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    MYO3A myosin IIIA [ Homo sapiens (human) ]

    Gene ID: 53904, updated on 2-Nov-2024

    GeneRIFs: Gene References Into Functions

    GeneRIFPubMed TitleDate
    The dynamics of actin protrusions can be controlled by tip-localized myosin motors.

    The dynamics of actin protrusions can be controlled by tip-localized myosin motors.
    Cirilo JA Jr, Liao X, Perrin BJ, Yengo CM., Free PMC Article

    02/7/2024
    Molecular insights into MYO3A kinase domain variants explain variability in both severity and progression of DFNB30 hearing impairment.

    Molecular insights into MYO3A kinase domain variants explain variability in both severity and progression of DFNB30 hearing impairment.
    Souissi A, Abdelmalek Driss D, Chakchouk I, Ben Said M, Ben Ayed I, Mosrati MA, Elloumi I, Tlili A, Aifa S, Masmoudi S.

    12/24/2022
    Deafness mutation in the MYO3A motor domain impairs actin protrusion elongation mechanism.

    Deafness mutation in the MYO3A motor domain impairs actin protrusion elongation mechanism.
    Gunther LK, Cirilo JA Jr, Desetty R, Yengo CM., Free PMC Article

    03/26/2022
    Frequency and origin of the c.2090T>G p.(Leu697Trp) MYO3A variant associated with autosomal dominant hearing loss.

    Frequency and origin of the c.2090T>G p.(Leu697Trp) MYO3A variant associated with autosomal dominant hearing loss.
    Bueno AS, Nunes K, Dias AMM, Alves LU, Mendes BCA, Sampaio-Silva J, Smits J, Yntema HG, Meyer D, Lezirovitz K, Mingroni-Netto RC., Free PMC Article

    03/26/2022
    Whole exome sequencing reveals pathogenic variants in MYO3A, MYO15A and COL9A3 and differential frequencies in ancestral alleles in hearing impairment genes among individuals from Cameroon.

    Whole exome sequencing reveals pathogenic variants in MYO3A, MYO15A and COL9A3 and differential frequencies in ancestral alleles in hearing impairment genes among individuals from Cameroon.
    Wonkam A, Manyisa N, Bope CD, Dandara C, Chimusa ER., Free PMC Article

    10/2/2021
    A novel missense variant in MYO3A is associated with autosomal dominant high-frequency hearing loss in a German family.

    A novel missense variant in MYO3A is associated with autosomal dominant high-frequency hearing loss in a German family.
    Doll J, Hofrichter MAH, Bahena P, Heihoff A, Segebarth D, Müller T, Dittrich M, Haaf T, Vona B., Free PMC Article

    05/15/2021
    Characterization of a novel MYO3A missense mutation associated with a dominant form of late onset hearing loss.

    Characterization of a novel MYO3A missense mutation associated with a dominant form of late onset hearing loss.
    Dantas VGL, Raval MH, Ballesteros A, Cui R, Gunther LK, Yamamoto GL, Alves LU, Bueno AS, Lezirovitz K, Pirana S, Mendes BCA, Yengo CM, Kachar B, Mingroni-Netto RC., Free PMC Article

    10/12/2019
    MYO3A is more efficient than MYO3B at increasing formation and elongation of stable microvilli on the surface of cultured epithelial cells.

    Impact of the Motor and Tail Domains of Class III Myosins on Regulating the Formation and Elongation of Actin Protrusions.
    Raval MH, Quintero OA, Weck ML, Unrath WC, Gallagher JW, Cui R, Kachar B, Tyska MJ, Yengo CM., Free PMC Article

    05/27/2017
    The structures of Myo3 in complex with Espin1 not only elucidate the mechanism of the binding, but also reveal a Myo3-induced release of Espin1 auto-inhibition mechanism.

    Myosin III-mediated cross-linking and stimulation of actin bundling activity of Espin.
    Liu H, Li J, Raval MH, Yao N, Deng X, Lu Q, Nie S, Feng W, Wan J, Yengo CM, Liu W, Zhang M., Free PMC Article

    01/14/2017
    Study reports an amino acid substitution in MYO3A motor-head domain disrupting its ATPase activity that can cause autosomal dominant progressive hereditary hearing loss. Also, these results uncovered a novel interaction between MYO3A and PCDH15 shedding new light on the function of myosin IIIA at stereocilia tips.

    MYO3A Causes Human Dominant Deafness and Interacts with Protocadherin 15-CD2 Isoform.
    Grati M, Yan D, Raval MH, Walsh T, Ma Q, Chakchouk I, Kannan-Sundhari A, Mittal R, Masmoudi S, Blanton SH, Tekin M, King MC, Yengo CM, Liu XZ., Free PMC Article

    12/31/2016
    A homozygous mutation, MYO3A:c.1841C>T (p.S614F), was identified to be responsible for non-syndromic congenital deafness in two members of a Kazakh family in China.

    Identification of a novel homozygous mutation in MYO3A in a Chinese family with DFNB30 non-syndromic hearing impairment.
    Qu R, Sang Q, Xu Y, Feng R, Jin L, He L, Wang L.

    12/17/2016
    Data suggest that, in enterocytes, MYO3A autophosphorylation of kinase domain at Thr184/Thr188 regulates kinase activity, translocation of MYO3A to tips of microvilli, and stability of actin cytoskeleton.

    Phosphorylation of the kinase domain regulates autophosphorylation of myosin IIIA and its translocation in microvilli.
    An BC, Sakai T, Komaba S, Kishi H, Kobayashi S, Kim JY, Ikebe R, Ikebe M., Free PMC Article

    02/21/2015
    The differential regulation of the kinase and motor activities allows for MYO3A to precisely self-regulate its concentration in the actin bundle-based structures of cells.

    Myosin 3A kinase activity is regulated by phosphorylation of the kinase domain activation loop.
    Quintero OA, Unrath WC, Stevens SM Jr, Manor U, Kachar B, Yengo CM., Free PMC Article

    02/22/2014
    Results suggest that Myo3A motor activity is regulated through a mechanism involving concentration-dependent autophosphorylation.

    Intermolecular autophosphorylation regulates myosin IIIa activity and localization in parallel actin bundles.
    Quintero OA, Moore JE, Unrath WC, Manor U, Salles FT, Grati M, Kachar B, Yengo CM., Free PMC Article

    02/26/2011
    Observational study and genome-wide association study of gene-disease association. (HuGE Navigator)

    Genome-wide association study for colorectal cancer identifies risk polymorphisms in German familial cases and implicates MAPK signalling pathways in disease susceptibility.
    Lascorz J, Försti A, Chen B, Buch S, Steinke V, Rahner N, Holinski-Feder E, Morak M, Schackert HK, Görgens H, Schulmann K, Goecke T, Kloor M, Engel C, Büttner R, Kunkel N, Weires M, Hoffmeister M, Pardini B, Naccarati A, Vodickova L, Novotny J, Schreiber S, Krawczak M, Bröring CD, Völzke H, Schafmayer C, Vodicka P, Chang-Claude J, Brenner H, Burwinkel B, Propping P, Hampe J, Hemminki K.

    09/15/2010
    Observational study and meta-analysis of gene-disease association. (HuGE Navigator)

    Supervised machine learning and logistic regression identifies novel epistatic risk factors with PTPN22 for rheumatoid arthritis.
    Briggs FB, Ramsay PP, Madden E, Norris JM, Holers VM, Mikuls TR, Sokka T, Seldin MF, Gregersen PK, Criswell LA, Barcellos LF., Free PMC Article

    04/7/2010
    behavioral inhibition-associated SNPs appear to be associated with differences in MYO3A- but not GAD2 lymphoblastoid-mRNA expression levels

    Polymorphisms in the GAD2 gene-region are associated with susceptibility for unipolar depression and with a risk factor for anxiety disorders.
    Unschuld PG, Ising M, Specht M, Erhardt A, Ripke S, Heck A, Kloiber S, Straub V, Brueckl T, Müller-Myhsok B, Holsboer F, Binder EB, Unschuld PG, Ising M, Specht M, Erhardt A, Ripke S, Heck A, Kloiber S, Straub V, Brueckl T, Müller-Myhsok B, Holsboer F, Binder EB.

    03/1/2010
    Observational study of gene-disease association. (HuGE Navigator)See all PubMed (2) articles

    Polymorphisms in the GAD2 gene-region are associated with susceptibility for unipolar depression and with a risk factor for anxiety disorders.
    Unschuld PG, Ising M, Specht M, Erhardt A, Ripke S, Heck A, Kloiber S, Straub V, Brueckl T, Müller-Myhsok B, Holsboer F, Binder EB, Unschuld PG, Ising M, Specht M, Erhardt A, Ripke S, Heck A, Kloiber S, Straub V, Brueckl T, Müller-Myhsok B, Holsboer F, Binder EB.

    A scan of chromosome 10 identifies a novel locus showing strong association with late-onset Alzheimer disease.
    Grupe A, Li Y, Rowland C, Nowotny P, Hinrichs AL, Smemo S, Kauwe JS, Maxwell TJ, Cherny S, Doil L, Tacey K, van Luchene R, Myers A, Wavrant-De Vrièze F, Kaleem M, Hollingworth P, Jehu L, Foy C, Archer N, Hamilton G, Holmans P, Morris CM, Catanese J, Sninsky J, White TJ, Powell J, Hardy J, O'Donovan M, Lovestone S, Jones L, Morris JC, Thal L, Owen M, Williams J, Goate A.

    03/25/2009
    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.

    The kinase domain alters the kinetic properties of the myosin IIIA motor.
    Dosé AC, Ananthanarayanan S, Moore JE, Corsa AC, Burnside B, Yengo CM.

    01/21/2010
    myosin IIIA can spend a majority of its ATP hydrolysis cycling time on actin

    Human myosin III is a motor having an extremely high affinity for actin.
    Kambara T, Komaba S, Ikebe M.

    01/21/2010
    mutation in humans causes progressive nonsyndromic hearing loss DFNB30

    From flies' eyes to our ears: mutations in a human class III myosin cause progressive nonsyndromic hearing loss DFNB30.
    Walsh T, Walsh V, Vreugde S, Hertzano R, Shahin H, Haika S, Lee MK, Kanaan M, King MC, Avraham KB., Free PMC Article

    01/21/2010
    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

    Kinetic mechanism of human myosin IIIA.
    Dosé AC, Ananthanarayanan S, Moore JE, Burnside B, Yengo CM.

    01/21/2010
    class III myosin is an actin-based motor protein having a protein kinase activity

    Determination of human myosin III as a motor protein having a protein kinase activity.
    Komaba S, Inoue A, Maruta S, Hosoya H, Ikebe M.

    01/21/2010
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