MYH11_RABIT SMMHC ELISA tesk kit
- Known as:
- MYH11_RABIT SMMHC Enzyme-linked immunosorbent assay test tesk reagent
- Catalog number:
- gen17199
- Product Quantity:
- 1
- Category:
- Peptides
- Supplier:
- Other suppliers
- Gene target:
- MYH11_RABIT SMMHC ELISA tesk kit
Related genes to: MYH11_RABIT SMMHC ELISA tesk kit
- Gene:
- MYH11 NIH gene
- Name:
- myosin heavy chain 11
- Previous symbol:
- -
- Synonyms:
- SMMHC, SMHC
- Chromosome:
- 16p13.11
- Locus Type:
- gene with protein product
- Date approved:
- 1991-09-13
- Date modifiied:
- 2016-06-22
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- Thoracic aortic dissection (TAD) is a life-threatening condition with a significant genetic contribution. This study evaluated the clinical implications of diagnostic screening of 368 TAD patients for (likely) pathogenic (LPP) variants in 23 TAD-associated genes and sought to identify genotype-phenotype correlations. Clinically relevant causative variants were identified in 12.5% of patients. Most patients were explained by LPP variants in FBN1 (n = 13), ACTA2 (n = 8), COL3A1 (n = 6), and TGFBR1 (n = 5), and all identified LPP variants were found in the genes identified by the ClinGen Aortopathy Expert Panel to be definitively or strongly associated with heritable aortopathy. LPP patients had a significantly younger age at dissection and had almost a two-fold increase in risk of dissection at any age compared to those without a rare genetic variant (HR, 1.98; 95% CI, 1.4-2.8; p < 0.001). COL3A1 LPP variant-harboring patients were particularly young, with a median age at dissection of 22 years. Patients with more than one variant of uncertain significance (VUS) experienced dissection at younger ages compared to single VUS-harboring individuals (p = 0.002). Presence of the MYH11 NM_001040113.2:c.3787_3789del (p.Lys1263del) VUS was indicative of a younger age at dissection. In conclusion, our study demonstrated the clinical utility of current genetic testing in TAD patients. Yet, it highlights the need for improved VUS interpretation and their consideration as risk factors. Further improvements in the screening approaches are needed to increase clinical utility and, hence, mitigate TAD morbidity and mortality by identification of at-risk individuals. - Source: PubMed
Publication date: 2026/06/03
Velchev Joe DavisKrebsová AliceVotýpka PavelZoubková VeronikaAmsel Bram JWildiers AntoonVerrijcken AntonLaga StevenGerber Bernhard LYildiz HalilFransen ErikMeester Josephina A NBoeckx NeleAlaerts MaaikeVoorendt MarshaKempers MarliesVan Laer LutLoeys Bart LVerstraeten Aline - The synthetic phenotype of vascular smooth muscle cells (VSMCs) accelerates the progression of atherosclerosis (AS) and plaque erosion (PE). EP4 enhances pro-inflammatory macrophages within plaques and impedes cholesterol efflux. However, evidence for EP4 regulating VSMC phenotypic switching remains weak. This study aims to elucidate the function of EP4 in the phenotypic transformation of VSMCs and its potential molecular mechanisms. - Source: PubMed
Publication date: 2026/06/01
Zhe ChunyangLi YangjieHe MingHe XiaoyanLi ZhuoLi HuiHu YanGao RuiDing Xumeng - Neointimal hyperplasia (NH) is a prominent pathological consequence following vascular injury and is driven in part by aberrant vascular smooth muscle cell (VSMC) proliferation. COP9 signalosome (CSN) subunit 5 (CSN5/JAB1/COPS5) is the deneddylase component of the CSN holocomplex responsible for deneddylation of cullin-RING ligases. Although CSN5/CSN is well studied in cancer biology, the role of CSN5/CSN in NH and vascular biology remain largely unexplored. Here, we investigated whether selective inhibition of CSN5 deneddylase activity using CSN5i-3 could mitigate neointimal remodeling following arterial injury. Adult mice were subjected to daily intraperitoneal injections of CSN5i-3 (20 mg/kg/day) or vehicle and left common carotid artery ligation. The left and the right common carotid arteries were then assessed for VSMC phenotypic modulation and neointima formation after 7 days of treatment. CSN5i-3 treatment markedly attenuated the ligation-induced changes in the mRNA level of , and , genes associated with extracellular matrix deposition and cell-cycle progression but did not alter expression changes of canonical smooth muscle differentiation markers () and in the ligated vessel. Importantly, CSN5i-3 significantly blunted the increases of PCNA expression and Ki67-positive VSMCs and reduced neointimal areas. These findings demonstrate that CSN deneddylase activity is dispensable for the dedifferentiation of contractile VSMCs into the synthetic state but promotes VSMC proliferation, supporting the concept that the dedifferentiation and proliferation of VSMCs in neointimal formation are separately regulated processes and differentially regulated by different CSN actions. This study also indicates that CSN5i-3 is highly promising in preventing neointimal hyperplasia. - Source: PubMed
Publication date: 2026/06/03
Giri SamikshaWang Xuejun - Moyamoya angiopathy (MMA) is a rare, chronic progressive cerebrovascular condition characterized by bilateral stenosis or occlusion of the terminal internal carotid arteries and their major branches. This progressive occlusion triggers the development of telangiectatic and fragile vessels at the base of the brain, creating the characteristic angiographic appearance of a "puff of smoke." Depending on the etiology, MMA is classified as Moyamoya Disease (MMD) when idiopathic and primary or Moyamoya Syndrome (MMS) when associated with underlying systemic conditions. While the gene, particularly the p.R4810K variant, is recognized as the major susceptibility locus for MMD in East Asian populations, it does not fully account for the global genetic landscape or the phenotypic diversity of the disease. This review provides a comprehensive overview of the genetic architecture of the entire MMA spectrum, exploring loci beyond . We analyze the role of genes involved in vascular smooth muscle cell contractility (, ), TGF-β signaling, and DNA repair mechanisms that drive MMS, alongside the genetic basis of syndromic forms associated with neurofibromatosis type 1, trisomy 21, and RASopathies. Understanding these diverse genetic drivers is crucial for early diagnosis, risk stratification, and the development of targeted molecular therapies. - Source: PubMed
Publication date: 2026/05/15
Sorte GiovanniCantone MariagiovannaBella RitaSalemi MicheleZedde MarialuisaZappia Mario - Intrauterine adhesions (IUA) are fibrotic scars that impair endometrial regeneration, and compromise fertility. Emerging evidence implicates circular RNAs (circRNAs) in fibrotic remodeling, but it remains unclear how the circRNA landscape and circRNA-associated splicing programs coordinately link uterine contractility, endometrial cell-cycle control, and immune activation in IUA. - Source: PubMed
Publication date: 2026/05/07
Chen YingqingJin JingXiang YingWang YanpingWu ShuangZhan NiXiong MengxinDeng Ali