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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 2 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 initia (show CASP8 Antibodies)tor caspase DRONC and regulates some of its non-a (show RIPK1 Antibodies)poptotic f (show CASP8 Antibodies)unctions. Results expose a conserved role for unconventional myosins in transducing caspase-d (show CASP3 Antibodies)ependent 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 (show ACTB Antibodies)-activated ATPase (show DNAH8 Antibodies) activity of tailless (show NR2E1 Antibodies) DM7A at low Ca(2 (show CA2 Antibodies)+) but not high Ca(2 (show CA2 Antibodies)+)
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.
MYO7A and PDZD7 (show PDZD7 Antibodies) 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 (show CASP8 Antibodies), revealing a new regulatory axis affecting RIPK1 (show RIPK1 Antibodies)>CASPASE-8 (show CASP8 Antibodies) signaling. Results expose a conserved role for unconventional myosins in transducing caspase (show CASP3 Antibodies)-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 (show RPE65 Antibodies), illustrating the involvement of a molecular motor (show MYO1B Antibodies) in the spatiotemporal organization of the retinoid cycle in vision.
the myosin VIIa is a "slow", monomeric molecular motor (show MYO1B Antibodies) with a duty ratio of 0.6.
we examine the effects of null mutation of the Ush1c (show USH1C Antibodies) gene on subcellular localization of Myo7a, Pcdh15 (show PCDH15 Antibodies) 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
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 (show ACSM3 Antibodies) (single a helix) lever arm extension in complex with apo (show C9orf3 Antibodies)- and Ca2 (show CA2 Antibodies)+-CaM, respectively, reveal that the motor contains an extended and rigid lever arm at low Ca2 (show CA2 Antibodies)+ concentration conditions. Increased cellular Ca2 (show CA2 Antibodies)+ 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 (show COCH Antibodies), DFNA11, DFNA15 (show POU4F3 Antibodies) and DFNA28 (show GRHL2 Antibodies).
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))