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our data suggests that MYO1E contributes to breast tumor malignancy and regulates the differentiation and proliferation state of breast tumor cells.
The ERK signaling pathway thus promotes cell motility through regulation of the subcellular localization of Myo1E.
Coinheritance of COL4A5 and MYO1E mutations accentuate the severity of kidney disease.
Myo1e is a key component contributing to the functional integrity of podocytes.
MYO1E mutations are not a major cause of Chinese familial Steroid-resistant nephrotic syndrome.
Homozygosity mapping and exome sequencing in a consanguineous kindred identified MYO1E and NEIL1 as novel candidate genes for human autosomal recessive steroid-resistant nephrotic syndrome.
MYO1E mutations are associated with childhood-onset, glucocorticoid-resistant focal segmental glomerulosclerosis.
myo1e binds lipids through nonspecific electrostatic interactions rather than a stereospecific protein-phosphoinositide interaction.
The kinetic mechanism of Myo1e (human myosin-IC).
Two proteins with prominent functions in endocytosis, synaptojanin-1 and dynamin, bind to the SH3 domain of human Myo1E.
MYO1E interacts directly with the FAK FERM-kinase linker and induce FAK kinase activity and tyrosine 397 phosphorylation.
the LSP1-myosin1e bimolecular complex plays a pivotal role in the regulation of actin cytoskeleton remodeling during Fc gamma receptor-driven phagocytosis.
Myo1e regulates TLR4-triggered macrophage spreading, chemokine release, and antigen presentation via MHC class II.
Overexpression of Myo1e can enhance podocyte migration ability, endocytosis, and attachment to the glomerular basement membrane
These findings suggest that myo1e represents a component of the slit diaphragm complex and may contribute to regulating junctional integrity in kidney podocytes.
depletion of Myo1E causes reduced transferrin endocytosis and a significant delay in transferrin trafficking to perinuclear compartments, demonstrating an integral role for Myo1E in these actin-mediated steps
myo1e expression in podocytes is necessary for normal glomerular filtration and that podocyte defects are likely to represent the primary pathway leading to glomerular disease associated with Myo1E mutations.
Expressed in both B-cell lines and primary B-lymphocytes.
Myo1e plays an important role in podocyte function and normal glomerular filtration.
This gene encodes a member of the nonmuscle class I myosins which are a subgroup of the unconventional myosin protein family. The unconventional myosin proteins function as actin-based molecular motors. Class I myosins are characterized by a head (motor) domain, a regulatory domain and a either a short or long tail domain. Among the class I myosins, this protein is distinguished by a long tail domain that is involved in crosslinking actin filaments. This protein localizes to the cytoplasm and may be involved in intracellular movement and membrane trafficking. Mutations in this gene are the cause of focal segmental glomerulosclerosis-6. This gene has been referred to as myosin IC in the literature but is distinct from the myosin IC gene located on chromosome 17.
MYO1E variant protein
, unconventional myosin 1E
, unconventional myosin-Ie
, Unconventional myosin from rat 5
, myosin heavy chain myr 3
, molecular motor
, LOW QUALITY PROTEIN: unconventional myosin-Ie