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anti-Mouse (Murine) Myosin VIIA Antibodies:
anti-Human Myosin VIIA Antibodies:
anti-Rat (Rattus) Myosin VIIA Antibodies:
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Human Polyclonal Myosin VIIA Primary Antibody for ICC, IF - ABIN4337560
Mellott, Devarajan, Shinogle, Moore, Talata, Laurence, Forrest, Noji, Tanaka, Staecker, Detamore: Nonviral Reprogramming of Human Wharton's Jelly Cells Reveals Differences Between ATOH1 Homologues. in Tissue engineering. Part A 2015
Show all 3 Pubmed References
Cow (Bovine) Polyclonal Myosin VIIA Primary Antibody for WB - ABIN267167
Tan, Lee, Ruan: Bone-marrow-derived cells that home to acoustic deafened cochlea preserved their hematopoietic identity. in The Journal of comparative neurology 2008
CK selectively interacts with the initiator caspase DRONC and regulates some of its non-apoptotic functions. Results expose a conserved role for unconventional myosins in transducing caspase-dependent regulation of kinases.
Data suggest that Crinkled acts in concert with Wingless targets to orchestrate the proper shaping of denticles in the Drosophila embryonic epidermis.
Product identified as myosin VIIA.
Loss of ck/myoVIIA function leads to complete deafness in Drosophila by disrupting the integrity of the scolopidia that transduce auditory signals.
myosin VIIA is classified to be a high duty ratio motor
kinetic behavior would allow myosin VIIa to exert and hold tension on actin filaments and, if dimerized, to function as a processive cargo transporter.
domain markedly inhibits the actin-activated ATPase activity of tailless DM7A at low Ca(2+) but not high Ca(2+)
Study identified a new hair cell-specific enhancer located within Intron 2-3 of zebrafish myo7aa gene and highly conserved between species
Zebrafish cone photoreceptors possess a large and well-differentiated accessory outer segment, in which the unconventional motor protein Myo7a is highly enriched.
Data show that myo7a is localized in actin-rich ellipsoids of fish cones.
Many of the genes found in the genetic network, pathways, and gene ontology categories of Myo7a are related to either deafness or blindness in Usher syndrome mouse model.
Here, the authors show that exophilin-8 accumulates granules in the cortical F-actin network not by direct interaction with myosin-Va, but by indirect interaction with a specific form of myosin-VIIa through its previously unknown binding partner, RIM-BP2.
MYO7A and PDZD7 interact in tissue-culture cells, and co-localize to the ankle-link region of stereocilia in wild-type but not Myo7a mutant mice.
MYO7A binds to and impinges on CASPASE-8, revealing a new regulatory axis affecting RIPK1>CASPASE-8 signaling. Results expose a conserved role for unconventional myosins in transducing caspase-dependent regulation of kinases.
Myo7a interacts with integrin beta5 and selectively promotes integrin alphavbeta5-mediated cell migration
Data show that myosin7a (Myo7a; sh1) deficiency causes severe retinal dysfunctions in albino sh1-/- mice.
The family was found to segregate novel mutations of two different genes: myosin VIIA (MYO7A), and phosphodiesterase 6B, which causes nonsyndromic retinitis pigmentosa.
the importance of MYO7A for the development and maintenance of bundle function
the results support a role for MYO7A in the translocation of RPE65, illustrating the involvement of a molecular motor in the spatiotemporal organization of the retinoid cycle in vision.
the myosin VIIa is a "slow", monomeric molecular motor with a duty ratio of 0.6.
we examine the effects of null mutation of the Ush1c gene on subcellular localization of Myo7a, Pcdh15 and Sans in the inner ear.
crystal structure of MYO7A MyTH4-FERM domains in complex with the central domain (CEN) of Sans at 2.8 angstrom resolution; MyTH4-FERM/CEN complex structure provides mechanistic explanations for known deafness-causing mutations in MYO7A MyTH4-FERM
Cadherin-23, myosin VIIa and harmonin form a ternary complex and interact with phospholipids.
MyosinVIIa interacts with Twinfilin-2 at the tips of mechanosensory stereocilia in the inner ear
The carboxy-terminal FERM domain of myosin VIIA is critical for melanosome transport in retinal pigment epithelial cells.
participates in anchoring and holding membrane-bound elements to the actin core of the stereocilium
Cdh23 and Myo7a are both required for establishing and/or maintaining the proper organisation of the stereocilia bundle and that they do not genetically interact to affect this process nor to cause age-related hearing loss.
Slac2-c interacts with Rab27, actin, myosin Va and this protein
the shaping of the hair bundle relies on a functional unit composed of myosin VIIa, harmonin b and cadherin 23 that is essential to ensure the cohesion of the stereocilia
Noise-induced hearing loss in 11-12-week-old mice heterozygous for a null allele of Myo7a ( Myo7a(4626SB)) is not significantly different from wild-type littermates.
The Russian USH cohort shows both novel and known USH mutations. Clinically the prevalence of USH2 is low (39.28%) and the frequency of MYO7A mutations responsible for USH1B is very high (63.63%, N = 7/11) compared to other cohorts. These seven patients carrying MYO7A mutations are preliminarily eligible for the UshStat(R) gene therapy.
Crystall structure shows the interactions between Myo7a protein domains and their partners, harmonin and SANS/ANKS4B.
pathogenic mutation c.2011G>A identified in Chinese family with autosomal dominant hearing loss
We report here novel homozygous mutations in various genes causing USH, extending the spectrum of causative mutations. We also prove combined sequencing techniques as useful tools to identify novel disease-causing mutations. To the best of our knowledge, this is the largest report of a genetic analysis of Israeli and Palestinian families (n = 74) with different USH subtypes.
This study extends the spectrum of known MYO7A mutations and proves next generation sequencing as a valuable tool in molecular diagnosis of Usher syndrome.
These findings broaden the phenotype spectrum of the MYO7A gene, and may facilitate understanding of the molecular pathogenesis of the disease, and genetic counseling for the family.
a novel stop gained variant c.4513G > T (p.Glu1505Ter) in MYO7A was found in an Iranian pedigree with two affected members with USH type 1
Two pathogenic variations (c.849+2T>C and c.5994G>A) in MYO7A were successfully identified and individually separated from parents
We found a remarkable genetic heterogeneity in the studied families with USH1 with a variety of mutations, among which three were novel. These novel mutations will be included in the NADf mutation screening chip that will allow a higher diagnosis efficiency of this extremely genetically heterogeneous disease.
Patients carrying mutations in MYO7A had a younger age of onset of hearing and visual impairments than those carrying mutations in USH2A, leading to an earlier diagnosis of the disease in the former patients.
We suggest that this new mutation named c.6079_6081del (p.H2027del) is the main cause of deaf-blindness found in this family clinically diagnosed as USH1B.
Results show the structures of Myo7a IQ5-SAH (single a helix) lever arm extension in complex with apo- and Ca2+-CaM, respectively, reveal that the motor contains an extended and rigid lever arm at low Ca2+ concentration conditions. Increased cellular Ca2+ concentration induces conformational flexibility of the motor and thus regulates its activity.
novel mutation c.3847_3848insTCTG (p. N1285LfsX24) in compound heterozygosity with c.2239_2240delAG in the MYO7A gene is the main cause of USH1 in the proband
report the results of genetic analyses performed on Moroccan families with autosomal recessive non syndromic hearing loss that identified two families with compound heterozygous MYO7A mutations
myosin VIIa movement appears to be suitable for translocating USH1 proteins on stereocilia actin bundles in inner-ear hair cells
In USH1B-MYO7A, constriction rate of EZ extent depends on the initial eccentricity of the transition. Ellipsoid zone edges in the macula correspond to large local changes in cone vision, but extramacular EZ edges show more pronounced losses on rod-based vision tests.
An unreported splice site mutation c.3924+1G > C compound with c.6028G > A in the MYO7A gene were detected to cosegregate with Usher syndrome type 2 in a Han Chinese family.
There are more than 39 deafness genes reported to cause non-syndromic hereditary hearing loss (HHL) in Iran, of which the most prevalent causative genes include GJB2, SLC26A4, MYO15A, and MYO7A. In addition, we highlight some of the more common genetic causes of syndromic HHL in Iran. [review]
This study showed that Mendelian sensorineural hearing loss exhibits vestibular dysfunction, including DFNA9, DFNA11, DFNA15 and DFNA28.
The novel compound heterozygous mutations (c.3671C>A and c.390_391insC) in MYO7A gene identified in this study were responsible for the autosomal recessive sensorineural hearing loss of this Chinese family
This gene is a member of the myosin gene family. Myosins are mechanochemical proteins characterized by the presence of a motor domain, an actin-binding domain, a neck domain that interacts with other proteins, and a tail domain that serves as an anchor. This gene encodes an unconventional myosin with a very short tail. Defects in this gene are associated with the mouse shaker-1 phenotype and the human Usher syndrome 1B which are characterized by deafness, reduced vestibular function, and (in human) retinal degeneration. Alternative splicing results in multiple transcript variants.
, lethal 27 in the black-reduced region
, lethal group D2
, myosin 7a
, myosin 7a heavy chain
, myosin VII
, myosin VIIa
, myosin heavy chain at 35BC
, mysoin VIIa
, stubby chaetae
, transcription unit D
, myosin VIIA
, myosin 7A
, motor protein
, shaker 1
, unconventional myosin-VIIa
, myosin VIIA (Usher syndrome 1B (autosomal recessive, severe))