Target intelligence / Profile preview

Myosin IC (MYO1C)

Target
MYO1C
Molecular classification
Enzyme (ATPase activity), Motor protein (Actin-based), Cytoskeletal protein, Membrane-associated protein
01

Overview

Myosin IC is a **class I unconventional myosin**—an actin-based molecular motor protein with ATPase activity. It is found throughout the cytoplasm and associates with membranes, including the plasma membrane and endosomes, using its pleckstrin homology (PH) domain to bind phosphoinositides. MYO1C supports membrane transport, vesicle trafficking, and remodeling, and is critical in linking the actin cytoskeleton to membrane structures. Its ATP-dependent power stroke features unique kinetics, making it highly responsive to mechanical tension and critical for adapting to cellular forces. In the nucleus, a specific isoform (NM1) regulates chromatin remodeling and gene transcription initiation. MYO1C is essential for processes such as glucose transporter recycling (insulin-stimulated GLUT4 movement), mechanotransduction in sensory hair cells, cell adhesion, and epithelial junction stability. Disease relevance includes its role in non-syndromic hereditary deafness, podocyte and epithelial integrity, and possibly metabolic regulation. This protein is highly conserved and involved in fundamental aspects of cell structure and signaling[2][5][6][7][9].

Other names
Unconventional myosin-IcMMI-betaMMIbmyr2NMIMyoICMyosin I betanuclear myosin IMyosin-Icmyosin-I betamyosin IC
02

Mechanism of action

Not applicable or documented for MYO1C directly. Drugs that influence actin dynamics, membrane tension, or insulin signaling could theoretically modulate MYO1C activity indirectly, but direct mechanisms are not described in the literature.

03

Biological functions

Intracellular transport (membrane and vesicle movement)Actin cytoskeleton dynamicsMembrane remodeling and tension sensingRegulation of transcription (participates in chromatin remodeling complexes)Mechanosensation (especially in sensory hair cells)Endocytosis and exocytosisCell adhesion and migration
04

Disease associations

Sensorineural deafness (Hereditary deafness, DFNA[5])Granulomatous amebic encephalitis[5]Involvement in diabetes/insulin signaling (GLUT4 recycling)[5][9]Possible roles in cell migration, cancer, tissue integrity (e.g., kidney podocyte function)[2][4]Neurodevelopment and mechanotransduction disorders
05

Safety considerations

Potential risk if altered MYO1C disrupts membrane trafficking, insulin response, or mechanosensation.Challenges include gene redundancy, compensation by other myosins, and systemic effects given its widespread tissue distribution.Off-target effects could impact hearing, metabolic pathways, or cell adhesion[5][9]
06

Biomarkers

Possible use in hereditary sensorineural deafness screening (DFNA hearing loss genes)Cytoskeletal/membrane trafficking disordersNot established for therapy monitoring; research context only[5]

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