Affinage

MYO1C

Unconventional myosin-Ic · UniProt O00159

Round 2 corrected
Length
1063 aa
Mass
121.7 kDa
Annotated
2026-04-29
119 papers in source corpus 37 papers cited in narrative 37 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

MYO1C is an actin-based unconventional class-I myosin motor that functions as a force-sensitive molecular tether and cargo transporter across diverse membrane trafficking, transcriptional, and cytoskeletal processes. In the cytoplasm, MYO1C drives insulin-stimulated GLUT4 vesicle translocation and tethering to cortical actin at the plasma membrane through a PI3K-independent pathway regulated by CaMKIIδ phosphorylation at S701, with RalA serving as the vesicular cargo receptor and calmodulin as the regulatory light chain (PMID:12490950, PMID:19046570, PMID:17765682, PMID:22918957); it additionally transports specific membrane cargoes—including Neph1, nephrin, rhodopsin, VEGFR2, Jagged1, and GPI-anchored proteins—to their surface destinations, stabilizes Golgi-associated actin for vesicle carrier arrival, delivers G-actin monomers to the leading edge of migrating cells, and promotes autophagosome–lysosome fusion through F-actin remodeling (PMID:21402783, PMID:34073294, PMID:23262137, PMID:22328521, PMID:22778278, PMID:30872458, PMID:25551774). A nuclear isoform (NM1, bearing a 16-amino-acid N-terminal extension) associates with RNA polymerases I and II, activates rDNA transcription via TIF-IA, binds gene promoters such as GDF-15, and regulates ERα enhancer clustering, while single-molecule biophysics reveals that tension of ≥2 pN converts MYO1C from a low- to a high-duty-ratio motor by slowing actin detachment, and cryo-EM structures show a unique actin interface and skewed lever-arm trajectory that explain its leftward gliding path and force-sensing through ATP binding rather than ADP release (PMID:15558034, PMID:11030652, PMID:31097328, PMID:18599791, PMID:28893906).

Mechanistic history

Synthesis pass · year-by-year structured walk · 17 steps
  1. 2000 High

    The discovery of a nuclear Myo1c isoform (NM1) bearing a unique 16-amino-acid N-terminal extension, co-immunoprecipitating RNA polymerase II and blocking in vitro RNA synthesis, established for the first time that an unconventional myosin operates in the nucleus during transcription.

    Evidence Isoform-specific antibody, confocal/EM colocalization, co-IP of Pol II, in vitro transcription inhibition in mammalian cells

    PMID:11030652

    Open questions at the time
    • No direct evidence for NM1-specific gene targets at this stage
    • Mechanism linking motor activity to transcription unknown
  2. 2002 High

    Identification of MYO1C on purified GLUT4 vesicles and demonstration that dominant-negative cargo domain and siRNA knockdown block insulin-stimulated GLUT4 translocation and glucose uptake answered how insulin mobilizes GLUT4 independently of PI3K, establishing MYO1C as the motor for this trafficking step.

    Evidence Vesicle purification, dominant-negative overexpression, siRNA knockdown, glucose uptake assay in 3T3-L1 adipocytes

    PMID:12490950

    Open questions at the time
    • Cargo receptor linking MYO1C to GLUT4 vesicle unknown
    • Upstream signaling events activating MYO1C unresolved
  3. 2004 High

    NM1 was shown to be essential for RNA polymerase I transcription at rDNA via direct binding to TIF-IA (requiring RSK-mediated S649 phosphorylation), extending the nuclear role of MYO1C from Pol II association to a defined mechanism in ribosomal RNA synthesis.

    Evidence Antibody microinjection, siRNA, overexpression, in vitro Pol I transcription on chromatin templates, co-IP of NMI–TIF-IA–Pol I

    PMID:15558034

    Open questions at the time
    • Whether NM1 plays a catalytic versus structural role in Pol I complex assembly unknown
    • No genome-wide assessment of NM1-dependent loci
  4. 2007 High

    Discovery that RalA acts as the cargo receptor linking MYO1C to GLUT4 vesicles—modulated by calmodulin—and simultaneously connects the exocyst for vesicle tethering resolved the missing cargo-recognition step in insulin-stimulated GLUT4 trafficking.

    Evidence Reciprocal co-IP, siRNA and dominant-negative RalA, glucose transport assay in adipocytes

    PMID:17765682

    Open questions at the time
    • Structural basis of RalA–MYO1C interaction unresolved
    • Whether calmodulin dissociation is the switch for RalA engagement unclear
  5. 2007 High

    Reconstituted kinetic studies showed that calcium binding to IQ1-associated calmodulin regulates MYO1C motor activity—moderately stimulating ATPase but completely inhibiting actin gliding—establishing the primary regulatory site and mechanism for calcium-dependent control of the motor.

    Evidence In vitro ATPase, actin gliding, stopped-flow fluorescence with labeled calmodulin, peptide binding assays

    PMID:17910470

    Open questions at the time
    • In vivo relevance of calcium-induced calmodulin dissociation from IQ1 not directly tested
    • Role of alternative light chains (CIB1, CaBP1) in modulating this regulation unclear
  6. 2008 High

    Single-molecule optical trapping revealed that MYO1C undergoes a dramatic load-dependent transition from low (<0.2) to high (>0.9) duty ratio at ≥2 pN tension, establishing it as a bona fide molecular force sensor—a property that explains its roles in membrane tethering and tension-dependent processes.

    Evidence Single-molecule optical trap measuring displacement and detachment kinetics under controlled loads

    PMID:18599791

    Open questions at the time
    • Structural basis for force-dependent detachment slowing unknown at this time
    • How force sensing integrates with cargo-specific functions in cells not addressed
  7. 2008 High

    Identification of CaMKIIδ-mediated phosphorylation of MYO1C at S701 as the insulin-responsive switch—enhancing ATPase activity, promoting 14-3-3 binding, reducing calmodulin binding, and being required for GLUT4 translocation—connected upstream insulin signaling to motor activation.

    Evidence In vitro kinase assay, S701A/K111A mutagenesis, siRNA rescue, GLUT4 translocation assay in adipocytes

    PMID:19046570

    Open questions at the time
    • How 14-3-3 binding alters MYO1C localization or interaction with RalA not defined
    • Whether S701 phosphorylation regulates non-GLUT4 cargoes unknown
  8. 2010 High

    Hearing-loss-associated motor-domain mutations (R156W, V252A, T380M) were shown to differentially impair ATPase kinetics, actin affinity, and motility, linking specific mechanochemical defects to human disease and validating the kinetic cycle as a drug/mutation target.

    Evidence Transient kinetic analyses, steady-state ATPase, in vitro motility with purified mutant proteins

    PMID:20640478 PMID:21265502

    Open questions at the time
    • No in vivo confirmation that these mutations cause hearing loss via MYO1C loss-of-function
    • Structural explanation for switch-1 disruption by R156W not yet available
  9. 2012 High

    A series of studies expanded MYO1C's cargo repertoire beyond GLUT4: it was shown to tether GLUT4 vesicles to cortical actin via TIRF imaging, selectively recycle GPI-anchored/lipid-raft cargo from the perinuclear compartment, transport Neph1 to the podocyte membrane, deliver G-actin monomers to the leading edge, and traffic VEGFR2 to the endothelial surface—establishing MYO1C as a general membrane-cargo transporter with selectivity for specific membrane domains.

    Evidence TIRF single-vesicle tracking, siRNA and dominant-negative studies, raft fractionation, mass spectrometry cargo identification, photoactivatable actin tracking, VEGFR2 surface assays in multiple cell types

    PMID:21402783 PMID:22328521 PMID:22778278 PMID:22918957 PMID:23262137

    Open questions at the time
    • Whether all cargoes use the same tail-domain binding surface unclear
    • Mechanisms selecting which cargo is loaded at a given time unknown
  10. 2013 High

    Zebrafish morpholino knockdown of Myo1c causing pericardial edema, dilated tubules, and absent slit diaphragm—rescued by mouse Myo1c mRNA—demonstrated an essential in vivo requirement for MYO1C in glomerular development and podocyte integrity.

    Evidence Morpholino knockdown in zebrafish, electron microscopy, mRNA rescue

    PMID:23715127

    Open questions at the time
    • Whether MYO1C loss causes kidney disease in mammals not yet shown at this point
    • Cargo(s) responsible for slit-diaphragm defect not identified in this model
  11. 2014 High

    MYO1C depletion was shown to block autophagosome–lysosome fusion selectively (without affecting endocytic degradation or lysosomal activity) by causing cholesterol-enriched membrane accumulation, revealing a lipid-homeostasis-dependent mechanism by which MYO1C supports autophagy.

    Evidence siRNA/dominant-negative knockdown, TEM, LC3/LAMP1 colocalization, EGFR degradation control, cholesterol quantification

    PMID:25551774

    Open questions at the time
    • Whether MYO1C directly transports cholesterol or indirectly regulates its distribution unclear
    • Actin remodeling contribution versus lipid redistribution not fully dissected
  12. 2017 High

    Full-length kinetic characterization of the three MYO1C splice isoforms revealed that N-terminal extensions allosterically shift the actomyosin equilibrium between open and closed states—mediated by a specific Arg-21/Glu-469 salt bridge in the NTR35 isoform—explaining how a single gene produces motors with distinct force-generating properties.

    Evidence Purified full-length isoform kinetics from HEK cells, global numerical simulation, R21G mutagenesis, NTR peptide addition

    PMID:28893906

    Open questions at the time
    • Isoform-specific cargo assignments not established
    • Tissue-specific expression ratios of isoforms not systematically mapped
  13. 2019 High

    Two studies revealed MYO1C's roles beyond vesicle transport: it stabilizes Golgi-associated actin required for both anterograde and retrograde carrier arrival (phenocopying Arp2/3 loss), and podocyte-specific knockout in mice conferred resistance to fibrotic kidney injury by blunting TGF-β signaling, with nuclear MYO1C directly binding the GDF-15 promoter.

    Evidence siRNA with Golgi transport assays and F-actin quantification; conditional KO mice with multiple injury models, ChIP at GDF-15 promoter

    PMID:30872458 PMID:31097328

    Open questions at the time
    • Whether Golgi actin stabilization requires MYO1C motor activity or passive tethering not tested
    • Genome-wide map of nuclear MYO1C promoter occupancy incomplete
  14. 2021 High

    Systemic Myo1c knockout mice exhibited progressive photoreceptor degeneration with rhodopsin mislocalization to inner segments, and direct MYO1C–rhodopsin binding was demonstrated, extending MYO1C's cargo transport function to sensory neurons.

    Evidence Myo1c KO mice, electroretinography, immunohistochemistry, direct binding assay

    PMID:34073294

    Open questions at the time
    • Whether MYO1C transports rhodopsin via the connecting cilium or an alternative route unknown
    • Other visual-cycle cargoes of MYO1C not explored
  15. 2024 Medium

    Non-canonical K27/K63-linked polyubiquitination of MYO1C by RNF41 was found to stabilize (rather than degrade) MYO1C, promoting actin remodeling and prostate cancer bone metastasis, identifying a post-translational mechanism controlling MYO1C protein levels.

    Evidence Ubiquitination assay defining linkage type, RNF41 knockdown, in vivo bone-metastasis xenograft, MYO1C rescue

    PMID:39112516

    Open questions at the time
    • Deubiquitinase counteracting RNF41 not identified
    • Whether K27/K63-Ub stabilization operates in non-cancer contexts unknown
  16. 2025 High

    Cryo-EM structures of actin-bound MYO1C ± ADP revealed a unique actin interface that reorients the motor domain relative to other myosin-I family members, skewing the lever-arm swing to explain leftward actin gliding; the N-terminal extension was shown to participate in force sensing through regulation of ATP binding rather than ADP release.

    Evidence Cryo-EM structure determination of actomyosin-MYO1C ± ADP, integration with crystallography for full-length modeling (preprint)

    PMID:bio_10.1101_2025.01.10.632429

    Open questions at the time
    • Structures not yet peer-reviewed
    • No structure with cargo bound to the tail domain
    • How NTR isoform differences alter the actin interface is not resolved structurally
  17. 2025 High

    MYO1C was shown to interact with the Notch ligand Jagged1 and to be required for its polarized trafficking under static conditions, with shear stress reducing the MYO1C–Jagged1 interaction, and separately, purified MYO1C was demonstrated sufficient to assemble an actin cage around giant membranes in vitro, explaining how Chlamydia exploits MYO1C for inclusion integrity.

    Evidence Proximity labeling + co-IP + KO with shear-stress platform for Jagged1; in vitro reconstitution of actin cage assembly with purified MYO1C for Chlamydia inclusion

    PMID:41242206 PMID:41321631

    Open questions at the time
    • Whether Jagged1 transport uses the same tail-domain surface as Neph1/rhodopsin not tested
    • In vitro actin cage assembly conditions may not recapitulate physiological membrane composition

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include: how isoform-specific cargoes are assigned in vivo; the full structural basis of tail-domain cargo recognition; whether nuclear MYO1C transcriptional functions require motor activity or tension; and how force sensing integrates with specific trafficking decisions at the single-molecule level inside cells.
  • No atomic-resolution structure of MYO1C tail bound to any cargo
  • Isoform-specific knockout models not yet reported
  • Single-molecule force measurements inside living cells not achieved

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0003774 cytoskeletal motor activity 8 GO:0008092 cytoskeletal protein binding 4 GO:0140657 ATP-dependent activity 4 GO:0140110 transcription regulator activity 3 GO:0008289 lipid binding 2
Localization
GO:0005886 plasma membrane 7 GO:0005634 nucleus 5 GO:0005856 cytoskeleton 4 GO:0031410 cytoplasmic vesicle 4 GO:0005829 cytosol 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 4 R-HSA-74160 Gene expression (Transcription) 3 R-HSA-382551 Transport of small molecules 2 R-HSA-9612973 Autophagy 2
Partners
CALM1EMDFLNAIKBKGKIRREL1RALARHORPTOR

Evidence

Reading pass · 37 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2002 Myo1c is present in GLUT4-containing vesicles purified from 3T3-L1 adipocytes and functions in a PI(3)K-independent insulin signaling pathway that controls movement of intracellular GLUT4-vesicles to the plasma membrane; dominant-negative Myo1c cargo domain inhibits insulin-stimulated GLUT4 translocation, and siRNA-mediated knockdown of Myo1c inhibits insulin-stimulated 2-deoxyglucose uptake. Subcellular fractionation/vesicle purification, dominant-negative overexpression, siRNA knockdown, glucose uptake assay, colocalization imaging in adipocytes Nature High 12490950
2004 Myo1c promotes membrane fusion of GLUT4-containing vesicles with the plasma membrane in adipocytes; enhanced Myo1c expression overrides PI3K inhibitor-induced block of membrane fusion and causes membrane ruffling that mobilizes GLUT4 vesicles to the cell surface. Overexpression in 3T3-L1 adipocytes with PI3K inhibitor LY294002, ultrafast microscopy of GLUT4-GFP vesicle dynamics Molecular and cellular biology High 15169906
2007 RalA interacts directly with Myo1c and functions as a cargo receptor for the Myo1c motor during insulin-stimulated GLUT4 trafficking; calmodulin, acting as Myo1c light chain, modulates the RalA–Myo1c interaction. RalA also links the exocyst complex to GLUT4 vesicle tethering at the plasma membrane. Co-immunoprecipitation, dominant-negative and siRNA knockdown of RalA, glucose transport assay in adipocytes Developmental cell High 17765682
2006 Myo1c interacts with NEMO/IKK-γ and is required for insulin-dependent trafficking of NEMO to membrane ruffles, where NEMO interacts with IRS-1; this Myo1c–NEMO axis is essential for TNF-α-induced serine-307 phosphorylation of IRS-1 and the resulting insulin resistance. Co-immunoprecipitation, dominant-negative Myo1c cargo domain overexpression, siRNA knockdown, immunofluorescence, phospho-IRS-1 immunoblotting The Journal of cell biology High 16754954
2008 CaMKIIδ phosphorylates Myo1c at serine 701 in response to insulin, leading to enhanced 14-3-3 binding and reduced calmodulin binding; phosphorylation increases Myo1c ATPase activity in vitro, and the phosphorylation-mimetic but not S701A or ATPase-dead (K111A) Myo1c rescues GLUT4 translocation after siRNA knockdown of endogenous Myo1c. In vitro CaMKII phosphorylation assay, siRNA knockdown of CaMKIIδ, mutagenesis (S701A, K111A), ATPase activity assay, GLUT4 translocation assay Cell metabolism High 19046570
2008 Rictor forms a biochemically distinct complex with Myo1c in adipocytes (separate from mTORC2); this Rictor–Myo1c complex participates in cortical actin remodeling and paxillin tyrosine-118 phosphorylation, and Myo1c-induced membrane ruffling is compromised after Rictor knockdown. Co-immunoprecipitation distinct from mTOR complex, RNAi depletion of Rictor and Myo1c, paxillin phosphorylation immunoblotting, morphological analysis of membrane ruffles Molecular and cellular biology High 18426911
2007 Calcium binding to regulatory-domain-associated calmodulin regulates myo1c motor activity: calcium moderately increases actin-activated ATPase but completely inhibits actin gliding; calmodulin dissociates most rapidly from IQ1 (adjacent to motor domain) in the presence of calcium (rate 60 s⁻¹), limited by a slow calcium-induced conformational change (3 s⁻¹), making IQ1-bound calmodulin the primary site of calcium regulation. Actin gliding assay, ATPase measurements, stopped-flow fluorescence kinetics, fluorescence anisotropy with labeled calmodulin mutant N111C, peptide binding assays Biochemistry High 17910470
2007 CIB1 and CaBP1 bind to the myo1c IQ motifs in the regulatory domain, compete with calmodulin for binding (more effectively in the presence of calcium), and colocalize with endogenous myo1c in cells; these myristoylated calcium-binding proteins may specify myo1c subcellular targeting. Pull-down experiments, fluorescence microscopy colocalization, competitive binding assays with calmodulin Journal of muscle research and cell motility Medium 17994197
2010 Expression of wild-type Myo1c in mouse tibialis anterior muscle in vivo significantly increases both contraction-stimulated and insulin-stimulated glucose uptake, whereas expression of the ATPase-dead mutant K111A-Myo1c decreases both, demonstrating that Myo1c motor activity is required for glucose uptake in skeletal muscle. In vivo electroporation of wild-type and K111A mutant Myo1c into mouse tibialis anterior, in vivo glucose uptake assay after contraction and insulin injection The Journal of biological chemistry High 21127070
2011 Myo1c directly interacts with the podocyte slit diaphragm protein Neph1 in an actin-dependent manner and mediates Neph1 transport to the podocyte cell membrane; dominant-negative Myo1c or Myo1c depletion significantly reduces Neph1 membrane localization and impairs tight junction formation and cell migration. In vitro and in vivo co-immunoprecipitation, dominant-negative Myo1c overexpression, siRNA knockdown, transepithelial electric resistance, BSA permeability assay, wound migration assay Molecular and cellular biology High 21402783
2011 A hearing-loss-associated myo1c point mutation R156W (in switch 1 region) decreases the actin-activated ATPase rate >4-fold (likely by reducing phosphate release), reduces the duty ratio, and renders actin gliding less sensitive to resisting forces in a frictional loading assay, without affecting ATP binding or ADP release rates substantially. Transient kinetic ATPase analysis at 37°C, in vitro motility assay at multiple myosin densities, frictional loading assay using recombinant myo1c(3IQ) and R156W-myo1c(3IQ) Biochemistry High 21265502
2012 Myo1c is a lipid-raft-associated motor protein that drives formation of recycling tubules from the perinuclear recycling compartment, selectively promoting recycling of GPI-linked raft cargo (but not transferrin receptor) back to the cell surface via an Arf6-dependent pathway; loss of Myo1c traps GPI-linked proteins in the recycling compartment and impairs cell spreading, migration, and Salmonella invasion. RNAi knockdown, dominant-negative overexpression, live-cell imaging of recycling tubules, biochemical lipid raft fractionation, Salmonella invasion assay, wound healing/migration assay Journal of cell science High 22328521
2012 Myo1c associates with both mobile and tethered GLUT4 vesicles in the TIRF zone beneath the plasma membrane of muscle cells; Myo1c knockdown or overexpression of an actin-binding-deficient mutant abolishes insulin-induced vesicle immobilization and increases vesicle velocity, preventing GLUT4 externalization. Interaction of vesicular Myo1c with cortical actin filaments is required for insulin-mediated tethering of GLUT4 vesicles. TIRF microscopy of GLUT4-GFP vesicle dynamics, siRNA knockdown, actin-binding-deficient mutant overexpression, single-vesicle tracking, GLUT4 surface exposure assay Molecular biology of the cell High 22918957
2012 Myo1c identifies G-actin as a cargo via its tail domain and transports G-actin (actin monomers) vectorially to the leading edge of migrating endothelial cells; the motor domain is required for transport. Local microinjection of Myo1c promotes G-actin accumulation and membrane ruffling, and Myo1c knockdown reduces G-actin delivery to the leading edge and impairs cell motility. Mass spectrometric identification of G-actin as Myo1c tail interactor, photoactivatable non-polymerizable actin tracking in live cells, Myo1c microinjection, siRNA knockdown with motility readout The Journal of cell biology High 22778278
2012 Myo1c is required for VEGFR2 delivery to the endothelial cell plasma membrane in response to VEGF; Myo1c depletion increases VEGFR2 lysosomal degradation, reduces VEGFR2 phosphorylation at Y1175, and attenuates ERK1/2 and c-Src activation, leading to reduced cell proliferation and migration. VEGFR2 colocalizes with Myo1c and caveolin-1 in response to VEGF. siRNA knockdown in primary human endothelial cells, surface VEGFR2 measurement, subcellular density-gradient fractionation, phospho-VEGFR2/ERK/Src immunoblotting, rescue with WT vs mutant Myo1c American journal of physiology. Heart and circulatory physiology High 23262137
2013 Myo1c is required for normal zebrafish glomerular development; morpholino knockdown of Myo1c in zebrafish causes pericardial edema, dilated renal tubules, abnormal podocyte morphology, and absence of the slit diaphragm, which is rescued by co-injection of mouse Myo1c mRNA. Antisense morpholino knockdown in zebrafish, immunofluorescence, in situ hybridization, electron microscopy, mRNA rescue experiment Kidney international High 23715127
2014 Loss of functional MYO1C disrupts autophagosome–lysosome fusion: MYO1C depletion causes accumulation of cholesterol-enriched membranes, increases total cellular cholesterol, and blocks autophagic cargo degradation without affecting endocytic cargo (EGFR) degradation or lysosomal pH/hydrolase activity, indicating that correct lipid (cholesterol) composition governed by MYO1C is required for autophagosome–lysosome fusion. siRNA and dominant-negative knockdown, transmission electron microscopy, immunofluorescence for LC3/LAMP1, EGFR degradation assay, lysosomal activity assay, cholesterol quantification Autophagy High 25551774
2010 Three hearing-loss-associated missense mutations in the Myo1c motor domain (R156W, V252A, T380M) differentially affect nucleotide binding and actin interactions: R156W disrupts the nucleotide-binding pocket and calcium binding by disrupting switch 1; V252A reduces actin affinity by disrupting communication between actin- and nucleotide-binding sites; T380M causes aberrant kinetic changes and uncoupling of ATPase from motility. Transient kinetic analyses, steady-state ATPase assay, in vitro motility assay, homology modeling with truncated Myo1c(1IQ-SAH) construct Cellular and molecular life sciences High 20640478
2004 Nuclear myosin I (NMI/Myo1c isoform with 16-aa N-terminal extension) is associated with rDNA and is required for RNA polymerase I transcription; antibody microinjection or siRNA depletion of NMI decreases Pol I transcription, overexpression augments pre-rRNA synthesis, and in vitro recombinant NMI activates Pol I transcription. NMI binds Pol I through the transcription initiation factor TIF-IA, requiring phosphorylation of TIF-IA at Ser649 by RSK kinase. Antibody microinjection, siRNA depletion, overexpression, in vitro Pol I transcription assay on naked DNA and chromatin, co-immunoprecipitation of NMI with TIF-IA/Pol I, kinase dependency assay Nature cell biology High 15558034
2000 A nuclear isoform of myosin I beta (Myo1c) containing a unique 16-amino acid N-terminal extension is identified; it colocalizes with RNA polymerase II in an alpha-amanitin- and actinomycin D-sensitive manner, co-immunoprecipitates RNA polymerase II, and antibody against the 16-aa extension blocks in vitro RNA synthesis. Affinity-purified antibody to 16-aa peptide, confocal and electron microscopy, co-immunoprecipitation, in vitro RNA synthesis inhibition assay Science High 11030652
2008 Myosin I (myo1c) acts as a molecular force sensor: single-molecule optical trap measurements show that the rate of myo1c detachment from actin decreases >75-fold under tension of ≤2 pN, causing myo1c to transition from a low duty-ratio (<0.2) to a high duty-ratio (>0.9) motor, supporting its role in tension-sensitive membrane and cytoskeletal processes. Single-molecule optical trap assay measuring displacement and actin-attachment kinetics under varying loads Science High 18599791
2016 The structural solution conformation of full-length Myo1c bound to its cargo protein Neph1 was determined by small-angle X-ray scattering, revealing an extended S-shaped Myo1c with Neph1 attached to the C-terminal tail without inducing significant conformational change in Myo1c. A critical Neph1 residue at the interaction surface was identified; point mutation at this site abolished Myo1c–Neph1 interaction in vitro and in live cells, and FRAP confirmed Myo1c-dependent vesicular movement of Neph1. Small-angle X-ray scattering (SAXS) structural modeling, point mutagenesis, in vitro binding assay, live-cell FRAP imaging Molecular and cellular biology High 27044863
2017 The MYO1C gene produces three alternatively spliced isoforms differing only in N-terminal regions (NTRs); full-length kinetic analysis shows MYO1Cc favors the actomyosin closed state (AMC), MYO1C16 populates AMC and AMO equally, and MYO1C35 favors the actomyosin open (AMO) state. The NTR35 residue Arg-21 engages Glu-469 in the post-relay helix, affecting power stroke mechanics; an R21G mutation abolishes MYO1C35-like kinetics, and adding NTR35 peptide to MYO1Cc transiently confers MYO1C35 behavior. Overexpression and purification of three full-length isoforms from HEK cells, transient kinetics, global numerical simulation, homology modeling, NTR peptide addition experiments, mutagenesis The Journal of biological chemistry High 28893906
2019 MYO1C depletion causes Golgi complex fragmentation and decompaction and loss of cellular F-actin; MYO1C accumulates at dynamic Golgi-associated actin dots and stabilizes actin at the Golgi, facilitating the arrival of both anterograde and retrograde transport carriers. This function is phenotypically similar to loss of the Arp2/3 complex. siRNA depletion, live-cell imaging of Golgi-associated structures, F-actin quantification, transport carrier arrival assay (anterograde and retrograde routes) Journal of cell science High 30872458
2019 Podocyte-specific Myo1c knockout mice are resistant to fibrotic injury (Adriamycin, nephrotoxic serum, unilateral ureteral obstruction); loss of Myo1c blunts canonical and non-canonical TGF-β signaling. Nuclear Myo1c directly binds the GDF-15 promoter and transcriptionally regulates this TGF-β-responsive gene, and GDF15 is upregulated in FSGS patient glomeruli. Conditional (podocyte-specific) Myo1c knockout mouse models, multiple injury paradigms, ChIP for nuclear Myo1c at GDF-15 promoter, differential gene expression analysis of nuclear Myo1c-associated promoters, TGF-β pathway immunoblotting Kidney international High 31097328
2019 Cepharanthine downregulates MYO1C, which in turn disrupts MYO1C/F-actin interaction with autophagic markers LC3 and LAMP1, blocking autophagosome–lysosome fusion; overexpression of MYO1C restores this colocalization. MYO1C promotes autophagosome–lysosome fusion through F-actin network remodeling. Co-immunoprecipitation of MYO1C with LC3/LAMP1, siRNA knockdown and overexpression, immunofluorescence colocalization, transmission electron microscopy Journal of experimental & clinical cancer research Medium 31699152
2021 Systemic MYO1C knockout mice show progressive loss of photoreceptor function; MYO1C localizes to photoreceptor inner and outer segments and directly interacts with rhodopsin (binding assay); in Myo1c-KO retinas, rhodopsin mislocalizes to rod inner segments and cell bodies, demonstrating MYO1C is required for rhodopsin transport to the outer segment. Myo1c knockout mice, electroretinogram analysis, immunohistochemistry, direct rhodopsin–MYO1C binding assay, ultrastructural examination Cells High 34073294
2016 Myo1c interacts with SHIP2 and filamin A in glioblastoma cells; Myo1c depletion impairs SHIP2 localization at lamellipodia, causes cells to cluster, reduces FAK Tyr397 phosphorylation, decreases focal adhesion length, and strongly reduces cell migration, demonstrating Myo1c is required for lamellipodia formation and a SHIP2-containing migration complex. Co-immunoprecipitation identifying Myo1c–SHIP2–filamin A complex, siRNA knockdown, immunofluorescence of lamellipodia, FAK phosphorylation immunoblotting, migration assay Biochemical and biophysical research communications Medium 27246739
2016 Lowered MYO1C expression in endometrial carcinoma cells stimulates cell proliferation, suppresses cell adhesion, and accelerates AKT phosphorylation in response to serum; conversely, MYO1C overexpression reduces basal pAKT, suggesting MYO1C suppresses the PI3K/AKT pathway. siRNA knockdown and overexpression in endometrial carcinoma cell lines, proliferation assay, adhesion assay, pAKT immunoblotting after serum stimulation PloS one Medium 27716847
2005 Myo1c expressed in M1 mouse collecting duct cells localizes to discrete plasma membrane domains; expression of full-length or truncated (dominant-negative, lacking ATPase/actin domains) Myo1c modulates antidiuretic hormone (ADH)-stimulated short-circuit current and reduces amiloride-sensitive Na+ channel activity; the IQ region is required for proper Myo1c targeting. Overexpression of WT and truncated Myo1c in M1 cells, electrophysiological short-circuit current measurements, EGFP-Myo1c targeting analysis American journal of physiology. Cell physiology Medium 15716323
2024 Liraglutide directly binds Myo1c at arginine 93, stabilizing Myo1c and enhancing the Myo1c/Dock5 interaction; this promotes Dock5-dependent keratinocyte proliferation, migration, and adhesion to accelerate diabetic wound healing. Keratinocyte-specific Dock5 knockout abrogates liraglutide's wound-healing effect. Molecular binding assay (liraglutide–Myo1c at R93), co-immunoprecipitation of Myo1c/Dock5, keratinocyte-specific Dock5 knockout mouse, wound closure assay in db/db and STZ diabetic mice Advanced science Medium 39159301
2024 RNF41 E3 ubiquitin ligase induces non-canonical K27- and K63-linked polyubiquitination of MYO1C to enhance its stability (rather than degradation), promoting actin remodeling and prostate cancer bone metastasis; inhibition of RNF41 reduces MYO1C levels and suppresses PCa metastasis in an intraarterial bone-metastasis xenograft model. Co-immunoprecipitation, ubiquitination assay defining K27/K63 linkage, RNF41 siRNA knockdown, in vivo bone-metastasis xenograft model, MYO1C rescue Oncogene Medium 39112516
2025 Cryo-EM structures of actin-bound myo1c in the presence and absence of ADP reveal a unique actin interface that reorients the motor domain compared with myo1b/other myosins, skewing the lever arm swing and explaining why myo1c propels actin in leftward circles. The N-terminal extension plays a unique role in force sensing. The structures explain why force primarily regulates ATP binding (not ADP release) in myo1c, and enable modeling of full-length myo1c during force generation. Cryo-EM structure determination of actin-bound myo1c ± ADP, integration with crystallography structures for full-length modeling bioRxivpreprint High bio_10.1101_2025.01.10.632429
2025 Nuclear Myo1c (NM1) positively regulates ERα clustering on enhancers and promotes condensate formation on chromatin genome-wide; NM1 depletion causes a genome-wide reduction in ERα occupancy and condensates, though estrogen-regulated gene expression remains largely robust, revealing a role for Myo1c in transcription factor clustering without strictly controlling transcriptional output. ChIP-seq for ERα occupancy, super-resolution/condensate imaging, NM1 depletion by siRNA, genome-wide analysis in estrogen-stimulated cells bioRxivpreprint Medium bio_10.1101_2025.01.29.635522
2025 Chlamydia trachomatis recruits MYO1C to its intracellular inclusion throughout its lifecycle; loss or inhibition of MYO1C activity reduces Ct infection and progeny production. In vitro reconstitution showed that purified MYO1C alone is necessary and sufficient to build an actin cage around giant membranous vesicles, functioning as a dynamic tether that assembles the actin cage around the inclusion membrane. Immunofluorescence of Ct-infected cells, MYO1C inhibition (pentachloropseudilin), siRNA depletion, in vitro reconstitution assay with purified MYO1C and giant membranous vesicles Microbiological research High 41242206
2007 Emerin directly binds nuclear myosin I (NMI/Myo1c) in vitro; bead-conjugated emerin affinity-purifies NMI from HeLa nuclear lysates, and this interaction is stable regardless of ATP (motor activity), placing NMI in a distinct emerin-containing complex at the nuclear envelope separate from gene-regulatory complexes. Recombinant bead affinity purification from HeLa nuclear lysates, in vitro direct binding assay, ATP-independence test, mass spectrometry identification Biochemistry Medium 17620012
2025 MYO1C interacts with Jagged1 (Notch ligand) under static conditions in endothelial cells, as confirmed by coimmunoprecipitation; shear stress reduces this interaction. Myo1c knockout inhibits Jagged1 polarization downstream of shear and its nucleograde transport, while Myo1c knockdown reduces membrane levels of Jagged1 under static but not shear conditions, revealing a role for Myo1c in hemodynamic control of Jagged1 localization. Jagged1-APEX2 proximity labeling, co-immunoprecipitation, Myo1c knockout/knockdown, orbital shaker shear stress platform, confocal imaging of Jagged1 localization iScience Medium 41321631

Source papers

Stage 0 corpus · 119 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2006 Global, in vivo, and site-specific phosphorylation dynamics in signaling networks. Cell 2861 17081983
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
2009 Defining the human deubiquitinating enzyme interaction landscape. Cell 1282 19615732
2004 Large-scale characterization of HeLa cell nuclear phosphoproteins. Proceedings of the National Academy of Sciences of the United States of America 1159 15302935
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
2007 Large-scale mapping of human protein-protein interactions by mass spectrometry. Molecular systems biology 733 17353931
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
2008 Large-scale proteomics and phosphoproteomics of urinary exosomes. Journal of the American Society of Nephrology : JASN 607 19056867
2011 Mapping the NPHP-JBTS-MKS protein network reveals ciliopathy disease genes and pathways. Cell 507 21565611
2022 OpenCell: Endogenous tagging for the cartography of human cellular organization. Science (New York, N.Y.) 432 35271311
2005 Diversification of transcriptional modulation: large-scale identification and characterization of putative alternative promoters of human genes. Genome research 409 16344560
2007 Functional specialization of beta-arrestin interactions revealed by proteomic analysis. Proceedings of the National Academy of Sciences of the United States of America 360 17620599
2021 A proximity-dependent biotinylation map of a human cell. Nature 339 34079125
2004 Nuclear actin and myosin I are required for RNA polymerase I transcription. Nature cell biology 327 15558034
2004 Transcriptome characterization elucidates signaling networks that control human ES cell growth and differentiation. Nature biotechnology 266 15146197
2022 EWSR1-induced circNEIL3 promotes glioma progression and exosome-mediated macrophage immunosuppressive polarization via stabilizing IGF2BP3. Molecular cancer 257 35031058
1999 Functional association of Nmi with Stat5 and Stat1 in IL-2- and IFNgamma-mediated signaling. Cell 251 9989503
2009 Proteomic analysis of human parotid gland exosomes by multidimensional protein identification technology (MudPIT). Journal of proteome research 237 19199708
2017 Optimized fragmentation schemes and data analysis strategies for proteome-wide cross-link identification. Nature communications 221 28524877
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
2015 ∆F508 CFTR interactome remodelling promotes rescue of cystic fibrosis. Nature 209 26618866
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
2018 An AP-MS- and BioID-compatible MAC-tag enables comprehensive mapping of protein interactions and subcellular localizations. Nature communications 201 29568061
2000 A myosin I isoform in the nucleus. Science (New York, N.Y.) 197 11030652
2008 Myosin I can act as a molecular force sensor. Science (New York, N.Y.) 192 18599791
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
2004 Unconventional myosin Myo1c promotes membrane fusion in a regulated exocytic pathway. Molecular and cellular biology 140 15169906
2002 A novel tricomplex of BRCA1, Nmi, and c-Myc inhibits c-Myc-induced human telomerase reverse transcriptase gene (hTERT) promoter activity in breast cancer. The Journal of biological chemistry 102 11916966
2008 CaMKII-mediated phosphorylation of the myosin motor Myo1c is required for insulin-stimulated GLUT4 translocation in adipocytes. Cell metabolism 98 19046570
1996 Isolation and characterization of Nmi, a novel partner of Myc proteins. Oncogene 93 8668343
2012 Myo1c regulates lipid raft recycling to control cell spreading, migration and Salmonella invasion. Journal of cell science 77 22328521
2017 NMI and IFP35 serve as proinflammatory DAMPs during cellular infection and injury. Nature communications 76 29038465
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
2009 Nmi (N-Myc interactor) inhibits Wnt/beta-catenin signaling and retards tumor growth. International journal of cancer 64 19358268
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
2013 Negative regulation of Nmi on virus-triggered type I IFN production by targeting IRF7. Journal of immunology (Baltimore, Md. : 1950) 55 23956435
2008 A Rictor-Myo1c complex participates in dynamic cortical actin events in 3T3-L1 adipocytes. Molecular and cellular biology 55 18426911
2006 The PH domain containing protein CKIP-1 binds to IFP35 and Nmi and is involved in cytokine signaling. Cellular signalling 55 17197158
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
2000 Interferon-inducible Myc/STAT-interacting protein Nmi associates with IFP 35 into a high molecular mass complex and inhibits proteasome-mediated degradation of IFP 35. The Journal of biological chemistry 51 10950963
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
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
1998 Interferon-induced upregulation and cytoplasmic localization of Myc-interacting protein Nmi. Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research 36 9781816
2012 A critical role of N-myc and STAT interactor (Nmi) in foot-and-mouth disease virus (FMDV) 2C-induced apoptosis. Virus research 35 22974759
2011 The Arabidopsis Myb genes MYR1 and MYR2 are redundant negative regulators of flowering time under decreased light intensity. The Plant journal : for cell and molecular biology 35 21255164
1999 Nmi protein interacts with regions that differ between MycN and Myc and is localized in the cytoplasm of neuroblastoma cells in contrast to nuclear MycN. Oncogene 34 10597290
2016 N-Myc-interacting protein (NMI) negatively regulates epithelial-mesenchymal transition by inhibiting the acetylation of NF-κB/p65. Cancer letters 33 27012186
2007 Calcium regulation of calmodulin binding to and dissociation from the myo1c regulatory domain. Biochemistry 33 17910470
2005 The high-mobility group transcription factor Sox10 interacts with the N-myc-interacting protein Nmi. Journal of molecular biology 32 16214168
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
1999 Subcellular localization of interferon-inducible Myc/stat-interacting protein Nmi is regulated by a novel IFP 35 homologous domain. Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research 29 10574616
2007 CIB1 and CaBP1 bind to the myo1c regulatory domain. Journal of muscle research and cell motility 25 17994197
2021 NMI Facilitates Influenza A Virus Infection by Promoting Degradation of IRF7 through TRIM21. American journal of respiratory cell and molecular biology 24 33761305
2021 Disruption of STAT5A and NMI signaling axis leads to ISG20-driven metastatic mammary tumors. Oncogenesis 24 34078871
2019 The motor protein Myo1c regulates transforming growth factor-β-signaling and fibrosis in podocytes. Kidney international 24 31097328
2017 NMI inhibits cancer stem cell traits by downregulating hTERT in breast cancer. Cell death & disease 23 28492540
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
2012 NMI mediates transcription-independent ARF regulation in response to cellular stresses. Molecular biology of the cell 22 23034180
2007 Stability of Nmi protein is controlled by its association with Tip60. Molecular and cellular biochemistry 22 17406968
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
2002 Intracellular redistribution of interferon-inducible proteins Nmi and IFP 35 in apoptotic cells. Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research 19 11911807
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
2017 NMI promotes hepatocellular carcinoma progression via BDKRB2 and MAPK/ERK pathway. Oncotarget 16 28077802
2005 STAT1 and Nmi are downstream targets of Ets-1 transcription factor in MCF-7 human breast cancer cell. FEBS letters 16 15996661
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
2023 Interaction of Nmi and IFP35 Promotes Mutual Protein Stabilization and IRF3 and IRF7 Degradation to Suppress Type I IFN Production in Teleost Fish. Journal of immunology (Baltimore, Md. : 1950) 12 37010945
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
2005 A comparison of the cyclooxygenase inhibitor-NO donors (CINOD), NMI-1182 and AZD3582, using in vitro biochemical and pharmacological methods. Biochemical pharmacology 9 16168964
2014 Nmi interacts with Hsp105β and enhances the Hsp105β-mediated Hsp70 expression. Experimental cell research 8 25088258
2019 NMI promotes cell proliferation through TGFβ/Smad pathway by upregulating STAT1 in colorectal cancer. Journal of cellular physiology 7 31230364
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
2017 Interferon activates promoter of Nmi gene via interferon regulator factor-1. Molecular and cellular biochemistry 7 28913576
2023 NMI Functions as Immuno-regulatory Molecule in Sepsis by Regulating Multiple Signaling Pathways. Inflammation 6 37679586
2017 NSR1/MYR2 is a negative regulator of ASN1 expression and its possible involvement in regulation of nitrogen reutilization in Arabidopsis. Plant science : an international journal of experimental plant biology 6 28818378
2017 Etoposide induced NMI promotes cell apoptosis by activating the ARF-p53 signaling pathway in lung carcinoma. Biochemical and biophysical research communications 6 29030066
2024 A noncanonical E3 ubiquitin ligase RNF41-mediated MYO1C stability promotes prostate cancer metastasis by inducing actin remodeling. Oncogene 4 39112516
2023 NMI promotes tumor progression and gemcitabine resistance in pancreatic cancer via STAT3-IFIT3 axis. Molecular carcinogenesis 3 37846815
2023 RAB31 in glioma-derived endothelial cells promotes glioma cell invasion via extracellular vesicle-mediated enrichment of MYO1C. FEBS open bio 3 37953466
2020 Strain-specific disruption of interferon-stimulated N-myc and STAT interactor (NMI) function by Toxoplasma gondii type I ROP18 in human cells. Parasitology 3 32729455
2022 Molecular characterization and transcriptional conservation of N-myc-interactor, Nmi, by type I and type II IFNs in mandarin fish Siniperca chuatsi. Developmental and comparative immunology 2 35051525
2015 DFT studies on the mechanism of alcohol oxidation by the (bpy)Cu(I)-TEMPO/NMI catalytic system. Dalton transactions (Cambridge, England : 2003) 2 25799480
2024 Recessive variants in MYO1C as a potential novel cause of proteinuric kidney disease. Pediatric nephrology (Berlin, Germany) 1 38904753
2026 NMI as a Novel pro-inflammatory Driver in Acute Pancreatitis Via PI3K-AKT Mediated Macrophage Activation. Inflammation 0 41553561
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 NMI promotes the secretion of IL-17 and exacerbates psoriasis. Proceedings of the National Academy of Sciences of the United States of America 0 41779795
2026 NMI Promotes Pro-Inflammatory Macrophage Polarization and Exacerbates. Inflammation 0 41862739
2025 Theranostic Near-Infrared Monoamine Oxidase Inhibitor (NMI) Protein Binding Interactions with MAOA and Albumin. Pharmaceutical research 0 39904854
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
2025 Multi-Source Porosity Image Normalization (NMI) in Selective Laser Melting for Reliable Reuse of Heterogeneous Microstructural Data. Materials (Basel, Switzerland) 0 41470352
2024 Recessive variants in MYO1C as a potential novel cause of proteinuric kidney disease. Research square 0 38659911
2024 NMI, POLR3G and APIP are the key molecules connecting glaucoma with high intraocular pressure: a clue for early diagnostic biomarker candidates. International journal of ophthalmology 0 39559319
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