MYH10

Last update 08 May 2025

Basic Info

Synonyms

Cellular myosin heavy chain, type B, MYH10, myosin heavy chain 10

+ [8]

Introduction

Cellular myosin that appears to play a role in cytokinesis, cell shape, and specialized functions such as secretion and capping. Involved with LARP6 in the stabilization of type I collagen mRNAs for CO1A1 and CO1A2. During cell spreading, plays an important role in cytoskeleton reorganization, focal contacts formation (in the central part but not the margins of spreading cells), and lamellipodial extension; this function is mechanically antagonized by MYH9. (Microbial infection) Acts as a receptor for herpes simplex virus 1/HHV-1 envelope glycoprotein B.

100 Clinical Results associated with MYH10

100 Translational Medicine associated with MYH10

0 Patents (Medical) associated with MYH10

288

Literatures (Medical) associated with MYH10

01 Apr 2025·Genetics in Medicine

Expanding the genetics and phenotypes of ocular congenital cranial dysinnervation disorders

Article

Author: Glaze, Carmen ; Demer, Joseph L. ; Isenberg, Sherwin J. ; Gerth-Kahlert, Christina ; Koc, Feray ; Kerr, Natalie C. ; Hanisch, Frank ; Larsen, Dorte Ancher ; Bothun, Erick D. ; Wabbels, Bettina ; Zubcov-Iwantscheff, Alexandra A. ; Traboulsi, Elias I. ; Mullineaux, Lisa ; Ferreira, Carlos R. ; Magli, Adriano ; Levy, Richard L. ; Curry, Cynthia J. ; Mackey, David A. ; Yang, Edward ; Halliday, Dorothy J. ; Berman, Jeffrey L. ; Poduri, Annapurna ; Elder, James E. ; Lee Dahm, Thomas ; O’Donnell-Luria, Anne ; Phalen, James A. ; Ciccarelli, Maria Laura ; Groopman, Emily ; Penzien, Johann ; Holder, Christopher ; Davitt, Bradley V. ; Staffieri, Sandra E. ; Drack, Arlene V. ; Hunter, David G. ; Prasov, Lev ; Talkowski, Michael E. ; MacArthur, Daniel G. ; Petersen, Robert ; Wirth, Megan M. ; Stalker, Heather J. ; Miller, Kathryn Bisceglia ; Al-Haddad, Christiane ; Singer-Berk, Moriel ; Ko, Melissa W. ; Mikail, Claudia N. ; Robson, Caroline D. ; Wilson, Michael W. ; Shaaban, Sherin ; Pandey, Pramod Kumar ; Mensching, Fiona M. ; Jurgens, Julie A. ; Hay, Eleanor ; Pratt, Brandon M. ; Sanchis-Juan, Alba ; Kahana, Alon ; Wong, Isaac ; Lee, Arthur S. ; Heidary, Gena ; Lek, Monkol ; Rivera-Quiles, Cristina ; Moller, H.U. ; Robb, Richard M. ; Désir, Julie ; Pavone, Piero ; Gottlob, Irene ; Whitman, Mary C. ; Christiansen, Stephen P. ; Zwaan, Johan ; Stasheff, Steven F. ; Woods, C. Geoffrey ; Wong, Agnes M.F. ; Lay-Son, Guillermo ; Singer, Harvey S. ; Taranath, Deepa Ajay ; Iannaccone, Alessandro ; Ugrin, Maria Cristina ; Zenteno, Juan C. ; Kazlas, Melanie ; Johnston, Suzanne C. ; Mantagos, Iason S. ; Berube, Lindsay ; Brand, Harrison ; Capasso, Jenina ; Strominger, Mitchell B. ; Strassberg, Sonya ; Elliott, Alexandra T. ; Polo, Claudia R. ; Thomas, Ioan Talfryn ; Soul, Janet S. ; Vogel G, Marlene C. ; Nishimura, Julie K. ; Lemire, Gabrielle ; Flaherty, Maree P. ; Smith, Lois E.H. ; Cordonnier, Monique ; Foster, Emma E. ; Wu, Carolyn ; Menezes, Manoj P. ; Feldman, Hagit Baris ; Bradford, Victoria R. ; Chacon-Camacho, Oscar Francisco ; De Berardinis, Teresa ; Maystadt, Isabelle ; Bekele, Sarah ; Weisburd, Ben ; Young, Terri L. ; Matos Ruiz, Paola M. ; Cox, Gerald F. ; Pais, Lynn ; Katowitz, James A. ; Dagi, Linda R. ; Zhao, Xuefang ; Mills, Monte D. ; Marti, Candice ; David, Karen L. ; McKenzie, Fiona ; Engle, Elizabeth C. ; Epley, K. David ; Noble, A. Gwendolyn ; VanderVeen, Deborah K. ; Chan, Wai-Man ; England, Eleina M. ; Miyana, Kaori ; Andrews, Caroline ; Yeung, Alison ; Barry, Brenda J. ; Horton, Jonathan C. ; D’Esposito, Fabiana ; Levin, Alex V. ; Sorkin, Jeffrey A. ; Rossillion, Béatrice ; MacKinnon, Sarah ; Russell, Kathryn A. ; Ledoux, Danielle M. ; Di Gioia, Silvio Alessandro ; Vincent, Andrea L. ; Ramos-Caceres, Maria ; Lyons, Christopher J. ; Fulton, Anne B. ; Toffoloni, Melissa ; Chang, Lan ; Ramos, Feliciano J. ; Grill, Stephen ; Eggenberger, Eric ; Sahin, Mustafa ; Miller, David T. ; Fu, Jack M. ; Abarca-Barriga, Hugo ; Kimonis, Virginia

PURPOSEThis study aimed to identify genetic etiologies and genotype/phenotype associations for unsolved ocular congenital cranial dysinnervation disorders (oCCDDs).METHODSWe coupled phenotyping with exome or genome sequencing of 467 probands (550 affected and 1108 total individuals) with genetically unsolved oCCDDs, integrating analyses of pedigrees, human and animal model phenotypes, and de novo variants to identify rare candidate single-nucleotide variants, insertion/deletions, and structural variants disrupting protein-coding regions. Prioritized variants were classified for pathogenicity and evaluated for genotype/phenotype correlations.RESULTSAnalyses elucidated phenotypic subgroups, identified pathogenic/likely pathogenic variant(s) in 43 of 467 probands (9.2%), and prioritized variants of uncertain significance in 70 of 467 additional probands (15.0%). These included known and novel variants in established oCCDD genes, genes associated with syndromes that sometimes include oCCDDs (eg, MYH10 [HGNC:7568], KIF21B [HGNC:29442], TGFBR2 [HGNC:11773], and TUBB6 [HGNC:20776]), genes that fit the syndromic component of the phenotype but had no prior oCCDD association (eg, CDK13 [HGNC:1733], TGFB2 [HGNC:11768]), genes with no reported association with oCCDDs or the syndromic phenotypes (eg, TUBA4A [HGNC:12407], KIF5C [HGNC:6325], CTNNA1 [HGNC:2509], KLB [HGNC:15527], FGF21 [HGNC:3678]), and genes associated with oCCDD phenocopies that had resulted in misdiagnoses.CONCLUSIONThis study suggests that unsolved oCCDDs are clinically and genetically heterogeneous disorders often overlapping other Mendelian conditions and nominates many candidates for future replication and functional studies.

01 Mar 2025·Journal of Cellular and Molecular Medicine

A Novel Disulfidptosis‐Related Diagnostic Gene Signature and Differential Expression Validation in Ischaemic Cardiomyopathy

Article

Author: Bo, Xiaohong ; Zhang, Ge ; Zeng, Yiyao ; Fan, Huimin ; Tang, Junnan ; Xu, Shuai ; Qin, Zhen ; Fan, Jili ; Zhou, Yafeng ; Yu, Fengyi ; Tan, Xin

ABSTRACTIschaemic cardiomyopathy (IC) predominantly arises from prolonged deprivation of oxygen in the coronary arteries, resulting in compromised cardiac contractility or relaxation. This study investigates the role of disulfidptosis‐associated genes (DiGs) in IC. Through the analysis of datasets GSE5406 and GSE57338, we explored the association between DiGs and immune characteristics to identify crucial genes contributing to IC development. The support vector machine model emerged as the most effective, identifying key genes such as MYH9, NUBPL, MYL6, MYH10 and NCKAP1. Validation with independent datasets GSE57345, GSE48166 and single‐cell GSE145154 further supported these findings, demonstrating high predictive accuracy. Experimental validation in an IC mouse model, using Western blot, immunohistochemistry and RT‐qPCR, confirmed the altered expression of these core genes in myocardial ischaemic regions. This research not only elucidates the significance of DiGs in IC but also underscores the diagnostic potential of identified core genes.

15 Feb 2025·The FASEB Journal

Exploring a novel risk model based on core disulfidptosis‐related genes in periodontitis: Bioinformatics analyses and experimental validation

Article

Author: Chen, Jia ; Liu, Qi ; Tian, Xue ; Yang, Yiqiang ; Lu, Xun ; Yang, Jiahui ; Wang, Yuran

AbstractBacteria in dental plaque invade periodontal tissues, causing chronic inflammation known as periodontitis. Despite advancements in understanding periodontitis, its molecular pathogenesis remains incompletely elucidated. In this study, a total of 247 samples were retrieved from the Gene Expression Omnibus (GEO) database, comprising 183 from individuals with periodontitis and 64 from healthy controls. Differentially expressed DRGs (DE‐DRGs) were identified, and their expression correlations were analyzed. Immune cell infiltration and its association with DE‐DRGs were assessed. Gene Set Variation Analysis (GSVA) was performed to determine key functions and pathways related to DE‐DRGs. Characteristic DE‐DRGs (CDE‐DRGs) were identified using the Least Absolute Shrinkage and Selection Operator (LASSO) analysis, and a risk model and personalized nomogram were constructed. Model performance was validated through calibration and decision curve analysis (DCA). External experiments, including qRT‐PCR and Western blot, confirmed the differential expression of DE‐DRGs. Fourteen DE‐DRGs were identified. Expression analysis revealed a strong synergistic correlation between MYH9 and ACTB (coefficient = 0.86) and an antagonistic correlation between NCKAP1 and FLNA (coefficient = −0.52). Immune profiling showed significant differences in the proportions of 22 immune cell types between groups, with 14 DE‐DRGs correlated with immune infiltration levels. Cluster analysis of periodontitis samples revealed distinct patterns of DE‐DRGs expression and immune cell infiltration across two clusters. A risk model incorporating four CDE‐DRGs (DSTN, SLC7A11, SLC3A2, and RPN1) was developed, alongside a personalized nomogram for predicting periodontitis risk. qRT‐PCR and Western blot analyses demonstrated downregulation of DSTN, SLC3A2, IQGAP1, CD2AP, and NCKAP1 and upregulation of SLC7A11, RPN1, FLNA, MYH9, TLN1, ACTB, MYH10, CAPZB, and PDLIM1 in periodontitis tissues. This study identified key DRGs in periodontitis, developed a predictive risk model and nomogram, and detailed the immune infiltration profile and its association with DRGs. These findings provide insights into the molecular pathogenesis of periodontitis and suggest potential strategies for personalized risk assessment, early diagnosis, and targeted therapy.

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