{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMYH9 encodes the nonmuscle myosin heavy chain IIA, a motor protein central to the regulation of actomyosin contractility, cell–cell adhesion, cytokinesis, and migration. Its physiological importance is underscored by the fact that germ‐line mutations in MYH9 underlie a spectrum of congenital disorders—including macrothrombocytopenia, May–Hegglin anomaly, and related syndromes—which manifest with abnormal platelet formation, hearing loss, cataracts, and nephritis. In cellular models, MYH9’s assembly into bipolar filaments is tightly modulated by phosphorylation and interactions with regulatory proteins, ensuring proper cytoskeletal dynamics and cell polarity."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "12"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nComprehensive genetic studies have revealed that polymorphisms at the MYH9 locus substantially contribute to kidney disease. Multiple genome‐wide and admixture analyses in populations—especially among individuals of African ancestry—have linked MYH9 risk variants with focal segmental glomerulosclerosis, hypertensive and non‐diabetic end‐stage renal disease, and proteinuria. These association studies indicate that MYH9 not only predisposes to glomerular injury but may also explain, in part, the ethnic disparities observed in kidney disease susceptibility, even though its exact pathogenic role in some forms (for example, type 2 diabetes–associated nephropathy) remains to be fully elucidated."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "13", "end_ref": "21"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its developmental and disease‐initiating roles, MYH9 is a key regulator of cytoskeletal dynamics that govern cell migration, adhesion turnover, and immune cell functions. For instance, studies in fibroblasts, mesenchymal stem cells, T lymphocytes, and natural killer cells have shown that MYH9 modulates contractility during cell spreading and directional movement, facilitates deadhesion at the uropod of migrating lymphocytes, and is essential for the transit of lytic granules through actin networks. In parallel, alterations in MYH9 function—such as those arising from fusion events (for example, MYH9–ALK chimeras) or altered interactions with signaling molecules—affect oncogenic processes. In various tumor models, MYH9 has been implicated both as a suppressor (where loss of MYH9 activity promotes invasive behavior) and as a promoter of tumor stemness through dysregulation of pathways (for example, the β‐catenin axis) in cancers such as hepatocellular carcinoma and breast cancer."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "22", "end_ref": "42"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "K E Heath, A Campos-Barros, A Toren, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Nonmuscle myosin heavy chain IIA mutations define a spectrum of autosomal dominant macrothrombocytopenias: May-Hegglin anomaly and Fechtner, Sebastian, Epstein, and Alport-like syndromes."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Am J Hum Genet (2001)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1086/324267"}], "href": "https://doi.org/10.1086/324267"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "11590545"}], "href": "https://pubmed.ncbi.nlm.nih.gov/11590545"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "Gian Marco Ghiggeri, Gianluca Caridi, Umberto Magrini, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Genetics, clinical and pathological features of glomerulonephritis associated with mutations of nonmuscle myosin IIA (Fechtner syndrome)."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Am J Kidney Dis (2003)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1053/ajkd.2003.50028"}], "href": "https://doi.org/10.1053/ajkd.2003.50028"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "12500226"}], "href": "https://pubmed.ncbi.nlm.nih.gov/12500226"}]}, {"type": "r", "ref": 3, "children": [{"type": "t", "text": "Marco Seri, Alessandro Pecci, Filomena Di Bari, et al. "}, {"type": "b", "children": [{"type": "t", "text": "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."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Medicine (Baltimore) (2003)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1097/01.md.0000076006.64510.5c"}], "href": "https://doi.org/10.1097/01.md.0000076006.64510.5c"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "12792306"}], "href": "https://pubmed.ncbi.nlm.nih.gov/12792306"}]}, {"type": "r", "ref": 4, "children": [{"type": "t", "text": "Laurence Lamant, Randy D Gascoyne, Marie Michèle Duplantier, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Non-muscle myosin heavy chain (MYH9): a new partner fused to ALK in anaplastic large cell lymphoma."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Genes Chromosomes Cancer (2003)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1002/gcc.10232"}], "href": "https://doi.org/10.1002/gcc.10232"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "12800156"}], "href": "https://pubmed.ncbi.nlm.nih.gov/12800156"}]}, {"type": "r", "ref": 5, "children": [{"type": "t", "text": "A Balduini, I Pallotta, A Malara, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Adhesive receptors, extracellular proteins and myosin IIA orchestrate proplatelet formation by human megakaryocytes."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "J Thromb Haemost (2008)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1111/j.1538-7836.2008.03132.x"}], "href": "https://doi.org/10.1111/j.1538-7836.2008.03132.x"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "18752571"}], "href": "https://pubmed.ncbi.nlm.nih.gov/18752571"}]}, {"type": "r", "ref": 6, "children": [{"type": "t", "text": "Doron M Behar, Saharon Rosset, Shay Tzur, et al. "}, {"type": "b", "children": [{"type": "t", "text": "African ancestry allelic variation at the MYH9 gene contributes to increased susceptibility to non-diabetic end-stage kidney disease in Hispanic Americans."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Hum Mol Genet (2010)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1093/hmg/ddq040"}], "href": "https://doi.org/10.1093/hmg/ddq040"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "20144966"}], "href": "https://pubmed.ncbi.nlm.nih.gov/20144966"}]}, {"type": "r", "ref": 7, "children": [{"type": "t", "text": "Alessandro Pecci, Alessandro Malara, Stefania Badalucco, et al. 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"}, {"type": "b", "children": [{"type": "t", "text": "MYH9 is a major-effect risk gene for focal segmental glomerulosclerosis."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Nat Genet (2008)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1038/ng.226"}], "href": "https://doi.org/10.1038/ng.226"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "18794856"}], "href": "https://pubmed.ncbi.nlm.nih.gov/18794856"}]}, {"type": "r", "ref": 15, "children": [{"type": "t", "text": "Barry I Freedman, Pamela J Hicks, Meredith A Bostrom, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Polymorphisms in the non-muscle myosin heavy chain 9 gene (MYH9) are strongly associated with end-stage renal disease historically attributed to hypertension in African Americans."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Kidney Int (2009)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1038/ki.2008.701"}], "href": "https://doi.org/10.1038/ki.2008.701"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "19177153"}], "href": "https://pubmed.ncbi.nlm.nih.gov/19177153"}]}, {"type": "r", "ref": 16, "children": [{"type": "t", "text": "Shay Tzur, Saharon Rosset, Revital Shemer, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Missense mutations in the APOL1 gene are highly associated with end stage kidney disease risk previously attributed to the MYH9 gene."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Hum Genet (2010)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1007/s00439-010-0861-0"}], "href": "https://doi.org/10.1007/s00439-010-0861-0"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "20635188"}], "href": "https://pubmed.ncbi.nlm.nih.gov/20635188"}]}, {"type": "r", "ref": 17, "children": [{"type": "t", "text": "Giulio Genovese, Stephen J Tonna, Andrea U Knob, et al. "}, {"type": "b", "children": [{"type": "t", "text": "A risk allele for focal segmental glomerulosclerosis in African Americans is located within a region containing APOL1 and MYH9."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Kidney Int (2010)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1038/ki.2010.251"}], "href": "https://doi.org/10.1038/ki.2010.251"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "20668430"}], "href": "https://pubmed.ncbi.nlm.nih.gov/20668430"}]}, {"type": "r", "ref": 18, "children": [{"type": "t", "text": "Takashi Sekine, Mutsuko Konno, Satoshi Sasaki, et al. 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"}, {"type": "b", "children": [{"type": "t", "text": "MYH9 and APOL1 are both associated with sickle cell disease nephropathy."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Br J Haematol (2011)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1111/j.1365-2141.2011.08832.x"}], "href": "https://doi.org/10.1111/j.1365-2141.2011.08832.x"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "21910715"}], "href": "https://pubmed.ncbi.nlm.nih.gov/21910715"}]}, {"type": "r", "ref": 20, "children": [{"type": "t", "text": "Jessica N Cooke, Meredith A Bostrom, Pamela J Hicks, et al. 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