MYH11_CHICK MYH11 ELISA tesk kit
- Known as:
- MYH11_CHICK MYH11 Enzyme-linked immunosorbent assay test tesk reagent
- Catalog number:
- gen17180
- Product Quantity:
- 1
- Category:
- Peptides
- Supplier:
- Other suppliers
- Gene target:
- MYH11_CHICK MYH11 ELISA tesk kit
Related genes to: MYH11_CHICK MYH11 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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- 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 - Core-binding factor (CBF) leukemias, including inv(16) AML, involve RUNX1/CBFβ chromosomal rearrangements that generate oncogenic fusion proteins. In inv(16) AML, the CBFβ-SMMHC fusion (CBFB-MYH11) dominantly perturbs RUNX1 by sequestering it in aberrant, high-affinity complexes. Structural studies reveal that CBFβ-SMMHC binds the RUNX1 Runt domain with higher affinity than wild-type CBFβ, aided by a second RUNX1-binding site in its SMMHC tail. This altered interface underlies the fusion's dominant-negative disruption of RUNX1 target-gene regulation. Chemical probes have been developed to disrupt this interface; notably, the bivalent inhibitor AI-10-49 selectively binds CBFβ-SMMHC, displacing RUNX1 and restoring RUNX1 transcriptional function. AI-10-49 delays leukemia progression in murine inv(16) models and induces apoptosis in human inv(16) AML cells. Mechanistically, uncoupling RUNX1 from CBFβ-SMMHC liberates RUNX1 to repress oncogenic programs: for example, RUNX1 rebinds distal MYC enhancers and recruits polycomb factors (RING1B) in place of SWI/SNF (BRG1) to silence MYC, triggering leukemia cell apoptosis. These chromatin and transcriptional consequences underscore how CBFβ-SMMHC sustains leukemic transcriptional programs. Importantly, combining CBFβ-SMMHC inhibitors with BET bromodomain inhibitors synergistically eradicates inv(16) leukemia in preclinical models. Together, these insights into the structural basis and functional role of the CBFβ-SMMHC-RUNX1 interface highlight protein-protein interaction disruption as a promising translational strategy in core-binding factor leukemia therapy. - Source: PubMed
Publication date: 2026/05/16
Kamel Emadeldin MKhadrawy Sally MostafaAli Mohamed A MAhmed Noha AAlkhedhairi SalehAlkhayl Faris F AbaLamsabhi Al Mokhtar - Although acute myeloid leukemia (AML) with CBFB::MYH11 rearrangement is classified as favorable-risk, approximately 40% of patients experience relapse. We evaluated the prognostic impact of CBFB::MYH11 transcript levels and the optimal timing of allogeneic hematopoietic cell transplantation (allo-HCT) at first complete remission (CR1). A total of 186 patients with CBFB::MYH11-rearranged AML treated with intensive induction chemotherapy were included. CBFB::MYH11 levels after cycles 2 and 3 were strongly correlated (P < 0.001). The post-cycle 2 CBFB::MYH11 transcript level emerged as the strongest prognostic marker for both disease-free survival (DFS) and overall survival (OS), outperforming assessments after cycles 1 or 3. CBFB::MYH11 ≥ 1% after cycle 2 was independently associated with inferior DFS (HR 3.84, P < 0.001) and OS (HR 3.98, P = 0.003). Among patients with post-cycle 2 CBFB::MYH11 ≥ 1.0%, the 3-year DFS and OS were both 91.7% in patients who received allo-HCT at CR1, compared with 47.8% and 72.9%, respectively, in the chemotherapy consolidation group. Multivariate analysis indicated that allo-HCT in CR1 improved 3-year DFS compared with chemotherapy consolidation (HR 0.24; P = 0.023). However, no significant improvement in OS was observed during follow-up. These findings suggest that post-cycle 2 CBFB::MYH11 level ≥1.0% identifies a high-risk subgroup that may benefit from allo-HCT in CR1. - Source: PubMed
Publication date: 2026/05/14
Wang MingyangZhang GuangjiGuo WenwenZhang HaixiaoCao JiaxinLuo JieyaYang MiaoCao YigengWang FengjiaoZhang RongliChen XinZhai WeihuaMa QiaolingWei JialinYang DonglinHe YiPang AimingFeng SizhouHan MingzheMi YingchangWang JianxiangWei HuiJiang Erlie - Severe burn injury induces a prolonged hypermetabolic state that is associated with undesirable metabolic consequences. Heat shock factor 1 (HSF1) is the predominant transcription factor that responds to thermal stress and has been reported to orchestrate the browning gene program of subcutaneous white adipose tissue (sWAT), thereby promoting energy expenditure. However, the role of sWAT HSF1 in the pathogenesis of burn injury remains unclear. In this study, we report that burn injury notably upregulates the expression of HSF1 in sWAT. Moreover, the genetic ablation of HSF1 in adipose tissues attenuated the burn-induced sWAT browning and lipolysis, circulating lipid dysfunction, and liver injury. Conversely, specific overexpression of the active form of HSF1 in sWAT exacerbated these phenotypes. Notably, we found that burn injury largely suppressed sWAT smooth muscle-related gene programs and shifted toward browning gene programs. Mechanistically, HSF1, in cooperation with PRDM16, drives this phenotypic switch by directly inhibiting the expression of Myh11, which is the smooth muscle marker for sWAT reprogramming. Furthermore, the pharmacological inhibition of HSF1 with DTHIB ameliorated burn injury. Overall, these findings highlight that sWAT HSF1 is a key mediator of pathological hypermetabolism following severe burn injury. - Source: PubMed
Publication date: 2026/05/07
Zhang YankangZheng YuhanChen BinLi XinqianZhang TingXu LingyanMa JingMa XinranLi Yu