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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- Inversion of chromosome 16 [inv(16)] generates the fusion gene CBFB::MYH11 (CM) and is one of the most common chromosomal rearrangements in Acute Myeloid Leukemia (AML). Expression of CM is required for leukemia initiation. Patients with inv(16) at diagnosis invariably have the rearrangement at relapse, leading to the assumption that CM is also required after leukemic transformation. However, a role for CM in leukemia maintenance has yet to be shown experimentally. To address this, we used an inducible CM knockdown (KD) mouse model and found that decreased CM eliminated leukemia cells from the peripheral blood and spleen, but not the bone marrow, despite all populations exhibiting significantly decreased CM mRNA and protein. The surviving CM KD cells in the bone marrow showed decreased apoptosis and proliferation, and increased expression of autophagy related genes. Surprisingly, with prolonged KD of CM, ~40% of mice re-established disease despite maintaining decreased CM. Our work indicates that CM is required for leukemia survival in the spleen and peripheral blood, but in the bone marrow CM KD leukemia cells can survive and re-establish disease independent of the fusion protein. These findings imply that targeting CM alone has potential to reduce leukemic burden but not cure the disease. - Source: PubMed
Publication date: 2026/08/17
Panda SipraWang YiqianDogiparthi Venkatasai RahulBecker MichelleDhir ArjunLam CalvinRivas CeciliaAlemu LemlemGarrett LisaXiao PengSwenson Samantha AHewitt Kyle JHyde R Katherine - Atherosclerosis is the primary underlying cause of coronary artery disease. is a coronary artery disease risk gene whose role in coronary artery pathophysiology is unknown. Whole-body loss of causes a lethal neonatal visceral myopathy in mice, necessitating unique approaches for the study of vascular smooth muscle cell (VSMC) phenotypes. - Source: PubMed
Publication date: 2026/08/04
Salem Amr RKumar AjayDoja JaserWally AlshimaaGe ChunyuRobichaud SabrinaSlivano Orazio JGriffin Susan HMarshall BrendanPerry ElizabethFranklin J LeeSeeley Erin HDong KunzheBoczkowska MalgorzataCsanyi GaborBryant W BartVazquez-Padron Roberto INanda VivekDominguez RobertoLong XiaochunMiano Joseph M - The cellular origin of smooth muscle cell (SMC)-derived populations in vascular lesions remains unresolved. Here we show, using single-cell transcriptomic analyses spanning carotid ligation injury, Myh11-CreERT-traced aortic homeostasis, and LDLR- and ApoE-deficient atherosclerosis, that a rare progenitor-like "Primed" SMC compartment pre-exists at baseline in all models and in the healthy human aorta. Relative to contractile SMCs, Primed SMCs attenuate sarcomeric and contractile programmes while inducing matricellular, progenitor-niche and chondrogenic-poised developmental programmes, resolving into conserved niche/progenitor () and matricellular () cores overlaid by vessel-specific signatures, on a retained SMC identity. Multiple orthogonal computational lineage-inference approaches indicate that this compartment expands predominantly through autonomous self-renewal and is the dominant inferred source of cycling and lesion fibrochondrocyte populations, while contractile SMCs are consistently depleted as a feeder source. These findings reframe lesional SMC cellularity as expansion of a pre-existing Primed compartment rather than widespread phenotypic switching of contractile SMCs. - Source: PubMed
Publication date: 2026/07/24
Wani ShwethaliKitching MichaelAboulhassanzadeh SobhanLungu Teodora-SimonaKilicgun IsilUlibarri KarsynLiu WeiminFloudas AchilleasRedmond Eileen MCahill Paul A - Radiation therapy for rectal cancer often causes long-term bowel dysfunction. We investigated radiation-associated motility changes in human rectal smooth muscle, focusing on the role of platelet-derived growth factor receptor alpha-positive (PDGFRα⁺) cells and interstitial cells of Cajal (ICC). Human rectal tissues were obtained from patients undergoing surgery with (n=61) or without (n=51) preoperative concurrent chemoradiotherapy (CCRT). Isometric tension recordings were used to assess myogenic responses to potassium chloride (KCl), acetylcholine (ACh), sodium nitroprusside (SNP), and adenosine triphosphate (ATP). Neurogenic components were assessed using electrical field stimulation. Intracellular microelectrode recordings measured slow wave activity. Expression of interstitial cells, neuronal cells and smooth muscle cells was assessed by immunohistochemistry and quantitative PCR. ATP-induced relaxation and ATP-associated suppression of slow wave activity were significantly attenuated in irradiated rectal tissue, while responses to KCl, ACh, and SNP were preserved. PDGFRα and Kit expression levels were markedly decreased in irradiated tissue (P < 0.001), whereas NOS1, VAChT, and MYH11 expression levels remained unchanged. Immunostaining confirmed reduced PDGFRα⁺ cells and ICC in irradiated tissue. Pelvic irradiation delivered in the context of preoperative CCRT was associated with reduced PDGFRα⁺ cells and ICC, with associated attenuation of ATP-mediated inhibitory responses, which may contribute to rectal dysmotility. These results suggest that preserving purinergic signaling may offer a potential therapeutic approach to improve long-term bowel function after pelvic radiotherapy. - Source: PubMed
Publication date: 2026/07/31
Kwon Yoon-HyeSung Tae SikYun Young HyunJung HyunjinSo InsukRyoo Seung-BumPark Kyu Joo - Analysis of stage transition in gastric cancer is the aim of this project. - Source: PubMed
Publication date: 2026/05/02
Montazer FatemehRezaei-Tavirani MostafaArjmand BabakAsri NastaranRazzaghi ZahraRazi FaridehBandarian Fatemeh