Affinage

MYO1E

Unconventional myosin-Ie · UniProt Q12965

Round 2 corrected
Length
1108 aa
Mass
127.1 kDa
Annotated
2026-04-29
97 papers in source corpus 15 papers cited in narrative 15 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

MYO1E is a long-tailed class I unconventional myosin that couples actin dynamics to membrane remodeling, functioning principally in clathrin-mediated endocytosis, podocyte maintenance, and immune-cell migration. Its motor domain exhibits fast ADP release and low K(ATPase), kinetic properties suited to rapid translocation through dense actin networks rather than sustained tension bearing (PMID:11940582); its C-terminal tail binds anionic phospholipids (PtdIns(4,5)P2, phosphatidylserine) through electrostatic interactions and recruits to clathrin-coated structures via its SH3 domain, which also mediates interactions with dynamin and synaptojanin-1 to drive vesicle internalization (PMID:17257598, PMID:20860408). In glomerular podocytes, MYO1E is required for slit-diaphragm protein trafficking and filtration-barrier integrity, and homozygous loss-of-function mutations cause childhood-onset steroid-resistant focal segmental glomerulosclerosis (PMID:21756023, PMID:36316095). In macrophages, MYO1E localizes to podosome bases via its TH2 domain and regulates podosome dynamics, TLR4-dependent intracellular transport, MHC class II surface expression, and cell migration (PMID:25263281).

Mechanistic history

Synthesis pass · year-by-year structured walk · 10 steps
  1. 1994 Medium

    Identification of MYO1E as a broadly expressed class I myosin gene in human epithelial and immune cells established the molecular existence of a new myosin-I family member, raising questions about its specific cellular function.

    Evidence PCR amplification, hybridization screening, and RNase protection assay across human cell lines

    PMID:8022818

    Open questions at the time
    • No functional or localization data; expression breadth established but cellular role unknown
  2. 2002 High

    In vitro kinetic characterization revealed that Myo1e has a unique ATPase cycle—fast ADP release, low K(ATPase), and weak actin affinity in ATP—distinguishing it from other vertebrate myosin-I isoforms and predicting it functions as a rapid translocator in dense actin meshworks rather than a tension sensor.

    Evidence Stopped-flow fluorescence and steady-state ATPase assays with truncated motor-IQ construct

    PMID:11940582

    Open questions at the time
    • Kinetics measured on truncated construct; full-length regulation unknown
    • No cellular context for the rapid-sliding model
  3. 2007 High

    Discovery that Myo1e interacts with dynamin and synaptojanin-1 through its SH3 domain and co-localizes with clathrin puncta answered the question of which membrane-trafficking pathway Myo1e participates in, establishing its role in clathrin-mediated endocytosis.

    Evidence Co-immunoprecipitation, GST pulldown, co-localization microscopy, dominant-negative tail-domain inhibition of transferrin uptake

    PMID:17257598

    Open questions at the time
    • Mechanism by which motor activity contributes to vesicle scission not resolved
    • Contributions of SH3-domain partners individually not dissected
  4. 2010 High

    Quantitative lipid-binding studies showed that the Myo1e tail associates with PtdIns(4,5)P2 and phosphatidylserine via nonspecific electrostatic interactions rather than stereospecific PH-domain recognition, explaining how the motor is targeted to the anionic inner leaflet of the plasma membrane and clathrin-coated vesicles.

    Evidence Sedimentation and stopped-flow assays with large unilamellar vesicles, PH-domain mutagenesis, in vivo imaging

    PMID:20860408

    Open questions at the time
    • How lipid binding is coordinated with actin engagement during endocytosis is unknown
    • Contribution of individual lipid species in vivo not determined
  5. 2011 High

    Identification of homozygous MYO1E mutations (A159P, Y695X) as the cause of childhood-onset steroid-resistant FSGS in independent families established MYO1E as essential for glomerular podocyte function and filtration-barrier integrity, linking the motor's actin-membrane coupling activity to human kidney disease.

    Evidence Genome-wide linkage and exome sequencing in two pedigrees, immunohistochemistry of podocytes, electron microscopy, mutant localization studies in transfected cells

    PMID:21697813 PMID:21756023

    Open questions at the time
    • Precise cargo transported by Myo1e in podocytes not identified
    • Whether heterozygous carriers have subclinical phenotypes is unknown
  6. 2013 High

    Zebrafish morpholino knockdown and podocyte siRNA studies demonstrated that Myo1e loss causes proteinuria-like phenotypes in vivo and disrupts actin organization, migration, adhesion, and endocytosis in cultured podocytes, confirming the functional requirement across species.

    Evidence Zebrafish morpholino knockdown (pericardial edema, pronephric cysts); siRNA in podocyte cell line with migration, endocytosis, adhesion assays

    PMID:23977349

    Open questions at the time
    • Morpholino off-target effects not fully excluded
    • Downstream signaling pathways in podocytes not mapped
  7. 2014 High

    Myo1e was shown to have a non-redundant immune function: in macrophages and dendritic cells it regulates TLR4-triggered spreading, CCL2 secretion, and MHC class II surface expression, with Myo1e-knockout cells exhibiting impaired CD4+ T-cell stimulation, extending its role to intracellular trafficking in innate immunity.

    Evidence Myo1e-KO bone marrow-derived macrophages and DCs; flow cytometry, ELISA, antigen-specific T-cell proliferation assay

    PMID:25263281

    Open questions at the time
    • Specific vesicular compartments regulated by Myo1e in antigen processing not identified
    • Whether Myo1e acts through endocytic or exocytic pathway for MHC-II maintenance unclear
  8. 2016 Medium

    Myo1e was placed upstream of the FAK–PI3K–RAC-1 signaling axis in B cells, where its loss reduces integrin and F-actin at membrane protrusions and impairs homing to lymph nodes, revealing a signaling-linked mechanism for Myo1e's role in immune-cell adhesion and migration.

    Evidence Intravital microscopy, phospho-immunoblotting for FAK/AKT/RAC-1, in vitro adhesion assays with Myo1e-KO B cells

    PMID:31756023

    Open questions at the time
    • Direct physical interaction between Myo1e and FAK not demonstrated
    • Single-lab finding; independent replication lacking
    • Whether this signaling axis operates in non-immune cells unknown
  9. 2022 High

    Mechanistic dissection of FSGS-associated motor-domain mutations showed that T119I disrupts targeting to junctions and clathrin-coated vesicles while D388H abolishes ATPase activity but retains localization, demonstrating that both membrane targeting and catalytic motor function are independently required for Myo1e's podocyte role.

    Evidence Adenoviral rescue in Myo1e-KO podocytes, FRAP, baculovirus-expressed truncated constructs for in vitro ATPase and actin-gliding assays, endocytosis assays

    PMID:36316095

    Open questions at the time
    • Structural basis for T119I mislocalization not resolved
    • Whether mutant proteins exert dominant-negative effects in heterozygous state unknown
  10. 2025 Medium

    Live-cell imaging in genome-edited hiPSCs revealed that Myo1e is recruited to clathrin-mediated endocytosis sites that stall under elevated membrane tension, where it promotes Arp2/3-dependent branched actin assembly to rescue internalization—providing a mechanosensory model for Myo1e's endocytic function.

    Evidence Super-resolution live-cell imaging of genome-edited hiPSCs, Myo1e-KO, membrane tension manipulation, Arp2/3 lifetime quantification (preprint)

    PMID:bio_10.1101_2025.11.12.688091

    Open questions at the time
    • Preprint; not yet peer-reviewed
    • Physical mechanism by which Myo1e senses tension not defined
    • Whether tension-dependent recruitment occurs in podocytes or immune cells not tested

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include the identity of specific cargoes transported by Myo1e in podocytes, the structural basis for its tension-responsive recruitment to endocytic sites, and the extent to which its immune-cell and podocyte functions share common molecular mechanisms versus cell-type-specific adaptations.
  • No high-resolution structure of full-length Myo1e
  • Direct cargo identification in podocytes lacking
  • Whether Myo1e's podosome and CME functions are mechanistically linked is unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0008092 cytoskeletal protein binding 3 GO:0003774 cytoskeletal motor activity 2 GO:0140657 ATP-dependent activity 2 GO:0008289 lipid binding 1
Localization
GO:0031410 cytoplasmic vesicle 4 GO:0005886 plasma membrane 3 GO:0005856 cytoskeleton 2
Pathway
R-HSA-5653656 Vesicle-mediated transport 5 R-HSA-1643685 Disease 4 R-HSA-168256 Immune System 2
Partners
ARPC2CALM1DNM1SYNJ1

Evidence

Reading pass · 15 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1994 MYO1E (myosin 1E) was identified as one of at least 11 unconventional myosin genes expressed in human epithelial cell lines and peripheral blood leukocytes, establishing it as a member of the myosin I family with overlapping expression across vertebrate cell types. PCR amplification, hybridization screening, RNase protection assay, immunoblot Proceedings of the National Academy of Sciences of the United States of America Medium 8022818
2002 Myo1e (human myosin-IC/myosin 1E) exhibits a distinct kinetic mechanism: its actin-activated ATPase has a low K(ATPase) (~1 µM) but weak actin affinity in the presence of ATP, with phosphate released while myo1e is dissociated from actin. ADP release from actomyo1e is >10-fold faster than other vertebrate myosin-I isoforms, suggesting myo1e is tuned for rapid sliding rather than tension maintenance, and functions best in regions of high concentrations of cross-linked actin filaments. In vitro kinetic ATPase analysis, stopped-flow fluorescence, equilibrium binding assays using truncated myo1e motor + single IQ motif construct The Journal of biological chemistry High 11940582
2007 Myo1E interacts via its SH3 domain with synaptojanin-1 and dynamin, two proteins with prominent roles in endocytosis. Myo1E co-localizes with clathrin- and dynamin-containing puncta at the plasma membrane in an SH3-domain-dependent manner. Expression of the Myo1E tail domain in a dominant-negative fashion inhibits transferrin endocytosis, establishing a role for Myo1E in clathrin-mediated endocytosis. Co-immunoprecipitation, GST pulldown assay, fluorescence microscopy co-localization, dominant-negative overexpression with transferrin uptake assay FEBS letters High 17257598
2011 Homozygous mutations in MYO1E (A159P and Y695X) cause childhood-onset, glucocorticoid-resistant focal segmental glomerulosclerosis (FSGS). The A159P mutation in the motor domain causes abnormal subcellular localization of Myo1E in transfected cells, while Y695X truncates the tail domain abolishing calmodulin binding. Myo1E is normally expressed in glomerular podocytes, establishing its role in podocyte function and glomerular filtration barrier integrity. Whole-genome linkage analysis, high-throughput sequencing, immunohistochemistry, electron microscopy, transfection/subcellular localization studies The New England journal of medicine High 21756023
2011 Exome sequencing in a consanguineous family with steroid-resistant nephrotic syndrome identified a homozygous A159P substitution in MYO1E as a candidate causative variant. The A159P variant is predicted to impair actin interaction in the MYO1E motor domain, consistent with the nephrotic phenotype observed in Myo1e-knockout mice. Homozygosity mapping, exome sequencing, bioinformatic structural modeling Kidney international Medium 21697813
2010 The myo1e C-terminal tail domain binds tightly to anionic phospholipids, particularly PtdIns(4,5)P2 and phosphatidylserine in large unilamellar vesicles, with near-diffusion-limited attachment kinetics and slow detachment (k_diss ≤ 0.4 s⁻¹). Lipid binding occurs through nonspecific electrostatic interactions rather than stereospecific PH domain-phosphoinositide interactions, as mutation of conserved PH domain residues has little effect on lipid binding in vitro or membrane localization in vivo. The myo1e tail localizes to clathrin-coated vesicles via its basic region. Sedimentation assays, stopped-flow fluorescence, fluorescence microscopy, site-directed mutagenesis of PH domain residues Biochemistry High 20860408
2013 Myo1e impairment in zebrafish via morpholino knockdown causes pericardial edema and pronephric cysts consistent with proteinuria. In cultured podocytes, Myo1e knockdown induces actin cytoskeleton rearrangement and defects in cell proliferation, migration, endocytosis, and adhesion to the glomerular basement membrane, demonstrating that Myo1e is a key component of the podocyte actin cytoskeleton required for glomerular filtration barrier integrity. Zebrafish morpholino knockdown, immunofluorescence, siRNA knockdown in cultured podocyte cell line, transwell migration assay, endocytosis assay, adhesion assay PloS one High 23977349
2014 Myo1e overexpression in mouse podocytes significantly enhances cell migration, endocytosis (FITC-transferrin internalization), and adhesion to the culture substrate, and protects against puromycin aminonucleoside-induced detachment, establishing Myo1e as a positive regulator of these podocyte functions. Myo1e overexpression in immortalized mouse podocyte cell line (MPC5), transwell migration assay, FITC-transferrin endocytosis, detachment assay after puromycin treatment Journal of cellular biochemistry Medium 24339252
2014 Myo1e regulates TLR4-triggered macrophage spreading, selectively suppresses CCL2 chemokine secretion, and maintains MHC class II surface expression in macrophages and dendritic cells. Myo1e-deficient cells show impaired antigen-specific CD4+ T-cell stimulation consistent with reduced MHC-II surface levels, and increased proteolytic cleavage of endocytosed antigen, revealing a non-redundant role of Myo1e in TLR4-controlled intracellular transport processes. Myo1e knockout mouse bone marrow-derived macrophages and DCs, flow cytometry for surface MHC-II, ELISA for CCL2, antigen-specific T-cell proliferation assay, macrophage spreading assay European journal of immunology High 25263281
2016 Myo1e modulates the recruitment of activated B cells to inguinal lymph nodes. Loss of Myo1e in B cells reduces integrin and F-actin levels at membrane protrusions, decreases phosphorylation of FAK, AKT, and RAC-1, disrupting the FAK-PI3K-RAC-1 signaling pathway and reducing B-cell adhesion and migration through high endothelial venules. Intravital microscopy in vivo, in vitro adhesion assays, flow cytometry for surface integrins, phospho-immunoblotting for FAK/AKT/RAC-1, Myo1e-knockout B cells Journal of cell science Medium 31964710
2020 Overexpression of Myo1e in mouse glomerular podocytes (MPC5) promotes albumin endocytosis in a dynamin-dependent manner; dynasore (a dynamin GTPase inhibitor) abolished the Myo1e-induced increase in FITC-BSA internalization. Myo1e overexpression also promotes expression of cytoskeletal F-actin and podocyte-specific molecules nephrin and podocin during albumin endocytosis. Myo1e overexpression and knockdown in MPC5 cells, FITC-BSA flow cytometry, dynasore inhibition, immunofluorescence for F-actin, western blot for nephrin/podocin PeerJ Medium 32211226
2022 Two SRNS-associated Myo1e motor domain mutations, T119I and D388H, have distinct functional defects: T119I is not enriched at cell junctions or clathrin-coated vesicles (CCVs) in Myo1e-KO podocyte cells, while D388H localizes similarly to wild-type but dissociates more slowly from junctions and CCVs. In vitro, D388H drastically reduces ATPase activity and actin filament translocation. Both mutations are loss-of-function but via different mechanisms—T119I affects targeting/localization while D388H impairs motor catalytic activity. Adenoviral delivery of EGFP-tagged Myo1e constructs into Myo1e-KO mouse podocyte cells, live-cell imaging of localization, FRAP, baculovirus-expressed truncated constructs for in vitro ATPase and actin gliding motility assays, clathrin-dependent endocytosis assay Journal of the American Society of Nephrology : JASN High 36316095
2022 Novel pathogenic MYO1E variants associated with FSGS map predominantly to the motor and neck domains of Myo1e, causing protein mislocalization in kidney sections. Histopathological analysis of all known pathogenic MYO1E variants reveals a characteristic pattern of podocyte damage and diffuse Alport-like glomerular basement membrane abnormalities, suggesting that Myo1e mutations disrupt podocyte contractile actin cables leading to GBM dysfunction. DNA/RNA sequencing, computer structural modeling, immunohistochemistry in kidney sections for Myo1e localization Pediatric nephrology (Berlin, Germany) Medium 35723736
2025 Myo1e (and Myo1f) localize specifically to the base of podosomes, underneath the actin core near the ventral plasma membrane in macrophages, with this localization primarily mediated by their TH2 domains. Knockout or knockdown of Myo1e/f leads to increased podosome size and altered podosome turnover and lateral mobility, indicating that Myo1e/f regulate attachment of podosome core actin filaments to the plasma membrane. Myo1e/f double-KO macrophages show reduced 2D and 3D migration despite increased matrix degradation capacity. TIRF microscopy, CRISPR knockout, siRNA knockdown, domain deletion analysis (TH2 domain), live-cell imaging, podosome size/turnover quantification, 3D migration assays, matrix degradation assays bioRxivpreprint Medium bio_10.1101_2025.04.28.651090
2025 In human induced pluripotent stem cells, Myo1E is recruited to clathrin-mediated endocytosis (CME) sites that have stalled due to increased membrane tension. As membrane tension rises, more CME sites recruit Myo1E. Loss of Myo1E results in increased Arp2/3 complex lifetime at CME sites under normal conditions, and at high tension these sites fail to recruit sufficient Arp2/3. Myo1E promotes assembly of a more effective branched actin network at stalled CME sites through motor activity and Arp2/3 recruitment, rescuing internalization. Live-cell imaging and super-resolution microscopy of genome-edited hiPSCs, membrane tension manipulation, Myo1E knockout, Arp2/3 recruitment quantification, CME dynamics analysis bioRxivpreprint Medium bio_10.1101_2025.11.12.688091

Source papers

Stage 0 corpus · 97 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2012 Insights into RNA biology from an atlas of mammalian mRNA-binding proteins. Cell 1718 22658674
2002 Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences. Proceedings of the National Academy of Sciences of the United States of America 1479 12477932
2017 Architecture of the human interactome defines protein communities and disease networks. Nature 1085 28514442
2015 A human interactome in three quantitative dimensions organized by stoichiometries and abundances. Cell 1015 26496610
2018 VIRMA mediates preferential m6A mRNA methylation in 3'UTR and near stop codon and associates with alternative polyadenylation. Cell discovery 829 29507755
2021 Dual proteome-scale networks reveal cell-specific remodeling of the human interactome. Cell 705 33961781
2012 A census of human soluble protein complexes. Cell 689 22939629
2011 Phylogenetic-based propagation of functional annotations within the Gene Ontology consortium. Briefings in bioinformatics 656 21873635
2020 Comparative host-coronavirus protein interaction networks reveal pan-viral disease mechanisms. Science (New York, N.Y.) 564 33060197
2022 OpenCell: Endogenous tagging for the cartography of human cellular organization. Science (New York, N.Y.) 432 35271311
2015 Panorama of ancient metazoan macromolecular complexes. Nature 407 26344197
2021 A proximity-dependent biotinylation map of a human cell. Nature 339 34079125
2010 Dynamics of cullin-RING ubiquitin ligase network revealed by systematic quantitative proteomics. Cell 318 21145461
2016 Identification of Zika Virus and Dengue Virus Dependency Factors using Functional Genomics. Cell reports 306 27342126
2012 A high-throughput approach for measuring temporal changes in the interactome. Nature methods 273 22863883
2010 MHC class II-associated proteins in B-cell exosomes and potential functional implications for exosome biogenesis. Immunology and cell biology 221 20458337
2002 Glucose transporter recycling in response to insulin is facilitated by myosin Myo1c. Nature 219 12490950
2016 An organelle-specific protein landscape identifies novel diseases and molecular mechanisms. Nature communications 211 27173435
2013 PRP19 transforms into a sensor of RPA-ssDNA after DNA damage and drives ATR activation via a ubiquitin-mediated circuitry. Molecular cell 204 24332808
2011 MYO1E mutations and childhood familial focal segmental glomerulosclerosis. The New England journal of medicine 191 21756023
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 171 17765682
2019 A protein-interaction network of interferon-stimulated genes extends the innate immune system landscape. Nature immunology 159 30833792
2007 An emerin "proteome": purification of distinct emerin-containing complexes from HeLa cells suggests molecular basis for diverse roles including gene regulation, mRNA splicing, signaling, mechanosensing, and nuclear architecture. Biochemistry 153 17620012
1994 Identification and overlapping expression of multiple unconventional myosin genes in vertebrate cell types. Proceedings of the National Academy of Sciences of the United States of America 149 8022818
2020 Comparative Application of BioID and TurboID for Protein-Proximity Biotinylation. Cells 146 32344865
2018 Identification of phagocytosis regulators using magnetic genome-wide CRISPR screens. Nature genetics 146 30397336
2022 A comprehensive SARS-CoV-2-human protein-protein interactome reveals COVID-19 pathobiology and potential host therapeutic targets. Nature biotechnology 140 36217030
2004 Unconventional myosin Myo1c promotes membrane fusion in a regulated exocytic pathway. Molecular and cellular biology 140 15169906
2019 Mapping the proximity interaction network of the Rho-family GTPases reveals signalling pathways and regulatory mechanisms. Nature cell biology 137 31871319
2017 RNA-binding activity of TRIM25 is mediated by its PRY/SPRY domain and is required for ubiquitination. BMC biology 135 29117863
2012 Novel Loci for metabolic networks and multi-tissue expression studies reveal genes for atherosclerosis. PLoS genetics 132 22916037
2019 The Functional Proximal Proteome of Oncogenic Ras Includes mTORC2. Molecular cell 124 30639242
2007 Myosin 1E interacts with synaptojanin-1 and dynamin and is involved in endocytosis. FEBS letters 124 17257598
2022 The ubiquitin-dependent ATPase p97 removes cytotoxic trapped PARP1 from chromatin. Nature cell biology 122 35013556
2008 CaMKII-mediated phosphorylation of the myosin motor Myo1c is required for insulin-stimulated GLUT4 translocation in adipocytes. Cell metabolism 98 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 76 21402783
2014 Loss of functional MYO1C/myosin 1c, a motor protein involved in lipid raft trafficking, disrupts autophagosome-lysosome fusion. Autophagy 65 25551774
2012 Myo1c binding to submembrane actin mediates insulin-induced tethering of GLUT4 vesicles. Molecular biology of the cell 63 22918957
2002 The kinetic mechanism of Myo1e (human myosin-IC). The Journal of biological chemistry 59 11940582
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
2011 Exome sequencing identified MYO1E and NEIL1 as candidate genes for human autosomal recessive steroid-resistant nephrotic syndrome. Kidney international 53 21697813
2010 Myo1e binds anionic phospholipids with high affinity. Biochemistry 50 20860408
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 42 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
2015 Coinheritance of COL4A5 and MYO1E mutations accentuate the severity of kidney disease. Pediatric nephrology (Berlin, Germany) 37 25739341
2011 A hearing loss-associated myo1c mutation (R156W) decreases the myosin duty ratio and force sensitivity. Biochemistry 37 21265502
2022 SMOC2 promotes aggressive behavior of fibroblast-like synoviocytes in rheumatoid arthritis through transcriptional and post-transcriptional regulating MYO1C. Cell death & disease 36 36513634
2005 Differential expression and molecular characterisation of Lmo7, Myo1e, Sash1, and Mcoln2 genes in Btk-defective B-cells. Cellular immunology 36 16137664
2007 Calcium regulation of calmodulin binding to and dissociation from the myo1c regulatory domain. Biochemistry 33 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
2014 Class I myosin Myo1e regulates TLR4-triggered macrophage spreading, chemokine release, and antigen presentation via MHC class II. European journal of immunology 27 25263281
2007 CIB1 and CaBP1 bind to the myo1c regulatory domain. Journal of muscle research and cell motility 25 17994197
2019 The motor protein Myo1c regulates transforming growth factor-β-signaling and fibrosis in podocytes. Kidney international 24 31097328
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
2014 Overexpression of Myo1e in mouse podocytes enhances cellular endocytosis, migration, and adhesion. Journal of cellular biochemistry 23 24339252
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 19 31699152
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 18 24698832
2005 Expression of the unconventional myosin Myo1c alters sodium transport in M1 collecting duct cells. American journal of physiology. Cell physiology 18 15716323
2020 Myo1e modulates the recruitment of activated B cells to inguinal lymph nodes. Journal of cell science 17 31964710
2013 Myo1e impairment results in actin reorganization, podocyte dysfunction, and proteinuria in zebrafish and cultured podocytes. PloS one 16 23977349
2024 Liraglutide Promotes Diabetic Wound Healing via Myo1c/Dock5. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 15 39159301
2016 Lowered Expression of Tumor Suppressor Candidate MYO1C Stimulates Cell Proliferation, Suppresses Cell Adhesion and Activates AKT. PloS one 15 27716847
2013 Myo1c is an unconventional myosin required for zebrafish glomerular development. Kidney international 15 23715127
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
2022 Focal segmental glomerulosclerosis and proteinuria associated with Myo1E mutations: novel variants and histological phenotype analysis. Pediatric nephrology (Berlin, Germany) 10 35723736
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
2023 Myo1e overexpression in lung adenocarcinoma is associated with increased risk of mortality. Scientific reports 8 36914720
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
2024 A noncanonical E3 ubiquitin ligase RNF41-mediated MYO1C stability promotes prostate cancer metastasis by inducing actin remodeling. Oncogene 4 39112516
2022 Steroid-Resistant Nephrotic Syndrome-Associated MYO1E Mutations Have Differential Effects on Myosin 1e Localization, Dynamics, and Activity. Journal of the American Society of Nephrology : JASN 4 36316095
2023 Analysis and validation of the potential of the MYO1E gene in pancreatic adenocarcinoma based on a bioinformatics approach. Oncology letters 3 37274465
2023 RAB31 in glioma-derived endothelial cells promotes glioma cell invasion via extracellular vesicle-mediated enrichment of MYO1C. FEBS open bio 3 37953466
2020 Overexpression of Myo1e promotes albumin endocytosis by mouse glomerular podocytes mediated by Dynamin. PeerJ 3 32211226
2023 Effect of cyclosporine A on focal segmental glomerulosclerosis caused by MYO1E mutation in a Chinese adult patient: A case report. Medicine 2 36705362
2022 Concordant nephrotic syndrome in twins with PAX2 and MYO1E mutations. Clinical nephrology. Case studies 2 35574290
2024 Recessive variants in MYO1C as a potential novel cause of proteinuric kidney disease. Pediatric nephrology (Berlin, Germany) 1 38904753
2014 [Mutational analysis of MYO1E in children with sporadic steroid-resistant nephrotic syndrome in Chinese Han ethnic group]. Zhonghua er ke za zhi = Chinese journal of pediatrics 1 25224051
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
2026 Steroid-Resistant Focal Segmental Glomerulosclerosis with Alport-like Glomerular Basement Membrane Lesions Due to a MYO1E Mutation: A Pediatric Case Report. International journal of molecular sciences 0 41898697
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
2014 [Mutational analysis of MYO1E in Chinese children with familial steroid-resistant nephrotic syndrome]. Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics 0 24750828