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Validated All-in-One™ qPCR Primer for CMA1(NM_001836.4) Search again
Product ID:
HQP002142
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
CYH, MCT1, chymase
Gene Description:
chymase 1
Target Gene Accession:
NM_001836.4(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
This gene product is a chymotryptic serine proteinase that belongs to the peptidase family S1. It is expressed in mast cells and thought to function in the degradation of the extracellular matrix, the regulation of submucosal gland secretion, and the generation of vasoactive peptides. In the heart and blood vessels, this protein, rather than angiotensin converting enzyme, is largely responsible for converting angiotensin I to the vasoactive peptide angiotensin II. Angiotensin II has been implicated in blood pressure control and in the pathogenesis of hypertension, cardiac hypertrophy, and heart failure. Thus, this gene product is a target for cardiovascular disease therapies. This gene maps to 14q11.2 in a cluster of genes encoding other proteases. [provided by RefSeq].
Gene References into function
- The S1 primary specificity pocket defines substrate specificity of chymases.
- The mast cell chymase A3255 allele was shown to have an effect on HDL cholesterol metabolism.
- The local release of mast cell chymase has potentially profound effects on airway smooth muscle cell function by disruption of the cell-associated matrix and inhibition of epidermal growth factor-induced smooth muscle cell proliferation.
- Results suggest the additive effect of angiotensin I-converting enzyme (ACE) and heart chymase (CMA) gene polymorphisms on the increase in left ventricular mass in NIDDM patients.
- Chymase may play a role in heart remodeling by increasing Ang II formation and activating MMP-9, and the regulation of collagen I gene expression.
- Both the ACE and chymase-like enzyme activities in the aneurysmal aortae were significantly higher than those in the control aortae.
- Degradation of phospholipid transfer protein (PLTP) and PLTP-generated pre-beta-high density lipoprotein by this enzyme in mast cells impairs high affinity efflux of cholesterol from macrophage foam cells.
- Interactions among the loops bordering and defining the active site appear to influence both the zymogen and the activated conformations of chymase in this model.
- albumin is a substrate of human chymase
- new class of chymase inhibitor through a substituent analysis of MWP00965 chemically synthesized
- chymase depletes pre-beta-high density lipoprotein, which impairs ATP-binding cassette transporter A1- but not scavenger receptor class B type I-mediated lipid efflux to high density lipoprotein
- MCT1 immunoreactivity was visible in blood vessel walls as early as the 13th week of gestation mainly in the visual cortical plate and subplate.
- mast cell chymase-1 is unlikely to influence blood pressure levels in the Japanese population.
- Bladder fibrosis may be mediated by mast cell chymase stimulation of collagen synthesis.
- The synthesis of new potential inhibitors of human chymase is described
- Tryptase and chymase and protein levels were determined in mast cells in fibrosarcoma.
- mast cell chymase activates ERK and p38 probably through G-protein-coupled receptor, and the ERK but not p38 cascade may have a crucial role in chymase-induced migration of eosinophils
- A novel (TG)n(GA)m repeat polymorphism 254 bp downstream of the mast cell chymase (CMA1) gene is associated with atopic asthma and total serum IgE levels.
- Chymase-induced apoptosis of conjunctival epithelial cells represents anoikis, which is a slowly occurring apoptotic process induced by lack of adhesion to an extracellular matrix.
- Significant association between the CMA1 promoter polymorphism rs1800875 and atopic eczema supports the hypothesis that CMA1 serves as candidate gene for atopic eczema.
- activated human skin mast cells (MCs) convert CTAP-III into biologically active NAP-2 through proteolytic cleavage by released chymase.
- The CMA1 polymorphisms studied do not contribute to disease susceptibility in Japanese or Dutch sarcoidosis patients.
- AGEs, a hallmark of diabetes, induce chymase via the RAGE-ERK1/2 MAP kinase pathway. Chymase initiates an important alternative angiotensin II-generating pathway in diabetes and may play a critical role in diabetic vascular disease.
- chymase in mast cells may have a role in inflammatory bowel disease
- There was higher angiotensin-converting enzyme (ACE) and chymase mRNA expression and mast cell density in failing than in control myocardium and no changes in ACE2 expression were detected.
- These observations suggest that mast cell chymase, possibly induced by interleukin-4-dependent phenotypic modulation, may be an important mediator in the inflammatory and fibrotic processes of idiopathic interstitial pneumonia in humans.
- Chymase promoted the migration of vascular smooth muscle cells in the matrix-coated invasion chambers and activated promatrix metalloproteinase-2 obtained from the culture medium of vascular smooth muscle cells.
- chymase inactivates the FAK-mediated cell survival signaling
- epithelial chymase is rapidly activated by a ligand-independent mechanism following mechanical stress via cytoskeletal and reactive oxygen species signaling and is associated with the onset of epithelial cell migration
- In Japan, carriage of the MMP-7-181 G allele and of the CMA/B A allele were each associated with an increased risk for H. pylori-related noncardia gastric cancer development.