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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Myosin, heavy chain 9, non-muscle

MHA, MYH9, myosin IIA
This gene encodes a conventional non-muscle myosin; this protein should not be confused with the unconventional myosin-9a or 9b (MYO9A or MYO9B). The encoded protein is a myosin IIA heavy chain that contains an IQ domain and a myosin head-like domain which is involved in several important functions, including cytokinesis, cell motility and maintenance of cell shape. Defects in this gene have been associated with non-syndromic sensorineural deafness autosomal dominant type 17, Epstein syndrome, Alport syndrome with macrothrombocytopenia, Sebastian syndrome, Fechtner syndrome and macrothrombocytopenia with progressive sensorineural deafness. [provided by RefSeq, Dec 2011] (from NCBI)
Top mentioned proteins: IIa, Actin, CAN, HAD, ACID
Papers using MHA antibodies
Performance standards for Antimicrobial Susceptibility Testing. Sixteenth informational supplement
Javaid SG et al., In The Libyan Journal of Medicine, 2002
... Lawns of each bacterial suspension were made on Mueller Hinton's agar (MHA) (Merck, Germany) using sterile cotton ...
Anion recognition effects in the structuring of bovine serum albumin films
Deng Linhong et al., In Nanoscale Research Letters, 2000
... 16-MHA, 1-ethyl-3-(dimethylaminopropyl) carbodi-imide hydrochloride (EDC), NHS, sulphathiazole sodium, tylosin, and levofloxacin were purchased from Sigma Aldrich Chemical Co ...
Papers on MHA
Sensitivity improvement of a sandwich-type ELISA immunosensor for the detection of different prostate-specific antigen isoforms in human serum using electrochemical impedance spectroscopy and an ordered and hierarchically organized interfacial supramolecular architecture.
Hernández-López et al., Mexico. In Anal Chim Acta, Feb 2016
To address and minimize the issue of non-specific protein adsorption, an organic matrix (amine-PEG3-biotin/avidin) was assembled on the previously functionalized electrode surface to build up an ordered and hierarchically organized interfacial supramolecular architecture: Au/16-MHA/EG3SH/amine-PEG3-biotin/avidin.
Downregulation of non‑muscle myosin IIA expression inhibits migration and invasion of gastric cancer cells via the c‑Jun N‑terminal kinase signaling pathway.
Wang et al., Zhengzhou, China. In Mol Med Report, Jan 2016
UNASSIGNED: Non‑muscle myosin IIA (NMIIA) has been found to be overexpressed in gastric cancer tissues.
Nerve growth factor stimulates axon outgrowth through negative regulation of growth cone actomyosin restraint of microtubule advance.
Bridgman et al., Saint Louis, United States. In Mol Biol Cell, Jan 2016
On fibronectin, NGF caused inactivation of myosin IIA that negatively regulated actin bundling.
Crawford et al., Cleveland, United States. In Pac Symp Biocomput, Dec 2015
Common genetic variants in the myosin, heavy chain 9, non-muscle (MYH9) gene were initially identified as associated with non-diabetic end-stage renal disease in African Americans, and it is now understood that these variants are in strong linkage disequilibrium with likely causal variants in neighboring APOL1.
Preoperative use of platelets in a 6-year-old with acute appendicitis and a myosin heavy chain 9-related disorder: a case report and review of literature.
Squires et al., Charleston, United States. In Transfusion, Nov 2015
BACKGROUND: Mutations of nonmuscle myosin heavy chain 9 (MYH9) gene are an autosomal dominant cause of inherited thrombocytopenia in children.
[Which genetic testing in renal disease].
Granata et al., In G Ital Nefrol, Sep 2015
The applicability of clinical genetics in nephrology is due to the fact that many kidney diseases are characterized by genetic mutations (e.g., von-Hippel Lindau syndrome, MYH9 related disorders, Fabry's syndrome, Liddle's and Bartter's Syndrome, and others).
Recent progress in the genetics of diabetic microvascular complications.
Chuang et al., Taipei, Taiwan. In World J Diabetes, Jul 2015
However, most of the identified risk loci could not be replicated by independent studies with a few exceptions including those in ELMO1, FRMD3, CARS, MYO16/IRS2, and APOL3-MYH9 genes.
African origins and chronic kidney disease susceptibility in the human immunodeficiency virus era.
Naicker et al., Johannesburg, South Africa. In World J Nephrol, Jun 2015
The APOL1 G1 and G2 alleles were more strongly associated with the risk for CKD than the previously examined MYH9 E1 risk haplotype in individuals of African ancestry.
Quantitative candidate gene association studies of metabolic traits in Han Chinese type 2 diabetes patients.
Li et al., Tianjin, China. In Genet Mol Res, 2014
We found that CAMTA1, ABI2, VHL, KAT2B, PKHD1, ESR1, TOX, SLC30A8, SFI1, and MYH9 polymorphisms were associated with HbA1c, FPG, and/or P2PG; GCK, HHEX, TCF7L2, KCNQ1, and TBX5 polymorphisms were associated with insulin resistance-related traits; ABCG2, SLC2A9, and PKHD1 polymorphisms were associated with SUA; CAMTA1, VHL, KAT2B, PON1, NUB1, SLITRK5, SMAD3, FTO, FANCA, and PCSK2 polymorphisms were associated with blood lipid traits; CAMTA1, SPAG16, TOX, KCNQ1, ACACB, and MYH9 polymorphisms were associated with blood pressure; and UBE2E3, SPAG16, SLC2A9, CDKAL1, CDKN2A/B, TCF7L2, SMAD3, and PNPLA3 polymorphisms were associated with BMI (all P values <0.05).
Myotonic dystrophy kinase-related Cdc42-binding kinases (MRCK), the ROCK-like effectors of Cdc42 and Rac1.
Manser et al., Singapore, Singapore. In Small Gtpases, 2014
Notably MRCK is a key regulator of myosin18A and myosin IIA/B, and through phosphorylation of their common regulatory light chains (MYL9 or MLC2) to promote actin stress fiber contractility.
Direct in vivo RNAi screen unveils myosin IIa as a tumor suppressor of squamous cell carcinomas.
Fuchs et al., New York City, United States. In Science, 2014
Seven of our top hits-including Myh9, which encodes nonmuscle myosin IIa-have not been linked to tumor development, yet tissue-specific Myh9 RNAi and Myh9 knockout trigger invasive SCC formation on tumor-susceptible backgrounds.
Centralspindlin and α-catenin regulate Rho signalling at the epithelial zonula adherens.
Yap et al., Brisbane, Australia. In Nat Cell Biol, 2012
Centralspindlin recruits the RhoGEF, ECT2, to activate Rho and support junctional integrity through myosin IIA.
Resolution doubling in live, multicellular organisms via multifocal structured illumination microscopy.
Shroff et al., Bethesda, United States. In Nat Methods, 2012
We captured dynamic changes in the zebrafish lateral line primordium and observed interactions between myosin IIA and F-actin in cells encapsulated in collagen gels, obtaining two-color 4D super-resolution data sets spanning tens of time points and minutes without apparent phototoxicity.
Whole-genome analysis informs breast cancer response to aromatase inhibition.
Mardis et al., Saint Louis, United States. In Nature, 2012
Eighteen significantly mutated genes were identified, including five genes (RUNX1, CBFB, MYH9, MLL3 and SF3B1) previously linked to haematopoietic disorders.
S100P dissociates myosin IIA filaments and focal adhesion sites to reduce cell adhesion and enhance cell migration.
Rudland et al., Liverpool, United Kingdom. In J Biol Chem, 2012
Data show wthat the S100P-induced dissociation of NMIIA filaments leads to a weakening of focal adhesion sites (FAS), reduced cell adhesion, and enhanced cell migration, the first major step in the metastatic cascade.
A Trp33Arg mutation at exon 1 of the MYH9 gene in a Korean patient with May-Hegglin anomaly.
Oh et al., South Korea. In Yonsei Med J, 2012
Study describe a Korean patient with May-Hegglin anomaly from a mutation of the MYH9 gene.
Crystal structure of the S100A4-nonmuscle myosin IIA tail fragment complex reveals an asymmetric target binding mechanism.
Nyitray et al., Budapest, Hungary. In Proc Natl Acad Sci U S A, 2012
Data suggest that the complex will facilitate the design of specific drugs that interfere with the S100A4-NMIIA interaction.
Asymmetric mode of Ca²⁺-S100A4 interaction with nonmuscle myosin IIA generates nanomolar affinity required for filament remodeling.
Barsukov et al., Liverpool, United Kingdom. In Structure, 2012
Asymmetric mode of Ca-S100A4 interaction with nonmuscle myosin IIA generates nanomolar affinity required for filament remodeling in epithelial carcinoma cells.
Alteration of liver enzymes is a feature of the MYH9-related disease syndrome.
Italian Registry for MYH9-releated diseases et al., Pavia, Italy. In Plos One, 2011
Elevation of liver enzymes is a frequent and previously unrecognized feature of the MYH9MYH9-related disease syndrome.
Non-muscle myosin IIA is a functional entry receptor for herpes simplex virus-1.
Kawaguchi et al., Tokyo, Japan. In Nature, 2010
non-muscle myosin heavy chain IIA (NMHC-IIA), a subunit of non-muscle myosin IIA (NM-IIA), functions as an HSV-1 entry receptor by interacting with gB
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