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Myosin IIIA

MYO3A, myosin IIIA, DFNB30
The protein encoded by this gene belongs to the myosin superfamily. Myosins are actin-dependent motor proteins and are categorized into conventional myosins (class II) and unconventional myosins (classes I and III through XV) based on their variable C-terminal cargo-binding domains. Class III myosins, such as this one, have a kinase domain N-terminal to the conserved N-terminal motor domains and are expressed in photoreceptors. The protein encoded by this gene plays an important role in hearing in humans. Three different recessive, loss of function mutations in the encoded protein have been shown to cause nonsyndromic progressive hearing loss. Expression of this gene is highly restricted, with the strongest expression in retina and cochlea. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: Actin, Myo3B, CAN, ATPase, HAIR
Papers on MYO3A
Class III myosins shape the auditory hair bundles by limiting microvilli and stereocilia growth.
Petit et al., Paris, France. In J Cell Biol, Feb 2016
Myosin IIIa, defective in the late-onset deafness form DFNB30, has been proposed to transport espin-1 to the tips of stereocilia, thereby promoting their elongation.
Identifying Children With Poor Cochlear Implantation Outcomes Using Massively Parallel Sequencing.
Wu et al., Taipei, Taiwan. In Medicine (baltimore), Jul 2015
Mutations in the WFS1, GJB3, ESRRB, LRTOMT, MYO3A, and POU3F4 genes were detected in 7 (23%) of the 30 matched controls.
Phosphorylation of the kinase domain regulates autophosphorylation of myosin IIIA and its translocation in microvilli.
Ikebe et al., Worcester, United States. In Biochemistry, 2015
To investigate the role of the kinase activity on the transporter function of myosin IIIA (Myo3A), we identified the phosphorylation sites of kinase domain (KD), which is responsible for the regulation of kinase activity and thus motor function.
Invertebrate and vertebrate class III myosins interact with MORN repeat-containing adaptor proteins.
O'Tousa et al., Richmond, United States. In Plos One, 2014
Co-precipitation experiments demonstrated that human MORN4 binds to human myosin IIIA (MYO3A).
Strategy for the customized mass screening of genetic sensorineural hearing loss in koreans.
Choi et al., Seoul, South Korea. In Korean J Audiol, 2014
The other causative genes were MRNR1, WFS1, COCH, TECTA, MYO6, COL11A2, EYA4, GJB3, OTOF, STRC, MYO3A, and GJB2.
Myosin 3A kinase activity is regulated by phosphorylation of the kinase domain activation loop.
Yengo et al., United States. In J Biol Chem, 2014
The kinase activity of MYO3A 2IQ with the phosphomimic (T184E) or phosphoblock (T184A) mutations demonstrates that kinase activity is reduced 30-fold as a result of the T184A mutation, although the Thr-178 site only had a minor impact on kinase activity.
Kinome-wide screening of HER2+ breast cancer cells for molecules that mediate cell proliferation or sensitize cells to trastuzumab therapy.
Mak et al., Toronto, Canada. In Oncogenesis, 2013
Antagonism using the SI identified MYO3A, MYO3B and MPZL1 as antagonizers to trastuzumab treatment among HER2+ cell lines.
Examination of whole blood DNA methylation as a potential risk marker for gastric cancer.
Issa et al., Philadelphia, United States. In Cancer Prev Res (phila), 2013
Quantitative methylation-specific real-time PCR was also conducted for 3 CpG island promoters (MINT25, MYO3A, and SOX11).
A study of GJB2 and delGJB6-D13S1830 mutations in Brazilian non-syndromic deaf children from the Amazon region.
dos Santos et al., Belém, Brazil. In Braz J Otorhinolaryngol, 2013
Mutations in the connexin 26 (GJB2) gene rank among the most frequent causes of non-syndromic deafness in different populations, while delGJB6-D13S1830 mutation located in the DFNB30 locus is known to cause sensorineural hearing loss.
Diagnostic application of targeted resequencing for familial nonsyndromic hearing loss.
Park et al., Seoul, South Korea. In Plos One, 2012
Finally NSHL-causing candidate mutations were identified in 13(65%) of the 20 probands of multiplex families, bringing the total solve rate (or detection rate) in our familial cases to be 78.1% (25/32) Damaging mutations discovered by the targeted resequencing were distributed in nine genes such as WFS1, COCH, EYA4, MYO6, GJB3, COL11A2, OTOF, STRC and MYO3A, most of which were private.
Myosin IIIB uses an actin-binding motif in its espin-1 cargo to reach the tips of actin protrusions.
Kachar et al., Bethesda, United States. In Curr Biol, 2012
Myosin IIIA (MYO3A) targets actin protrusion tips using a motility mechanism dependent on both motor and tail actin-binding activity [1].
Detection of bladder cancer using novel DNA methylation biomarkers in urine sediments.
Issa et al., Houston, United States. In Cancer Epidemiol Biomarkers Prev, 2011
RESULTS: Based on a multigene predictive model, we discovered 6 methylation markers (MYO3A, CA10, SOX11, NKX6-2, PENK, and DBC1) as most promising for detecting bladder cancer.
A mouse model for human hearing loss DFNB30 due to loss of function of myosin IIIA.
King et al., Seattle, United States. In Mamm Genome, 2011
Homozygosity and compound heterozygosity for loss-of-function mutations in MYO3A, which encodes myosin IIIA, are responsible for inherited human progressive hearing loss DFNB30.
Intermolecular autophosphorylation regulates myosin IIIa activity and localization in parallel actin bundles.
Yengo et al., State College, United States. In J Biol Chem, 2010
Results suggest that Myo3A motor activity is regulated through a mechanism involving concentration-dependent autophosphorylation.
Genome-wide association study for colorectal cancer identifies risk polymorphisms in German familial cases and implicates MAPK signalling pathways in disease susceptibility.
Hemminki et al., Heidelberg, Germany. In Carcinogenesis, 2010
Two other unreported SNPs, rs6038071, 40 kb upstream of CSNK2A1 (casein kinase 2, alpha 1 polypeptide) and an intronic marker in MYO3A (myosin IIIA), rs11014993, associated with CRC only in the familial CRC cases (P = 2.5 x 10(-3), recessive model, and P = 2.7 x 10(-4), dominant model).
Polymorphisms in the GAD2 gene-region are associated with susceptibility for unipolar depression and with a risk factor for anxiety disorders.
Binder et al., München, Germany. In Am J Med Genet B Neuropsychiatr Genet, 2010
behavioral inhibition-associated SNPs appear to be associated with differences in MYO3A- but not GAD2 lymphoblastoid-mRNA expression levels
The kinase domain alters the kinetic properties of the myosin IIIA motor.
Yengo et al., Berkeley, United States. In Biochemistry, 2008
A model in which the activity and concentration of myosin IIIA localized to the tips of actin bundles mediates the morphology of the tips in sensory cells.
Kinetic mechanism of human myosin IIIA.
Yengo et al., Berkeley, United States. In J Biol Chem, 2007
the actomyosin-ADP state may be important for the ability of myosin III to function as a cellular transporter and actin cross-linker in the actin bundles of sensory cells
Human myosin III is a motor having an extremely high affinity for actin.
Ikebe et al., Worcester, United States. In J Biol Chem, 2007
myosin IIIA can spend a majority of its ATP hydrolysis cycling time on actin
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