High

    Demonstrated tissue-level cargo specificity in vision, showing MYO1C directly binds rhodopsin and is required for its localization and photoreceptor outer-segment maintenance.

    Evidence Myo1c knockout mice, ERG, IHC, EM, direct rhodopsin binding assay

    PMID:34073294

    Open questions at the time
    • Trafficking route of rhodopsin via MYO1C not mapped
    • Relationship to ciliary/connecting cilium transport unaddressed
  12. 2024 Medium

    Revealed regulation of MYO1C stability and small-molecule targeting, showing RNF41-mediated noncanonical K27/K63 ubiquitination stabilizes MYO1C to drive metastasis, and liraglutide binds R93 to stabilize MYO1C and promote wound healing.

    Evidence Co-IP, K27/K63 ubiquitination assays, RNF41 silencing, xenograft metastasis; direct liraglutide binding (R93), Dock5 keratinocyte KO mice

    PMID:39112516 PMID:39159301

    Open questions at the time
    • Single-lab findings, mechanism linking stabilization to actin remodeling indirect
    • How ubiquitin linkage type alters motor function unresolved
  13. 2025 High

    Provided the structural basis of MYO1C's distinctive mechanics and extended its roles, with cryo-EM defining a unique actin interface, skewed lever arm and ATP-binding force-sensing, plus chiral F-actin flow, ERα chromatin clustering, and shear-regulated Jagged1 trafficking.

    Evidence Cryo-EM of actin-MYO1C ±ADP (preprint); Drosophila genetics and in vitro motility (preprint); ChIP-seq/condensate imaging (preprint); APEX2 proteomics and co-IP with KO/KD

    PMID:41321631 PMID:bio_10.1101_2025.01.10.632429 PMID:bio_10.1101_2025.01.29.635522 PMID:bio_10.1101_2025.05.06.648335

    Open questions at the time
    • Several findings are preprints awaiting peer review
    • Whether nuclear ERα clustering role has transcriptional consequence is unresolved given unchanged output

Open questions

Synthesis pass · forward-looking unresolved questions
  • How a single motor is partitioned and regulated to select among its many cargoes (GLUT4, raft cargo, slit-diaphragm proteins, VEGFR2, rhodopsin, Jagged1) and between cytoplasmic trafficking and nuclear chromatin functions remains unresolved.
  • No unified model of cargo-selection determinants
  • Mechanism of nuclear targeting and promoter recognition undefined
  • Isoform-to-function mapping incomplete

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0008092 cytoskeletal protein binding 5 GO:0140657 ATP-dependent activity 5 GO:0003774 cytoskeletal motor activity 4 GO:0140110 transcription regulator activity 2 GO:0003677 DNA binding 1
Localization
GO:0005886 plasma membrane 5 GO:0005856 cytoskeleton 4 GO:0005634 nucleus 2 GO:0005764 lysosome 2 GO:0005794 Golgi apparatus 1
Pathway
R-HSA-5653656 Vesicle-mediated transport 6 R-HSA-162582 Signal Transduction 4 R-HSA-9609507 Protein localization 3 R-HSA-74160 Gene expression (Transcription) 2 R-HSA-9612973 Autophagy 2
Partners
JAGGED1NEMONEPH1NEPHRINRALARHODOPSINRICTORRNF41
Complex memberships
SHIP2-filamin A lamellipodial complex

Evidence

Reading pass · 31 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2002 Myo1c is present in GLUT4-containing vesicles purified from adipocytes and functions in a PI(3)K-independent insulin signaling pathway to control movement of intracellular GLUT4-containing vesicles to the plasma membrane; dominant-negative Myo1c cargo domain inhibits insulin-stimulated GLUT4 translocation, and siRNA knockdown of Myo1c inhibits insulin-stimulated 2-deoxyglucose uptake. GLUT4 vesicle purification, co-localization microscopy, dominant-negative expression, siRNA knockdown, 2-deoxyglucose uptake assay Nature High 12490950
2004 Myo1c motor activity is required for membrane fusion of GLUT4-containing vesicles at the plasma membrane; enhanced Myo1c expression drives membrane ruffling and overrides the PI 3-kinase inhibitor block on membrane fusion, restoring GLUT4 display on the cell surface. PI 3-kinase inhibitor treatment (LY294002), Myo1c overexpression, ultrafast fluorescence microscopy of GLUT4-containing vesicle mobilization Molecular and cellular biology High 15169906
2007 RalA interacts with Myo1c and functions as a cargo receptor for the Myo1c motor during insulin-stimulated GLUT4 trafficking; this interaction is modulated by calmodulin, which acts as the light chain for Myo1c. RalA also signals to the exocyst complex for GLUT4 targeting to the plasma membrane. Co-immunoprecipitation, dominant-negative mutants, siRNA knockdown, glucose transport assay Developmental cell Medium 17765682
2007 Calcium regulates calmodulin binding to Myo1c IQ motifs: calcium increases actin-activated ATPase activity but completely inhibits actin gliding; calmodulin bound to IQ1 (adjacent to motor domain) dissociates most rapidly in calcium (rate 60 s⁻¹), limited by a slow calcium-induced conformational change (3 s⁻¹), and is responsible for regulation of Myo1c ATPase and motile activity. Actin gliding assays, ATPase measurements, fluorescence spectroscopy, stopped-flow kinetics with fluorescently labeled calmodulin mutant Biochemistry High 17910470
2007 CaBP1 and CIB1 bind to the Myo1c regulatory domain IQ motifs and compete with calmodulin for binding; both proteins colocalize with endogenous Myo1c in cells and may specify subcellular localization of Myo1c. Pull-down experiments, fluorescence microscopy co-localization, in vitro binding competition assays Journal of muscle research and cell motility Medium 17994197
2008 CaMKIIδ phosphorylates Myo1c at S701 in response to insulin, enhancing 14-3-3 binding and reducing calmodulin binding; CaMKII phosphorylation increases Myo1c ATPase activity in vitro; expression of S701A or ATPase-dead K111A Myo1c fails to rescue GLUT4 translocation after siRNA knockdown, demonstrating that insulin-regulated GLUT4 trafficking requires CaMKII-dependent phosphorylation and motor activity of Myo1c. In vitro kinase assay with recombinant CaMKII, siRNA knockdown of CaMKIIδ, site-directed mutagenesis (S701A, K111A), GLUT4 translocation assay, ATPase assay Cell metabolism High 19046570
2008 Rictor forms a biochemically distinct complex with Myo1c (separate from mTORC2) in adipocytes; both Rictor and Myo1c are required for paxillin Y118 phosphorylation and cortical actin remodeling (membrane ruffling), and Myo1c-induced membrane ruffling is compromised by Rictor knockdown. Co-immunoprecipitation, RNAi knockdown, paxillin phosphorylation assay, membrane ruffling imaging Molecular and cellular biology Medium 18426911
2010 Myo1c motor activity is required for both contraction-stimulated and insulin-stimulated glucose uptake in mouse skeletal muscle in vivo; expression of ATPase-dead K111A-Myo1c decreases both stimulated glucose uptake, while wild-type Myo1c increases it, without altering GLUT4 expression or upstream signaling. In vivo electroporation of skeletal muscle, ATPase-dead mutant (K111A), in vivo glucose uptake assay, in situ contraction The Journal of biological chemistry High 21127070
2011 Myo1c directly interacts with Neph1 and nephrin in an actin-dependent manner, and this interaction is required for targeting these slit diaphragm proteins to the podocyte cell membrane; dominant-negative Myo1c and Myo1c depletion reduce membrane localization of Neph1 and nephrin, and impair cell migration and tight junction formation. Co-immunoprecipitation, in vitro binding assay, dominant-negative expression, RNAi knockdown, transepithelial resistance assay, wound migration assay Molecular and cellular biology High 21402783
2011 A disease-associated Myo1c R156W mutation (associated with hearing loss) has a lower duty ratio than wild-type; it reduces ATPase activity >4-fold likely by decreasing phosphate release rate, and is less force-sensitive than wild-type in frictional loading assays, while actin gliding rate is unaffected at high myosin density but reduced at low surface densities. Recombinant protein expression, transient kinetic analyses, steady-state ATPase assay, in vitro motility assay, frictional loading assay Biochemistry High 21265502
2012 Myo1c binding to submembrane actin filaments is required for insulin-induced tethering of GLUT4 vesicles at the plasma membrane in muscle cells; actin-binding-deficient Myo1c mutant abolishes vesicle immobilization and increases vesicle velocity in the TIRF zone, while Myo1c overexpression promotes vesicle tethering and GLUT4 surface delivery. TIRF microscopy, GLUT4 vesicle tracking, actin-binding-deficient mutant expression, RNAi knockdown, GLUT4 externalization assay Molecular biology of the cell High 22918957
2012 Myo1c is the first motor protein identified to drive formation of recycling tubules from the perinuclear recycling compartment, specifically mediating recycling of lipid-raft-associated GPI-linked cargo proteins (but not transferrin receptor) to the cell surface; Myo1c depletion traps GPI-linked raft markers in the perinuclear compartment and impairs cell spreading, migration, and Salmonella invasion. RNAi knockdown, dominant-negative overexpression, fluorescence microscopy of recycling tubules and GPI-cargo trafficking, cell spreading and migration assays, Salmonella invasion assay Journal of cell science High 22328521
2012 Myo1c tail domain interacts with G-actin (monomeric actin), and Myo1c motor domain activity is required for vectorial transport of G-actin to the leading edge of migrating endothelial cells; Myo1c knockdown reduces G-actin delivery to the leading edge and impairs cell motility. Mass spectrometry identification, photoactivatable non-polymerizable actin tracking in live cells, Myo1c knockdown, microinjection of Myo1c The Journal of cell biology High 22778278
2006 Myo1c interacts with NEMO/IKK-γ and acts as a motor to traffic NEMO to membrane ruffles; enhanced Myo1c expression increases the NEMO-IRS-1 interaction required for TNF-α-induced Ser307 phosphorylation of IRS-1, while dominant-negative Myo1c cargo domain inhibits this interaction and blocks IRS-1 phosphorylation. Co-immunoprecipitation, dominant-negative and overexpression constructs, IRS-1 phosphorylation assay, glucose uptake assay The Journal of cell biology Medium 16754954
2010 Myo1c mutations associated with hearing loss (R156W, V252A, T380M) cause defects in nucleotide and/or actin interactions: R156W disrupts switch 1 movement affecting nucleotide binding and calcium regulation; V252A reduces actin affinity; T380M uncouples ATPase from motility. Transient kinetic analyses, steady-state ATPase assay, in vitro motility assay, homology modeling with truncated Myo1c construct Cellular and molecular life sciences High 20640478
2014 Loss of functional MYO1C causes accumulation of autophagic structures due to a block in autophagosome-lysosome fusion, while endocytic EGFR degradation remains unaffected; this is attributable to abnormal cholesterol/lipid distribution in autophagosomes and lysosomes caused by MYO1C loss. RNAi knockdown, dominant-negative expression, transmission electron microscopy, fluorescence microscopy of autophagosome markers, EGFR degradation assay, cholesterol staining Autophagy Medium 25551774
2012 Myo1c is required for VEGFR2 delivery to the cell surface in endothelial cells; VEGF stimulation recruits VEGFR2 to caveolin-1- and Myo1c-enriched membrane fractions, and Myo1c depletion reroutes VEGFR2 to lysosomes, reducing VEGFR2 phosphorylation (Y1175), ERK1/2 and c-Src activation, and cell proliferation/migration. siRNA knockdown, wild-type vs. mutant Myo1c rescue, subcellular density gradient fractionation, surface VEGFR2 measurement, VEGFR2 phosphorylation assay American journal of physiology. Heart and circulatory physiology Medium 23262137
2013 Myo1c interacts directly with nephrin and neph1 and is required for podocyte morphogenesis in zebrafish; morpholino knockdown of Myo1c causes loss of slit diaphragm and abnormal podocyte morphology, rescued by co-injection with mouse Myo1c mRNA. Antisense morpholino knockdown in zebrafish, mRNA rescue, immunofluorescence, in situ hybridization, transmission electron microscopy of glomerulus Kidney international Medium 23715127
2016 Myo1c is a structural component of a SHIP2-containing protein complex (with filamin A) at lamellipodia; Myo1c depletion impairs SHIP2 localization at lamellipodia and ruffles, reduces FAK Tyr397 phosphorylation, focal adhesion length, and PI(4,5)P2 levels, and strongly reduces cell migration. Co-immunoprecipitation, siRNA knockdown, immunofluorescence localization, FAK phosphorylation assay, cell migration assay Biochemical and biophysical research communications Medium 27246739
2016 Structural analysis by small angle X-ray scattering of full-length Myo1c reveals an extended S-shaped conformation; Neph1 attaches to the C-terminal tail of Myo1c without inducing a significant conformational change; a critical point mutation in Neph1 abolishes the Myo1c interaction in vitro and in live cells; FRAP analysis confirmed Myo1c-dependent vesicular movement and turnover of Neph1 at the membrane. Small angle X-ray scattering (SAXS), site-directed mutagenesis, in vitro binding assay, live-cell imaging, FRAP Molecular and cellular biology High 27044863
2017 The three alternatively spliced MYO1C isoforms (MYO1CC, MYO1C16, MYO1C35), differing only in N-terminal regions (NTRs), have distinct ATPase kinetics: MYO1CC favors the actomyosin closed state, MYO1C16 equally populates open and closed states, and MYO1C35 favors the open state; full-length constructs undergo an isomerization before ADP release not seen in truncated constructs; NTR35 residue Arg-21 interaction with post-relay helix Glu-469 affects power stroke mechanics. Recombinant protein purification from HEK cells, ATPase kinetic assays, global numerical simulation, homology modeling, NTR peptide addition experiments, R21G mutagenesis The Journal of biological chemistry High 28893906
2019 MYO1C stabilizes F-actin at Golgi-associated actin dots and is required for Golgi complex integrity; MYO1C depletion causes Golgi fragmentation and decompaction, loss of cellular F-actin, and delays arrival of incoming transport carriers from both anterograde and retrograde routes. siRNA depletion, fluorescence microscopy of Golgi morphology and actin structures, transport carrier arrival assay Journal of cell science Medium 30872458
2019 Nuclear Myo1c (rather than cytoplasmic) controls TGF-β signaling in podocytes by directly binding to the GDF-15 promoter and regulating transcription of TGF-β-responsive genes; podocyte-specific Myo1c knockout mice are resistant to fibrotic injury and show blunted canonical and non-canonical TGF-β signaling. Podocyte-specific knockout mouse model, chromatin immunoprecipitation (ChIP) for GDF-15 promoter binding, differential gene expression analysis, fibrosis models (Adriamycin, nephrotoxic serum, UUO) Kidney international High 31097328
2019 MYO1C interacts with F-actin and associates with LC3 (autophagosome marker) and LAMP1 (lysosome marker); cepharanthine downregulates MYO1C, blocking MYO1C and F-actin colocalization with LC3/LAMP1 and preventing autophagosome-lysosome fusion; overexpression of MYO1C restores this colocalization. Co-immunoprecipitation, immunofluorescence colocalization, siRNA knockdown, MYO1C overexpression, Western blot for autophagy markers, transmission electron microscopy Journal of experimental & clinical cancer research Medium 31699152
2021 MYO1C localizes to photoreceptor inner and outer segments and directly interacts with rhodopsin; loss of MYO1C in knockout mice causes rhodopsin mislocalization to rod inner segments and cell bodies, progressive shortening of outer segments, and progressive loss of photoreceptor function. Myo1c knockout mice, electroretinogram, immunohistochemistry, direct binding assay (rhodopsin-MYO1C), histology and electron microscopy Cells High 34073294
2024 RNF41 induces K27- and K63-linked noncanonical polyubiquitination of MYO1C to enhance its stability, promoting actin remodeling and prostate cancer bone metastasis; RNF41 silencing or targeting MYO1C stability suppresses bone metastasis in xenograft models. Co-immunoprecipitation, ubiquitination assays (K27/K63-linkage), RNF41 silencing, MYO1C stability assay, in vitro and in vivo metastasis models Oncogene Medium 39112516
2024 Liraglutide directly binds to Myo1c at arginine 93, stabilizing Myo1c and enhancing its interaction with Dock5 (dedicator of cytokinesis 5) by targeting the Dock5 promoter, thereby promoting keratinocyte proliferation, migration, and adhesion to accelerate diabetic wound healing; these effects are abrogated in keratinocyte-specific Dock5 knockout mice. Direct binding assay (liraglutide-Myo1c), site identification (R93), Dock5 keratinocyte-specific knockout mice, diabetic mouse wound models, cell proliferation/migration/adhesion assays Advanced science Medium 39159301
2025 Cryo-EM structures of actin-bound myo1c with and without ADP reveal a unique actin interface that reorients the motor domain relative to other myosins, a skewed lever arm swing trajectory (explaining leftward circular actin gliding), and unique nucleotide-dependent behavior of the N-terminal extension that underlies force-sensing via ATP binding isomerization rather than ADP release. Cryo-EM structure determination of actin-myo1c complexes (±ADP), integration with crystallographic data, full-length atomic modeling bioRxivpreprint High bio_10.1101_2025.01.10.632429
2025 Nuclear myosin 1 (NM1/Myo1c) acts as a positive regulator of ERα clustering on enhancers and promotes condensate formation on chromatin; NM1 depletion leads to genome-wide reduction in ERα occupancy and condensates, though transcriptional output remains largely unaffected despite disrupted clustering. ChIP-seq, ERα occupancy mapping, NM1 depletion, condensate imaging, estrogen-regulated gene expression analysis bioRxivpreprint Medium bio_10.1101_2025.01.29.635522
2025 Myo1c (Drosophila ortholog) directs counterclockwise circumferential F-actin flows in macrophages and dictates sinistral cell chirality; in a modified in vitro motility assay, Myo1c induces random (non-chiral) F-actin flow, contrasting with Myo1D which induces clockwise chiral F-actin rings. Drosophila genetics, live-cell F-actin flow imaging in macrophages, modified in vitro motility assay with near-physiological actin concentrations bioRxivpreprint Medium bio_10.1101_2025.05.06.648335
2025 Myo1c interacts with the Notch ligand Jagged1 under static conditions (confirmed by co-immunoprecipitation), and this interaction is reduced by shear stress; Myo1c knockout inhibits Jagged1 polarization downstream of shear and Myo1c knockdown reduces membrane levels of Jagged1 under static conditions. Proximity labeling (APEX2) followed by proteomics, co-immunoprecipitation, Myo1c knockout and knockdown, Jagged1 localization assay under shear stress iScience Medium 41321631

Source papers

Stage 0 corpus · 48 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2002 Glucose transporter recycling in response to insulin is facilitated by myosin Myo1c. Nature 219 12490950
2007 Activation of RalA is required for insulin-stimulated Glut4 trafficking to the plasma membrane via the exocyst and the motor protein Myo1c. Developmental cell 172 17765682
2004 Unconventional myosin Myo1c promotes membrane fusion in a regulated exocytic pathway. Molecular and cellular biology 141 15169906
2008 CaMKII-mediated phosphorylation of the myosin motor Myo1c is required for insulin-stimulated GLUT4 translocation in adipocytes. Cell metabolism 101 19046570
2012 Myo1c regulates lipid raft recycling to control cell spreading, migration and Salmonella invasion. Journal of cell science 77 22328521
2011 Motor protein Myo1c is a podocyte protein that facilitates the transport of slit diaphragm protein Neph1 to the podocyte membrane. Molecular and cellular biology 77 21402783
2014 Loss of functional MYO1C/myosin 1c, a motor protein involved in lipid raft trafficking, disrupts autophagosome-lysosome fusion. Autophagy 66 25551774
2012 Myo1c binding to submembrane actin mediates insulin-induced tethering of GLUT4 vesicles. Molecular biology of the cell 63 22918957
2006 Myosin motor Myo1c and its receptor NEMO/IKK-gamma promote TNF-alpha-induced serine307 phosphorylation of IRS-1. The Journal of cell biology 57 16754954
2008 A Rictor-Myo1c complex participates in dynamic cortical actin events in 3T3-L1 adipocytes. Molecular and cellular biology 55 18426911
2012 The myosin motor Myo1c is required for VEGFR2 delivery to the cell surface and for angiogenic signaling. American journal of physiology. Heart and circulatory physiology 54 23262137
2010 Myo1c regulates glucose uptake in mouse skeletal muscle. The Journal of biological chemistry 49 21127070
2012 Myo1c facilitates G-actin transport to the leading edge of migrating endothelial cells. The Journal of cell biology 47 22778278
2023 m6A-modified circRNA MYO1C participates in the tumor immune surveillance of pancreatic ductal adenocarcinoma through m6A/PD-L1 manner. Cell death & disease 43 36781839
2016 miR-137 plays tumor suppressor roles in gastric cancer cell lines by targeting KLF12 and MYO1C. Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine 42 27468717
2022 SMOC2 promotes aggressive behavior of fibroblast-like synoviocytes in rheumatoid arthritis through transcriptional and post-transcriptional regulating MYO1C. Cell death & disease 37 36513634
2011 A hearing loss-associated myo1c mutation (R156W) decreases the myosin duty ratio and force sensitivity. Biochemistry 37 21265502
2007 Calcium regulation of calmodulin binding to and dissociation from the myo1c regulatory domain. Biochemistry 35 17910470
2019 MYO1C stabilizes actin and facilitates the arrival of transport carriers at the Golgi complex. Journal of cell science 30 30872458
2008 Are MYO1C and MYO1F associated with hearing loss? Biochimica et biophysica acta 29 19027848
2019 The motor protein Myo1c regulates transforming growth factor-β-signaling and fibrosis in podocytes. Kidney international 26 31097328
2007 CIB1 and CaBP1 bind to the myo1c regulatory domain. Journal of muscle research and cell motility 25 17994197
2015 Analysis of an independent tumor suppressor locus telomeric to Tp53 suggested Inpp5k and Myo1c as novel tumor suppressor gene candidates in this region. BMC genetics 23 26170120
2019 Downregulation of MYO1C mediated by cepharanthine inhibits autophagosome-lysosome fusion through blockade of the F-actin network. Journal of experimental & clinical cancer research : CR 21 31699152
2024 Liraglutide Promotes Diabetic Wound Healing via Myo1c/Dock5. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 19 39159301
2014 Molecular motor MYO1C, acetyltransferase KAT6B and osteogenetic transcription factor RUNX2 expression in human masseter muscle contributes to development of malocclusion. Archives of oral biology 19 24698832
2005 Expression of the unconventional myosin Myo1c alters sodium transport in M1 collecting duct cells. American journal of physiology. Cell physiology 18 15716323
2013 Myo1c is an unconventional myosin required for zebrafish glomerular development. Kidney international 16 23715127
2016 Lowered Expression of Tumor Suppressor Candidate MYO1C Stimulates Cell Proliferation, Suppresses Cell Adhesion and Activates AKT. PloS one 15 27716847
2010 Myo1c mutations associated with hearing loss cause defects in the interaction with nucleotide and actin. Cellular and molecular life sciences : CMLS 15 20640478
2016 The SHIP2 interactor Myo1c is required for cell migration in 1321 N1 glioblastoma cells. Biochemical and biophysical research communications 14 27246739
2021 Loss of Motor Protein MYO1C Causes Rhodopsin Mislocalization and Results in Impaired Visual Function. Cells 13 34073294
2017 N-terminal splicing extensions of the human MYO1C gene fine-tune the kinetics of the three full-length myosin IC isoforms. The Journal of biological chemistry 13 28893906
2018 Monodisperse magnetic poly(glycidyl methacrylate) microspheres for isolation of autoantibodies with affinity for the 46 kDa form of unconventional Myo1C present in autoimmune patients. Mikrochimica acta 11 29687337
2013 Alternative splicing of Myb-related genes MYR1 and MYR2 may modulate activities through changes in dimerization, localization, or protein folding. Plant signaling & behavior 11 24309816
2020 Glioma-derived endothelial cells promote glioma cells migration via extracellular vesicles-mediated transfer of MYO1C. Biochemical and biophysical research communications 10 32081419
2016 Structural Analysis of the Myo1c and Neph1 Complex Provides Insight into the Intracellular Movement of Neph1. Molecular and cellular biology 9 27044863
2012 Molecular roles of Myo1c function in lipid raft exocytosis. Communicative & integrative biology 9 23739769
2024 A noncanonical E3 ubiquitin ligase RNF41-mediated MYO1C stability promotes prostate cancer metastasis by inducing actin remodeling. Oncogene 7 39112516
2017 Magnetic poly(2-hydroxyethyl methacrylate) microspheres for affinity purification of monospecific anti-p46 kDa/Myo1C antibodies for early diagnosis of multiple sclerosis patients. Bioscience reports 7 28351895
2023 RAB31 in glioma-derived endothelial cells promotes glioma cell invasion via extracellular vesicle-mediated enrichment of MYO1C. FEBS open bio 3 37953466
2024 Recessive variants in MYO1C as a potential novel cause of proteinuric kidney disease. Pediatric nephrology (Berlin, Germany) 1 38904753
2026 MYO1C is a urinary extracellular vesicle biomarker and mediator of podocyte injury in diabetic nephropathy. JCI insight 0 41569692
2026 VPS4A activates glycolytic metabolism via MYO1C to promote radioresistance in ESCC. European journal of medical research 0 41654990
2025 Chlamydia trachomatis highjacks host MYO1C for actin cage recruitment at the bacterial inclusion. Microbiological research 0 41242206
2025 Mechanosensitive interactions between Jag1 and Myo1c control Jag1 trafficking in endothelial cells. iScience 0 41321631
2024 Recessive variants in MYO1C as a potential novel cause of proteinuric kidney disease. Research square 0 38659911
2023 In Silico Prediction of MYO1C-Rhodopsin Interactions and Its Significance in Protein Localization and Visual Function. Advances in experimental medicine and biology 0 37440078

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