Use your antibodies-online credentials, if available.
No Products on your Comparison List.
Your basket is empty.
Find out more
Show all species
Show all synonyms
Select your species and application
anti-Mouse (Murine) Antibodies:
anti-Rat (Rattus) Antibodies:
Go to our pre-filtered search.
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 (show MYO1D Antibodies) and Myosin IC (show MYO1C Antibodies) 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 (show CAD Antibodies) distribution
the actin (show ACTB Antibodies) 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 (show DCTN2 Antibodies), DNAH10 (show DNAH10 Antibodies), 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 (show TH1L Antibodies) 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 (show PKLR Antibodies)-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.
Myo1a and Myo6 (show MYO6 Antibodies) play essential roles in response to intestinal mucosal injury
The data indicates that Myo1a is an important regulator of CFTR (show CFTR Antibodies) 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 (show MYO1B Antibodies) 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.
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