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the LSP1 (show LSP1 ELISA Kits)-myosin1e bimolecular complex plays a pivotal role in the regulation of actin cytoskeleton remodeling during Fc gamma receptor (show FCGR1A ELISA Kits)-driven phagocytosis.
We propose a novel genome-wide mechanism where myosin synergizes with Pol II-associated actin to link the polymerase machinery with permissive chromatin for transcription activation.
Our observations demonstrate specific changes in the expression of myosin IC (show MYO1C ELISA Kits) isoform A that are concurrent with the occurrence of prostate cancer in the TRAMP (show DPT ELISA Kits) mouse prostate cancer model that closely mimics clinical prostate cancer
Myo1e regulates TLR4-triggered macrophage spreading, chemokine release, and antigen presentation via MHC class II.
Ca(2+) binding to calmodulin induces major conformational changes in both IQ motifs and the post-IQ domain and increases flexibility of the myosin-1c tail.
Myo1e is a key component contributing to the functional integrity of podocytes.
Overexpression of Myo1e can enhance podocyte migration ability, endocytosis, and attachment to the glomerular basement membrane
The v-Crk-myosin-1c interaction, which modulates membrane dynamics by regulating Rac1 activity, is crucial for cell adhesion and spreading.
These findings suggest that myo1e represents a component of the slit diaphragm complex and may contribute to regulating junctional integrity in kidney podocytes.
Mouse nuclear myosin I knock-out shows interchangeability and redundancy of myosin isoforms in the cell nucleus.
The ERK (show EPHB2 ELISA Kits) signaling pathway thus promotes cell motility through regulation of the subcellular localization of Myo1E.
Coinheritance of COL4A5 (show COL4a5 ELISA Kits) and MYO1E mutations accentuate the severity of kidney disease.
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 ELISA Kits) 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 ELISA Kits)).
Two proteins with prominent functions in endocytosis, synaptojanin-1 (show SYNJ1 ELISA Kits) and dynamin (show DNM1 ELISA Kits), bind to the SH3 domain (show ITSN1 ELISA Kits) of human Myo1E.
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.
, myosin I beta
, nuclear myosin I beta
, unconventional myosin-Ic
, MYO1E variant protein
, unconventional myosin 1E
, unconventional myosin-Ie
, molecular motor
, Unconventional myosin from rat 5
, myosin heavy chain myr 3