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these results reveal the molecular motor Myo1D as a chiral determinant that is sufficient to break symmetry at all biological scales through chiral interaction with the actin cytoskeleton.
Myo31DF-overexpressing cells suggest that cell-shape chirality was established in each cell and reflects intrinsic planar cell chirality.
DE-Cadherin regulates unconventional Myosin ID and Myosin IC in Drosophila left-right asymmetry establishment.
left-right(LR)directional rotation of hindgut epithelial tube; DECad is distributed to cell boundaries with LR asymmetry which is responsible for planar cell-shape chirality formation; myosin ID switches LR polarity found in PCC and in DE-Cad distribution
the actin cytoskeleton and myosin I proteins may be crucial for generating left-right asymmetry in invertebrates
Myo31DF interacts and colocalizes with beta-catenin, suggesting that situs inversus genes can direct left-right development through the adherens junction
the organ specificities of the Myo31DF and Myo61F activities depended on their head regions
These data do not support a causal relationship of variants in MYO1A to sensorineural hearing loss. We suggest that the genotypic ascertainment method is useful to objectively evaluate gene-phenotype associations.
This is the first time a haplotype on chromosome 12 containing sequence variants in the genes DCTN2, DNAH10, LRIG3, and MYO1A has been linked to an inherited neuropathy in humans.
One missense variant, p.R544W, was found in the MYO1A gene, and in silico analysis suggested that this variant has deleterious effects on protein function.
Most of the altogether 10 MYO1A mutations are annotated in dbSNP, and population frequencies (dbSNP, 1000 Genomes, Exome Sequencing Project) above 0.1% contradict pathogenicity under a dominant model
findings suggest that MYO1A has tumor suppressor activity in the normal gastric epithelium but not in the normal endometrium and inactivation of MYO1A either genetically or epigenetically may confer gastric epithelial cells a growth ad
Myo1a targeting to microvilli is driven by membrane binding potential that is distributed throughout TH1 rather than localized to a single motif.
results identify MYO1A as a unique tumor-suppressor gene in colorectal cancer and demonstrate that the loss of structural brush border proteins involved in cell polarity are important for tumor development
MYO1A (brush border myosin I) dynamics in the brush border of LLC-PK1-CL4 cells
mapping of a novel autosomal dominant non-syndromic deafness locus, DFNA48, to chromosome 12q13-q14 in an Italian family
Multiple mutations of MYO1A, a cochlear-expressed gene, were studied in sensorineural hearing loss.
This movement is based on an active and directed process that is facilitated by an acto-NMI complex, establishing for the first time a functional role for a motor complex consisting of actin and a myosin in the nucleus.
These data are the first to suggest that mechanical activity is essential for proper localization of Myo1a in microvilli.
Sensing molecular tension is crucial for a wide array of cellular processes. Myosin I dramatically alters its motile properties in response to tension.
Myo1a and Myo6 play essential roles in response to intestinal mucosal injury
The data indicates that Myo1a is an important regulator of CFTR traffic and anion transport in the brush border membrane of villus enterocytes.
Data suggest that Myo1d may be the primary compensating class I myosin in the Myo1a KO model; they also suggest that dynamics govern the localization and function of different yet closely related myosins that target common actin structures.
Actin filaments and myosin I alpha cooperate with microtubules for the movement of lysosomes
RT-PCR analysis of RNA extracted from the inner ear and cochlea of mice helped in the evaluation of MYO1A expression.
critical multifunctional component of the enterocyte, required for maintaining the normal composition and highly ordered structure of the brush border
These studies show that class I myosins directly control the mechanical properties of the cell membrane; they also position these motor proteins as master regulators of cellular events involving membrane deformation.
This gene encodes a member of the myosin superfamily. The protein represents an unconventional myosin\; it should not be confused with the conventional skeletal muscle myosin-1 (MYH1). Unconventional myosins contain the basic domains characteristic of conventional myosins and are further distinguished from class members by their tail domains. They function as actin-based molecular motors. Mutations in this gene have been associated with autosomal dominant deafness. Alternatively spliced variants have been found for this gene.
, myosin 1D
, myosin 1a
, myosin 31DF
, myosin I
, myosin IA
, myosin ID
, unconventional myosin 31DF
, brush border myosin I
, myosin I heavy chain
, myosin, heavy polypeptide-like (100kD)
, unconventional myosin-Ia
, brush border myosin 1
, myosin, heavy polypeptide-like (110kD)
, brush border myosin-I
, myosin heavy polypeptide 1 skeletal muscle adult
, brush border 110 kDa protein
, brush border myosin I heavy chain