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Last update 08 May 2025

MYH9

Last update 08 May 2025

Basic Info

Synonyms

Cellular myosin heavy chain, type A, DFNA17, EPSTS

+ [13]

Introduction

Cellular myosin that appears to play a role in cytokinesis, cell shape, and specialized functions such as secretion and capping. Required for cortical actin clearance prior to oocyte exocytosis (By similarity). Promotes cell motility in conjunction with S100A4 (PubMed:16707441). During cell spreading, plays an important role in cytoskeleton reorganization, focal contact formation (in the margins but not the central part of spreading cells), and lamellipodial retraction; this function is mechanically antagonized by MYH10 (PubMed:20052411). (Microbial infection) Acts as a receptor for herpes simplex virus 1/HHV-1 envelope glycoprotein B.

Drugs associated with MYH9

NMIIA Inhibitor(University of Cincinnati)

Target

MYH9

Mechanism

MYH9 inhibitors

Active Org.

University of Cincinnati Physicians Co. LLC

Originator Org.

University of Cincinnati Physicians Co. LLC

Active Indication

HER2 Positive Breast Cancer

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Blebbistatin

Target

Cardiac myosin x MYH2 x MYH9

Mechanism

Cardiac myosin inhibitors [+2]

Active Org.

Harvard Medical School [+1]

Originator Org.

Harvard Medical School

Active Indication

Colitis

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Compound-011 (Protheragen)

Target

MYH9

Mechanism

MYH9 inhibitors

Active Org.

Protheragen, Inc.

Originator Org.

Protheragen, Inc.

Active Indication

Thrombosis

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with MYH9

100 Translational Medicine associated with MYH9

0 Patents (Medical) associated with MYH9

1,143

Literatures (Medical) associated with MYH9

01 May 2025·Modern Pathology

Clinical, Morphologic, and Genomic Findings in Spitz Tumors With RET Fusion: A Series of 31 Cases

Article

Author: De la Fouchardiere, Arnaud ; Gerami, Pedram ; Goto, Keisuke ; Donati, Michele ; Lemahieu, Julie ; Mansour, Boulos ; Goutas, Dimitrios ; Macagno, Nicolas ; Pissaloux, Daniel ; Van der Meulen, Joni ; Olivares, Shantel ; Nosek, Daniel ; Kervarrec, Thibault ; Kazakov, Dmitry V ; Perrone, Giuseppe ; Loontiens, Siebe

RET-fused Spitz neoplasms are rare and poorly characterized. We describe clinical, histologic and molecular findings of 31 Spitz neoplasms with RET fusion diagnosed as 16 Spitz nevus (SN), 13 atypical Spitz tumors (AST) and 2 Spitz melanoma (SM). The lesions mainly occurred in children and young adults of both sexes with predilection for the extremities. Microscopically, there were mainly symmetrical compound melanocytic neoplasms with a dome-shaped/slightly raised silhouette predominantly composed of epithelioid, spindled and/or smaller nevoid melanocytes arranged in confluent nests. Dyscohesive melanocytes within the nests in the upper part of the lesions, prominent Kamino bodies, giant multinucleated melanocytes, variable pigmentation and increased vascularity with vascular ectasia were frequent features. RNA sequencing detected 9 different 5' (N-terminus) fusion partners, including KIF5B (n= 8), LMNA (n= 7), CCDC6 (n= 6), OPTN (n= 3), MYO5A (n= 2) and NCOA4, ERC1, MYH9, AGAP3 (n= 1). Of these, OPTN::RET and AGAP3::RET represent novel fusions, and 3 further 5' fusion partners, namely NCOA4, ERC1 and MYH9 have never been reported in Spitz tumors. Although as a whole group, the tumors showed a heterogenous histopathologic presentation, correlation of the morphological features and the 5' fusion partners demonstrated certain associations. Nevoid melanocytes were exclusively encountered in cases with KIF5B fusion partner. Neuroid-like appearances with intersecting fascicles of spindled cells typified both MYO5A-fused cases. Epithelioid melanocyte population dominated cases with LMNA and CCDC6 fusion partners. Transepidermal elimination/floating intraepidermal nests of pigmented both spindled and epithelioid melanocytes were observed in the OPTN subgroup. The remaining cases with less frequent 5' fusion partners manifested in general more atypical histopathologic features, including nuclear pleomorphism, high mitotic count, atypical mitoses and sheet-like growth pattern. Melanoma fluorescence in situ hybridization (FISH) Probe Kit targeting RREB1, MYC, CDKN2A, and CCND1, was negative for copy number variation in 4 cases tested, including 2 cases with complete p16 nuclear loss on immunohistochemistry. Array comparative genomic hybridization (aCGH) performed in 3 lesions detected numerous segmental chromosomal imbalances in 2 cases diagnosed SM. DNA and RNA sequencing detected several further genomic alterations, including POU2F3 overexpression in 3 highly pigmented lesions. Further studies are needed to confirm possible correlations between the microscopic features and a particular fusion partner (or additional genetic events) in RET-fused Spitz neoplasms.

01 May 2025·Gene

Analysis of ferroptosis-related key genes and regulatory networks in diabetic foot ulcers

Article

Author: Wang, Juan ; Chen, Jianguo ; Zhong, Lin ; Wang, Jiale ; Zhang, Xuanfen ; Qiao, Jianxiong ; Zhou, Hanghang

BACKGROUNDDiabetic foot ulcers (DFUs) is a severe complication of diabetes. Recent evidence suggests that ferroptosis, a form of regulated necrosis, may play a significant role in the progression of DFU. However, the precise molecular mechanisms remain elusive.OBJECTIVEThis study aims to identify ferroptosis-related genes (FRGs) and the signaling pathways involved in DFU progression by analyzing the gene expression profiles of DFU.METHODSDifferentially expressed genes (DEGs) were identified by analyzing gene expression data from two DFU-related datasets (GSE38396, and GSE143735). FRGs were collected from both datasets and the literature. DEGs were then intersected with FRGs to identify ferroptosis-related differentially expressed genes (FRDEGs) in DFU. Functional enrichment analysis, protein-protein interaction (PPI) network analysis, receiver operating characteristic (ROC) curve analysis, and regulatory network interaction analysis (including mRNA-miRNA, mRNA-transcription factor (TF), and mRNA-drug interactions) were performed on the FRDEGs. Additionally, immune infiltration analysis was conducted using CIBERSORTx. Finally, skin tissue samples from clinical patients were collected, and the expression levels of FRDEGs in DFU samples were validated through reverse transcription quantitative real-time PCR (RT-qPCR), immunohistochemistry (IHC) and Immunofluorescence (IF), to uncover potential new targets for the diagnosis and treatment of DFU.RESULTSA total of 14 DFUs samples (non-healing group) and 12 control samples (healing group) were obtained in this study. We identified 276 DEGs in DFUs samples compared to controls, with 121 up-regulated and 155 down-regulated genes. By intersecting DEGs with ferroptosis-related genes, we identified 10 FRDEGs (AURKA, CTH, FBLN1, FTL, GLS2, KDM5C, MYH9, PCNA, PYCR1, and SPARC). The GO and KEGG analysis results showed that FRDEGs were mainly enriched in biological processes such as amino acid biosynthesis and tight junction pathways. Further analysis of FRDEGs identified ten hub genes closely associated with 112 TFs, 34 miRNAs, and 50 drugs or molecular compounds. Additionally, RT-qPCR validation of skin tissue samples from 8 DFU patients and 8 controls showed that AURKA were significantly up-regulated in DFU, IHC and IF analysis further demonstrated elevated AURKA protein expression in DFU samples. Moreover, AURKA was identified as a potential diagnostic marker for diabetic wound healing, with high diagnostic accuracy based on ROC curve analysis (AUC = 0.950 in the combined dataset, and AUC = 0.881 in the validation dataset). These findings highlight AURKA as a key gene involved in ferroptosis and a potential target for the diagnosis and monitoring of DFUs.CONCLUSIONThis study identified FRDEGs associated with DFUs, highlighting AURKA as a key diagnostic marker. These findings offer valuable insights into the molecular mechanisms driving DFUs and suggest potential therapeutic targets for their management.

01 Apr 2025·Acta Pharmacologica Sinica

Endothelial FOSL1 drives angiotensin II-induced myocardial injury via AT1R-upregulated MYH9

Article

Author: Yang, Ai-Hua ; Qian, Hong-Yan ; Zhang, Yi-Feng ; Qian, Yi ; Zhao, Wen-Jing ; Zhu, Wei-Zhong ; Liu, Yi ; Cao, Jia-Xin

Vascular remodeling represents a pathological basis for myocardial pathologies, including myocardial hypertrophy and myocardial infarction, which can ultimately lead to heart failure. The molecular mechanism of angiotensin II (Ang II)-induced vascular remodeling following myocardial infarction reperfusion is complex and not yet fully understood. In this study, we examined the effect of Ang II infusion on cardiac vascular remodeling in mice. Single-cell sequencing showed Ang II induced cytoskeletal pathway enrichment and that FOS like-1 (FOSL1) affected mouse cardiac endothelial dysfunction by pseudotime analysis. Myosin heavy chain 9 (MYH9) was predominantly expressed in primary cardiac endothelial cells. The Ang II type I receptor blocker telmisartan and the protein kinase C inhibitor staurosporine suppressed Ang II-induced upregulation of MYH9 and FOSL1 phosphorylation in human umbilical vein endothelial cells. Silencing MYH9 abolished Ang II-mediated inhibition of angiogenesis in human umbilical vein endothelial cells, and attenuated AngII-induced vascular hyperpermeability. We found that FOSL1 directly bound to the MYH9 promoter and thus activated transcription of MYH9 by the dual luciferase reporter and chromatin immunoprecipitation assays, leading to vascular dysfunction. In vivo, 6 weeks after injecting adeno-associated virus-ENT carrying the TEK tyrosine kinase (tie) promoter-driven short hairpin RNA for silencing FOSL1 (AAV-tie-shFOSL1), cardiac function represented by the ejection fraction and fractional shortening was improved, myocardial fibrosis was decreased, protein levels of phosphorylated FOSL1, MYH9, and collagen type I alpha were reduced, and cardiac vascular density was recovered in mice with endothelial Fosl1-specific knockdown in Ang II-infused mice. In ischemia-reperfusion mice, AAV-shFosl1 mice had a reduced infarct size and preserved cardiac function compared with control AAV mice. Our findings suggest a critical role of the FOSL1/MYH9 axis in hindering Ang II-induced vascular remodeling, and we identified FOSL1 as a potential therapeutic target in endothelial cell injuries induced by myocardial ischemia-reperfusion.

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MYH9

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