MYH9 - Knowledge (XXG)

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visceral endoderm does not specifically depend on NM IIA since its function can be restored by genetically replacing the NMHC IIA with cDNA encoding NMHC II B (or NMHC IIC) that is under control of the NMHC IIA promoter. These "replacement" mice have a normal visceral endoderm and continue to proceed through gastrulation and undergo organogenesis. However, they die when they fail to develop a normal placenta. Absence of NM IIA results in a compact and underdeveloped labyrinthine layer in the placenta which lacks fetal blood vessel invasion. Moreover, mutant p.R702C NM IIA mice show similar defects in placental formation and mice specifically ablated for NM IIA in the mouse trophoblast-lineage cells demonstrate placental defects similar to mice in which NMHC IIA is genetically replaced by NMHC IIB. There are significant differences in the relative abundance of the three NM II paralogs in various cells and tissues. However, NM IIA appears to be the predominant paralog in both tissues and cells in humans and mice. Mass spectroscopy analysis of the relative abundance of NMHC IIs in mouse tissues and human cell lines shows that NM IIA is predominant, although tissues like the heart vary from cell to cell; myocardial cells contain only NM IIB but NM IIA is more abundant in the non-myocyte cells. NM IIB is predominant in most parts of the brain and spinal cord but NM IIA is relatively more abundant in most other organs and cells lines. Both NM IIA and IIB are expressed early in development with NM IIC expression starting at E 11.5 in mice. Not only do most cells contain more than one paralog but there is evidence that the paralogs can co-assemble intracellularly into heterotypic filaments in a variety of settings in cultured cells.

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of the two heavy chains together form the tail domain. The motor domain, which is organized into four subdomains (SH3-like motif, the upper and the lower 50kDa subdomains, and the converter region) connected by flexible linkers, interacts with filamentous actin to generate force through magnesium-dependent hydrolysis of ATP. The neck acts as a lever arm that amplifies the movement produced by conformational changes of the motor domain, and is the binding site for the light chains through two IQ motifs. The tail domain is fundamental for both dimerization of the heavy chains and formation of NM IIA functional filaments. Two heavy chains dimerize through the tail domain forming a long alpha-helical coiled-coil rod composed of typical heptad repeats. Dimers self-associate though the coiled-coil rods to form myosin filaments. The tail domain ends at the C-terminus with a 34-residue non-helical tailpiece.

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distinct roles during vertebrate development and adulthood (for general reviews on NM IIs, see ). All NM IIs have two important features: they are MgATPase enzymes that can hydrolyze ATP thereby converting chemical energy into mechanical movement. In addition, they can form bipolar filaments which can interact with and exert tension on actin filaments. These properties provide the basis for all NM II functions. The path to myosin filament formation, which is shared by NM II and smooth muscle myosin, starts with a folded inactive conformation of the NM II monomer which, upon phosphorylation of the 20 KDa light chain unfolds the molecule to produce a globular head region followed by an extended alpha-helical coiled-coil tail. The tail portion of the molecule can interact with other NM IIA hexamers to form bipolar filaments composed of 14-16 molecules.

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expression is associated with enhanced cell migration through maintenance of cell polarization and inhibition of cell turning. Similar to heavy chain phosphorylation, in vitro binding of S100A to the carboxy-terminal end of the NM IIA coiled-coil region prevents filament formation and S100A4 binding to previously formed filaments promotes filament disassembly. The tumor suppressor protein Lgl1 also inhibits the ability of NM IIA to assemble into filaments in vitro. In addition, it regulates the cellular localization of NM IIA and contributes to the maturation of focal adhesions. Other proteins that are known to interact with NM IIA include the actin binding protein tropomyosin 4.2 and a novel actin stress fiber associated protein, LIM and calponin-homology domains1 (LIMCH1).

1478:-RD patients develop sensorineural hearing loss. Severity of the hearing impairment is greatly variable, as it ranges from a mild hearing defect that occurs in mid or advanced age to a progressive hearing loss that is evident in the first years of life and rapidly evolves to severe deafness. Kidney damage occurs in about 25% of patients. It presents with proteinuria and often progresses to kidney failure, which, in its most severe forms, may require dialysis and/or kidney transplantation. Around 20% of patients develop presenile cataracts. About 50% of 315: 292: 189: 214: 1500:-RD is caused by missense mutations affecting the head or tail domain of the NMHC IIA. Nonsense or frameshift alterations resulting in the deletion of a C-terminal fragment of the NMHC IIA (17 to 40 residues) are involved in approximately 20% of families. In-frame deletions or duplications have been identified in a few cases. The disease is transmitted as an autosomal-dominant trait, however, about 35% of index cases are sporadic. Sporadic forms mainly derive from 566: 321: 220: 1474:-RD patients are characterized by a very large size: platelets larger than red blood cells (called "giant platelets") are always present at the examination of peripheral blood smears. Granulocyte inclusions of the NMHC IIA may be evident at the analysis of blood films after conventional staining as cytoplasmic basophilic (light blue) inclusions, called "Döhle-like bodies". More than 50% of 1648: 1446:-RD). All affected individuals present congenital hematological alterations consisting in thrombocytopenia, platelet macrocytosis, and inclusions of the MYH9 protein in the cytoplasm of granulocytes. Most patients develop one or more non-congenital manifestations, including sensorineural deafness, kidney damage, presenile cataracts, and/or elevation of liver enzymes. The term 1362:

part of a superfamily composed of more than 30 classes. Class II myosins include muscle and non-muscle myosins that are organized as hexameric molecules consisting of two heavy chains (230 kDa), two regulatory light chains (20 KDa) controlling the myosin activity, and two essential light chains (17 kDa), which stabilize the heavy chain structure.

1466:-RD is a rare disease: prevalence is estimated around 3:1,000,000. The actual prevalence is expected to be higher, as mild forms are often discovered incidentally and patients are frequently misdiagnosed with other disorders. The disease has been reported worldwide and there is no evidence of variation in prevalence across ethnic populations. 1403:

the MgATPase activity due to the folded conformation. In addition to phosphorylation of the 20 KDa light chains, the NMHC IIs can also be phosphorylated, but the sites phosphorylated differ among the paralogs. In most cases phosphorylation of NMHC IIA can act to either dissociate the myosin filaments or to prevent filament formation.

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Thrombocytopenia can result in a variable degree of bleeding tendency. The majority of patients have no spontaneous bleeding or only mild cutaneous bleeding (easy bruising) and are at risk of significant hemorrhages only after surgery or other invasive procedures, deliveries, or trauma. Some patients

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Non-muscle myosin IIA (NM IIA) is expressed in most cells and tissues where it participates in a variety of processes requiring contractile force, such as cytokinesis, cell migration, polarization and adhesion, maintenance of cell shape, and signal transduction. Myosin IIs are motor proteins that are

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Phosphorylation of the 20 KDa light chains on Serine 19 and Threonine 18 by a number of different kinases, but most prominently by Rho-dependent kinase and/or by the calcium-calmodulin-dependent myosin light chain kinase, not only linearizes the folded structure but removes the inhibition imposed on

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Like all class II myosins, the two NMHC IIAs dimerize producing an asymmetric molecular structure recognizable by two heads and a tail domain: the N-terminal half of each heavy chain generates the head domain, which consists of the globular motor domain and the neck domain, and the C-terminal halves

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is a large gene spanning more than 106 kilo base pairs on chromosome 22q12.3. It is composed of 41 exons with the first ATG of the open reading frame localized in exon 2 and the stop codon in exon 41. It encodes non-muscle myosin heavy chain IIA (NMHC IIA), a protein of 1,960 amino acids. Consistent

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There are three paralogs of non-muscle myosin II (NM II), NM IIA, IIB, and IIC, with each having the heavy chain encoded on a different chromosome. All three paralogs appear to bind the same or very similar light chains and share basic properties as to structure and activation, but all three play

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In addition to phosphorylation, NM IIA filament assembly and localization can be modulated by interaction with other proteins including S100A4 and Lethal giant larvae (Lgl1). The former is a calcium binding protein and is also known as metastatin, a well-characterized metastatic factor. S100A4

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which is disorganized due to a loss of E-cadherin mediated cell-cell adhesions. Lacking a normal polarized columnar layer of endoderm, the abnormal visceral endoderm of NM IIA knockout embryos fails to support the critical step of gastrulation. However, the development of a normal functioning

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mutation. The recent definition of genotype-phenotype correlations allows prediction of the clinical evolution of the disease in most cases. Genotype-phenotype correlations have been reported also for the severity of thrombocytopenia, platelet size, and the features of leukocyte inclusions.

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Verver EJ, Topsakal V, Kunst HP, Huygen PL, Heller PG, Pujol-Moix N, et al. (January 2016). "Nonmuscle Myosin Heavy Chain IIA Mutation Predicts Severity and Progression of Sensorineural Hearing Loss in Patients With MYH9-Related Disease".

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D'Apolito M, Guarnieri V, Boncristiano M, Zelante L, Savoia A (March 2002). "Cloning of the murine non-muscle myosin heavy chain IIA gene ortholog of human MYH9 responsible for May-Hegglin, Sebastian, Fechtner, and Epstein syndromes".

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Seri M, Cusano R, Gangarossa S, Caridi G, Bordo D, Lo Nigro C, et al. (September 2000). "Mutations in MYH9 result in the May-Hegglin anomaly, and Fechtner and Sebastian syndromes. The May-Heggllin/Fechtner Syndrome Consortium".

8337: 1489:-RD is confirmed by the identification of the NMHC IIA inclusions in granulocytes through an immunofluorescence assay on peripheral blood smears and/or by the detection of the causative mutation through mutational screening of the 3816:

Savoia A, De Rocco D, Panza E, Bozzi V, Scandellari R, Loffredo G, et al. (April 2010). "Heavy chain myosin 9-related disease (MYH9 -RD): neutrophil inclusions of myosin-9 as a pathognomonic sign of the disorder".

1386:) is localized in a syntenic region on chromosome 15 and has the same genomic organization as that of the human gene. It encodes a protein of the same length, with 97.1% amino acid identity with the human MYH9 protein. 1523:-RD. ACE-inhibitors or angiotensin II receptor blockers may be effective in reducing proteinuria when given at the early stage of kidney involvement. Cochlear implantation is effective in restoring hearing function in 5684:

Lalwani AK, Linthicum FH, Wilcox ER, Moore JK, Walters FC, San Agustin TB, et al. (1998). "A five-generation family with late-onset progressive hereditary hearing impairment due to cochleosaccular degeneration".

1450:-RD encompasses four syndromic pictures that were considered for many years as distinct disorders, namely May-Hegglin anomaly, Sebastian syndrome, Fechtner syndrome, and Epstein syndrome. After the identification of 5866:

Sajid M, Hu Z, Lele M, Stouffer GA (May 2000). "Protein complexes involving alpha v beta 3 integrins, nonmuscle myosin heavy chain-A, and focal adhesion kinase from in thrombospondin-treated smooth muscle cells".

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in African Americans and in Hispanic Americans. However, subsequent studies showed that this association is explained by strong linkage disequilibrium with two haplotypes (haplotypes G1 and G2) in the neighboring

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Kelley MJ, Jawien W, Lin A, Hoffmeister K, Pugh EW, Doheny KF, et al. (May 2000). "Autosomal dominant macrothrombocytopenia with leukocyte inclusions (May-Hegglin anomaly) is linked to chromosome 22q12-13".

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Kas SM, de Ruiter JR, Schipper K, Annunziato S, Schut E, Klarenbeek S, et al. (August 2017). "Insertional mutagenesis identifies drivers of a novel oncogenic pathway in invasive lobular breast carcinoma".

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Kitamura K, Yoshida K, Shiraishi Y, Chiba K, Tanaka H, Furukawa K, et al. (November 2013). "Normal neutrophil myosin IIA localization in an immunofluorescence analysis can rule out MYH9 disorders".

1482:-RD patients present chronic or intermittent elevation of liver transaminases or gamma-glutamyl transferases: this alteration appears to be benign, as no patients showed evolution to liver dysfunction. 5495:

Obermann WM, Plessmann U, Weber K, Fürst DO (October 1995). "Purification and biochemical characterization of myomesin, a myosin-binding and titin-binding protein, from bovine skeletal muscle".

5380:"Cellular myosin heavy chain in human leukocytes: isolation of 5' cDNA clones, characterization of the protein, chromosomal localization, and upregulation during myeloid differentiation" 3419:"MYH9-related disease: May-Hegglin anomaly, Sebastian syndrome, Fechtner syndrome, and Epstein syndrome are not distinct entities but represent a variable expression of a single illness" 1549:

in the tongue epithelium led to the development of tongue SCC. In mice predisposed to invasive lobular breast carcinoma (ILBC) because of E-cadherin ablation, the inactivation of

5267:"Enzymic and immunochemical properties of lysozyme. Accurate definition of the antigenic site around the disulphide bridge 30-115 (site 3) by 'surface-simulation' synthesis" 1545:

in the epithelial cells in mice was associated with the development of squamous cell carcinoma (SCC) of the skin and the head and neck. In another mouse model, ablation of

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Kunishima S, Yoshinari M, Nishio H, Ida K, Miura T, Matsushita T, et al. (March 2007). "Haematological characteristics of MYH9 disorders due to MYH9 R702 mutations".

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NM IIA plays a major role in early vertebrate development. Ablation of NM IIA in mice results in lethality by embryonic day (E) 6.5 due to abnormalities in the visceral

49: 328: 227: 4290:"Renin-angiotensin system blockade is effective in reducing proteinuria of patients with progressive nephropathy caused by MYH9 mutations (Fechtner-Epstein syndrome)" 5829:

Miyamoto CA, Fischman DA, Reinach FC (October 1999). "The interface between MyBP-C and myosin: site-directed mutagenesis of the CX myosin-binding domain of MyBP-C".

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as the gene responsible for all of these entities, it was recognized that they actually represent different clinical presentations of the same disease, now known as

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Within a phase 2 trial, eltrombopag, an agonist of the thrombopoietin receptor, significantly increased platelet count in 11 out of 12 patients affected with

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Maupin P, Phillips CL, Adelstein RS, Pollard TD (November 1994). "Differential localization of myosin-II isozymes in human cultured cells and blood cells".

4685:"African ancestry allelic variation at the MYH9 gene contributes to increased susceptibility to non-diabetic end-stage kidney disease in Hispanic Americans" 1470:

have spontaneous mucosal bleeding, such as menorrhagia, epistaxis, and gum bleeding. Severe and life-threatening hemorrhages are not frequent. Platelets of

5651:"Cleavage of human and mouse cytoskeletal and sarcomeric proteins by human immunodeficiency virus type 1 protease. Actin, desmin, myosin, and tropomyosin" 5089:

Kim SJ, Lee S, Park HJ, Kang TH, Sagong B, Baek JI, et al. (October 2016). "Genetic association of MYH genes with hereditary hearing loss in Korea".

8307: 3774:"Immunofluorescence analysis of neutrophil nonmuscle myosin heavy chain-A in MYH9 disorders: association of subcellular localization with MYH9 mutations" 150: 1069: 1050: 4053:

Kunishima S, Takaki K, Ito Y, Saito H (April 2009). "Germinal mosaicism in MYH9 disorders: a family with two affected siblings of normal parents".

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Kelley MJ, Jawien W, Ortel TL, Korczak JF (September 2000). "Mutation of MYH9, encoding non-muscle myosin heavy chain A, in May-Hegglin anomaly".

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Husi H, Ward MA, Choudhary JS, Blackstock WP, Grant SG (July 2000). "Proteomic analysis of NMDA receptor-adhesion protein signaling complexes".

8327: 5126:"Targeted exon sequencing successfully discovers rare causative genes and clarifies the molecular epidemiology of Japanese deafness patients" 1805: 6627: 1787: 5714:

Ford HL, Silver DL, Kachar B, Sellers JR, Zain SB (December 1997). "Effect of Mts1 on the structure and activity of nonmuscle myosin II".

5032:"Application of massively parallel sequencing to genetic diagnosis in multiplex families with idiopathic sensorineural hearing impairment" 3529:"MYH9-related disease: a novel prognostic model to predict the clinical evolution of the disease based on genotype-phenotype correlations" 314: 5992: 3638:

Savoia A, Pecci A (1993). "MYH9-Related Disease". In Adam MP, Ardinger HH, Pagon RA, Wallace SE, Bean LJ, Stephens K, Amemiya A (eds.).

3072:"Keratin 5-Cre-driven excision of nonmuscle myosin IIA in early embryo trophectoderm leads to placenta defects and embryonic lethality" 2592:"Direct evidence for functional smooth muscle myosin II in the 10S self-inhibited monomeric conformation in airway smooth muscle cells" 5745:"Mapping of a myosin-binding domain and a regulatory phosphorylation site in M-protein, a structural protein of the sarcomeric M band" 4791:"Missense mutations in the APOL1 gene are highly associated with end stage kidney disease risk previously attributed to the MYH9 gene" 1277: 1284: 291: 2690:

Li ZH, Bresnick AR (May 2006). "The S100A4 metastasis factor regulates cellular motility via a direct interaction with myosin-IIA".

4938:"Polymorphisms in the nonmuscle myosin heavy chain 9 gene (MYH9) are associated with the progression of IgA nephropathy in Chinese" 121:, BDPLT6, DFNA17, EPSTS, FTNS, MHA, NMHC-II-A, NMMHC-IIA, NMMHCA, myosin, heavy chain 9, non-muscle, myosin heavy chain 9, MATINS 7146: 1774: 1753: 8342: 7415: 7258: 5985: 1586: 213: 188: 3916:"Diagnosis of inherited platelet disorders on a blood smear: a tool to facilitate worldwide diagnosis of platelet disorders" 1770: 5310:"Large tidal volume ventilation improves pulmonary gas exchange during lower abdominal surgery in Trendelenburg's position" 8294: 7848: 5183:

England K, Ashford D, Kidd D, Rumsby M (June 2002). "PKC epsilon is associated with myosin IIA and actin in fibroblasts".

2727:"The tumor suppressor Lgl1 forms discrete complexes with NMII-A and Par6α-aPKCζ that are affected by Lgl1 phosphorylation" 1557:

expression is associated with oncogenesis and/or tumor progression in human SCC and ILBC, thus also supporting a role for

4139:"Position of nonmuscle myosin heavy chain IIA (NMMHC-IIA) mutations predicts the natural history of MYH9-related disease" 1749: 130: 6555: 1613: 4331:"Patients with Epstein-Fechtner syndromes owing to MYH9 R702 mutations develop progressive proteinuric renal disease" 1655:

The 2018 version of this article was updated by an external expert under a dual publication model. The corresponding

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led to the development of tumors recapitulating the features of human ILBC. Some observations suggest that defective

2923:"Defects in cell adhesion and the visceral endoderm following ablation of nonmuscle myosin heavy chain II-A in mice" 327: 226: 8026: 3121:"Ablation of nonmuscle myosin II-B and II-C reveals a role for nonmuscle myosin II in cardiac myocyte karyokinesis" 320: 219: 1966:"Drawing the tree of eukaryotic life based on the analysis of 2,269 manually annotated myosins from 328 species" 8259: 1114: 138: 4483:"Conditional deletion of nonmuscle myosin II-A in mouse tongue epithelium results in squamous cell carcinoma" 5555:"Identification and overlapping expression of multiple unconventional myosin genes in vertebrate cell types" 1095: 3957:"Mutation spectrum and genotype-phenotype correlations in a large French cohort of MYH9-Related Disorders" 2649:

Grum-Schwensen B, Klingelhofer J, Berg CH, El-Naaman C, Grigorian M, Lukanidin E, et al. (May 2005).

1577: 6678: 6032: 5415:"Human nonmuscle myosin heavy chain mRNA: generation of diversity through alternative polyadenylylation" 2490:"Head-head and head-tail interaction: a general mechanism for switching off myosin II activity in cells" 1656: 202: 2362:

Eddinger TJ, Meer DP (August 2007). "Myosin II isoforms in smooth muscle: heterogeneity and function".

3668:"Platelet diameters in inherited thrombocytopenias: analysis of 376 patients with all known disorders" 3276:"Self-sorting of nonmuscle myosins IIA and IIB polarizes the cytoskeleton and modulates cell motility" 6947: 5799: 5566: 5426: 5137: 5043: 4745: 4494: 4437: 4004:

Kunishima S, Matsushita T, Yoshihara T, Nakase Y, Yokoi K, Hamaguchi M, et al. (February 2005).

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Genovese G, Friedman DJ, Ross MD, Lecordier L, Uzureau P, Freedman BI, et al. (August 2010).

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Saposnik B, Binard S, Fenneteau O, Nurden A, Nurden P, Hurtaud-Roux MF, et al. (July 2014).

3896: 3852: 3751: 3475:"Recent advances in the understanding and management of MYH9-related inherited thrombocytopenias" 3448: 3392: 3348: 2651:"Suppression of tumor development and metastasis formation in mice lacking the S100A4(mts1) gene" 2387: 1573: 1378:

is typical of housekeeping genes having no TATA box but high GC content, with multiple GC boxes.

162: 5608:"Cellular titin localization in stress fibers and interaction with myosin II filaments in vitro" 4098:"Somatic mosaicism in MYH9 disorders: the need to carefully evaluate apparently healthy parents" 1260: 1235: 1209: 1188: 5345:"Human nonmuscle myosin heavy chains are encoded by two genes located on different chromosomes" 3914:

Greinacher A, Pecci A, Kunishima S, Althaus K, Nurden P, Balduini CL, et al. (July 2017).

1825:"Human nonmuscle myosin heavy chains are encoded by two genes located on different chromosomes" 8105: 7808: 6469: 5953: 5915: 5876: 5846: 5817: 5774: 5731: 5702: 5672: 5637: 5594: 5541: 5512: 5483: 5454: 5401: 5366: 5331: 5296: 5253: 5200: 5165: 5106: 5071: 5008: 4959: 4918: 4869: 4820: 4771: 4714: 4665: 4616: 4585:

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4403: 4352: 4311: 4262: 4241:"Eltrombopag for the treatment of the inherited thrombocytopenia deriving from MYH9 mutations" 4213: 4170: 4119: 4070: 4027: 3986: 3937: 3888: 3844: 3795: 3743: 3697: 3645: 3620: 3558: 3496: 3440: 3384: 3340: 3305: 3256: 3199: 3150: 3101: 3052: 3003: 2944: 2903: 2854: 2797: 2748: 2707: 2672: 2631: 2568: 2519: 2470: 2428: 2379: 2341: 2305: 2251: 2199: 2150: 2098: 2046: 1997: 1946: 1895: 1846: 1709: 1691: 110: 42: 7828: 4840:"APOL1 genetic variants in focal segmental glomerulosclerosis and HIV-associated nephropathy" 4481:

Conti MA, Saleh AD, Brinster LR, Cheng H, Chen Z, Cornelius S, et al. (September 2015).

1866:"Human nonsyndromic hereditary deafness DFNA17 is due to a mutation in nonmuscle myosin MYH9" 8053: 7760: 7745: 7740: 7735: 7730: 7720: 7641: 7350: 7330: 7300: 7295: 7177: 6532: 6527: 5945: 5905: 5897: 5838: 5807: 5764: 5756: 5723: 5694: 5662: 5627: 5619: 5584: 5574: 5533: 5504: 5475: 5444: 5434: 5391: 5356: 5321: 5286: 5278: 5243: 5235: 5192: 5155: 5145: 5098: 5061: 5051: 4998: 4990: 4949: 4908: 4900: 4859: 4851: 4810: 4802: 4789:

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3234: 2979: 2832: 2607: 2539:"Visualization of head-head interactions in the inhibited state of smooth muscle myosin" 8158: 8021: 6718: 6549: 6058: 5667: 5650: 5632: 5607: 5291: 5266: 5248: 5223: 5160: 5125: 5066: 5031: 5003: 4978: 4913: 4888: 4864: 4839: 4815: 4790: 4766: 4733: 4709: 4684: 4683:

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4660: 4635: 4611: 4586: 4515: 4482: 4458: 4425: 4398: 4371: 3981: 3956: 3790: 3773: 3692: 3667: 3615: 3580: 3553: 3528: 3300: 3275: 3251: 3218: 3194: 3169: 3145: 3120: 3096: 3071: 3047: 3022: 2998: 2963: 2898: 2873: 2849: 2816: 2792: 2767: 2626: 2591: 2587: 2563: 2538: 2514: 2489: 2448:"Structures of smooth muscle myosin and heavy meromyosin in the folded, shutdown state" 2300: 2275: 2246: 2221: 2194: 2169: 2145: 2120: 2093: 2068: 2041: 2016: 1992: 1965: 1941: 1914: 1890: 1865: 1704: 1674: 1669: 5196: 4889:"Polymorphisms in MYH9 are associated with diabetic nephropathy in European Americans" 3435: 3418: 2447: 2423: 2406: 2337: 1881: 984: 979: 974: 969: 964: 959: 954: 949: 944: 939: 934: 929: 924: 919: 914: 909: 904: 899: 894: 889: 884: 879: 874: 869: 864: 859: 854: 838: 833: 828: 823: 818: 813: 808: 803: 798: 793: 788: 783: 778: 773: 768: 763: 758: 753: 748: 743: 738: 733: 728: 723: 718: 713: 708: 703: 687: 682: 677: 672: 667: 662: 657: 652: 647: 642: 637: 632: 627: 622: 617: 612: 607: 8321: 8311: 8222: 8217: 7182: 7052: 7001: 6951: 6891: 6813: 6781: 6722: 6508: 6027: 5769: 5744: 5589: 5554: 5508: 5479: 5449: 5414: 4734:"Association of trypanolytic ApoL1 variants with kidney disease in African Americans" 4274: 4209: 4082: 4066: 4022: 4005: 3491: 3474: 594: 5927: 5858: 4329:

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