Ask about this productRelated genes to: MYOM1 antibody
- Gene:
- MYOM1 NIH gene
- Name:
- myomesin 1
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 18p11.31
- Locus Type:
- gene with protein product
- Date approved:
- 1998-12-09
- Date modifiied:
- 2019-04-23
Related products to: MYOM1 antibody
Related articles to: MYOM1 antibody
- Vandetanib is a novel multi-targeted tyrosine kinase inhibitor (TKI) that has demonstrated clinical efficacy in the long-term treatment of medullary thyroid carcinoma. However, its use is frequently associated with cardiovascular side effects, some of which may be life-threatening. Notably, multi-targeted TKIs have been increasingly implicated in the risk of cardiotoxicity. Among these, cardiac contractile dysfunction has emerged as a critical concern, yet the underlying mechanisms remain incompletely elucidated-particularly the phenomenon of excitation-contraction uncoupling. This study aims to investigate how vandetanib affects cardiac contractility, with a specific focus on sarcomeric protein degradation, and to identify potential molecular targets for reversing myofilament degradation. Chronic treatment with vandetanib led to a significant reduction in myocardial contractile function, the disruption of cardiac troponin T (cTnT), cardiac troponin I (cTnI) organization and downregulation of essential myofilament proteins, including cTnT (42.3% ± 5.6% protein loss)and MYOM1 (32.7% ± 4.9% protein loss), without notable suppression of calcium-handling proteins such as JPH2, p-PLN, and p-CaMKII. Calcium imaging revealed preserved sarcoplasmic reticulum (SR) calcium release, suggesting contractile dysfunction was not primarily calcium-driven. Instead, reduced myofilament calcium sensitivity and partial sarcomere disassembly were observed. Mechanistically, we identified upregulation of calpain expression and enzymatic overactivation as key mediators of sarcomeric protein degradation. Inhibition of calpain activity partially rescued vandetanib-induced loss of contractile proteins and preserved myofilament structure. Calpain1 overexpression aggravated, while calpain1 knockdown partially rescued, vandetanib-induced cTnT degradation. Our findings uncover a novel mechanism underlying TKI-induced cardiotoxicity, involving calpain-dependent degradation of cardiac myofilament proteins and independent of calcium dysregulation. This study highlights the critical role of sarcomere stability in maintaining cardiac function during TKI therapy and identifies calpain as a promising therapeutic target for cardioprotection, with calpain activation rather than calcium dysregulation being the key driver of vandetanib-induced cardiac dysfunction. - Source: PubMed
Publication date: 2026/02/27
Ji FangHuang JieYan JieLv SiLu LinWen HuLu JianYuan HuanGu YinshanLiao BinWu LinXie BingbinLi Miaoling - MYOM1, a major component of the vertebrate myofibrillar M band, binds myosin, titin, and light meromyosin, has been linked to cardiomyopathy and unexpected sudden death, yet the pathogenic mechanisms remain unclear. Leveraging the UK Biobank, we identified a significant association between dilated cardiomyopathy (DCM) and loss-of-function (LoF) MYOM1 variants. Functional studies showed that MYOM1 deficiency precipitates DCM with overt heart failure, accompanied by sarcomeric disorganization, pathological structural remodeling, and mitochondrial abnormalities. Optical mapping of cardiac electrophysiology revealed slowed ventricular conduction with increased heterogeneity, alongside marked prolongation of action potential duration and depolarization. At the molecular level, transcriptomic and immunoblot analyses demonstrated downregulation of key sarcoplasmic reticulum regulators, including RYR2 and SERCA2. Consistent with these findings, calcium imaging documented impaired calcium conduction velocity and blunted intracellular calcium transients, indicating sarcoplasmic reticulum dysfunction. Our study provided significant insights into the role of MYOM1 variants in DCM. LoF of MYOM1 contributes to DCM and heart failure by disrupting sarcomere integrity and destabilizing sarcoplasmic reticulum calcium homeostasis, with secondary mitochondrial abnormalities. These data establish MYOM1 as a disease-relevant determinant of myocardial remodeling and excitation-contraction coupling, and support MYOM1 as a potential target for risk stratification and therapy in DCM. - Source: PubMed
Publication date: 2026/02/10
Ruan JinghuaGuan YutingLe KaixingZhang AoTan PingpingRan YuqingWu HuilanPeng YongmiaoWang YijiaFeng XingLi XuekunZhang BingLiu ZhigangMa DaqingShu QiangGuo Xiaoling - To characterize the reproductive tract microbiota in patients with ovarian chocolate cysts (CC) and adenomyosis (AM) compared to controls (NC), and investigate the in vitro effects of representative differential bacteria on human endometrial stromal cells (T-HESC). - Source: PubMed
Publication date: 2025/11/05
Li JunchiZhang YulinZhang JunliYue ChongGuo LanYang GuangjiJiang ZhimeiRen DongyanYu Tao - The prevalence of RNA binding proteins (RBPs) in regulating alternative splicing (AS) in age-related sensorineural hearing loss (SNHL) is unclear. To address this question, we comprehensively analyzing RNA-seq data from a mouse model to identify deregulated AS events (RASEs) and differentially expressed RNA binding proteins (DERBPs) associated with age-related SNHL, and constructed the networks between these two levels of changes. We have identified 198 and 187 RASEs related to severe and mild symptoms, respectively. Genes harboring these RASEs are significantly enriched in positive regulation of GTPase activity and cytoskeleton organization. We further identified 25 and 14 DERBPs related to severe and mild symptoms, respectively, and constructed the regulatory network between DERBPs and RASEs. Among these DERBPs, the significantly increased expression of Isg15 and Myom1, the decreased expression of Acan, as well as some of their regulated RASEs including two in Uap1 also demonstrated in cochlear transcriptomes obtained from the age-related SNHL mouse model constructed in this study. Analysis of human pluripotent stem cell-derived macrophages containing ISG15 knockout samples revealed that ISG15 is a key splicing regulator, and can directly regulate the alternative splicing of UAP1 in human cells. These findings prove insights into the involvement of a large number of alternative splicing events driven by RNA-binding proteins (RBPs) in the pathogenesis of age-related SNHL, and suggest their potentials as therapeutic targets and disease markers. - Source: PubMed
Publication date: 2025/10/22
Yu WeiQin ZepingLiang XinYuZhu XianbaiTan GuojingRen BaiyangXiang YanghongZou CanZhou XueqinWang HongyangDeng Anchun - This study aimed to investigate population genetic differences related to reproductive traits between Duroc and Yorkshire (Dutch Large White) pigs using two approaches: linear mixed models that dissect additive and dominant effects, and selective sweep analysis. (1) Methods: Genome-wide single-nucleotide polymorphism (SNP) data of 3917 Duroc and 3217 Yorkshire pigs were analyzed. The first principal component (PC1) was used as a simulated phenotype to capture population-level variance. Additive and dominant genetic effects were partitioned and evaluated by using the combination of the linear mixed models (LMM) and ADDO's algorithm (LMM + ADDO). In parallel, selective sweep signals were detected using fixation index () and nucleotide diversity (θ) analyses. A comparative assessment was then conducted between the LMM + ADDO and the selective sweep analysis results. Significant loci were annotated using quantitative trait loci (QTL) databases and the Ensembl genome browser. (2) Results: There are 39040 SNPs retained after quality control. Using the LMM + ADDO framework with PC1 as a simulated phenotype, a total of 632 significant SNPs and 184 candidate genes were identified. Notably, 587 SNPs and 171 genes were uniquely detected by the LMM + ADDO method and not among loci detected by the top 5% of and θ values. Key candidate genes associated with litter size included , , , and , while , , and were associated with teat number traits. (3) Conclusions: This study demonstrates the power of integrating additive and dominant effect modeling with population genetics approaches for the detection of genomic regions under selection. The findings provide novel insights into the genetic architecture of reproductive traits in pigs and have practical implications for understanding the inheritance of complex traits. - Source: PubMed
Publication date: 2025/07/11
Chen ChangyiHe YuKe JuanZhang XiaoranFei JunwenSun BoxingSun HaoBai Chunyan