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anti-Human MYO1E Antibodies:
anti-Rat (Rattus) MYO1E Antibodies:
anti-Mouse (Murine) MYO1E Antibodies:
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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 (show EPHB2 Antibodies) signaling pathway thus promotes cell motility through regulation of the subcellular localization of Myo1E.
Coinheritance of COL4A5 (show COL4a5 Antibodies) 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 (show NEIL1 Antibodies) 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 (show MYO1C Antibodies)).
Two proteins with prominent functions in endocytosis, synaptojanin-1 (show SYNJ1 Antibodies) and dynamin (show DNM1 Antibodies), bind to the SH3 domain (show ITSN1 Antibodies) of human Myo1E.
the LSP1 (show LSP1 Antibodies)-myosin1e bimolecular complex plays a pivotal role in the regulation of actin cytoskeleton remodeling during Fc gamma receptor (show FCGR1A Antibodies)-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.
Myo1e plays an important role in podocyte function and normal glomerular filtration.
Myosins are actin-based motor molecules with ATPase activity. Unconventional myosins serve in intracellular movements. Their highly divergent tails are presumed to bind to membranous compartments, which would be moved relative to actin filaments (By similarity).
MYO1E variant protein
, unconventional myosin 1E
, unconventional myosin-Ie
, Unconventional myosin from rat 5
, myosin heavy chain myr 3
, molecular motor
, unconventional myosin-If
, LOW QUALITY PROTEIN: unconventional myosin-Ie