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Validated All-in-One™ qPCR Primer for TPSAB1(NM_003294.3) Search again
Powered by BiozBy 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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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
Tryptases comprise a family of trypsin-like serine proteases, the peptidase family S1. Tryptases are enzymatically active only as heparin-stabilized tetramers, and they are resistant to all known endogenous proteinase inhibitors. Several tryptase genes are clustered on chromosome 16p13.3. These genes are characterized by several distinct features. They have a highly conserved 3' UTR and contain tandem repeat sequences at the 5' flank and 3' UTR which are thought to play a role in regulation of the mRNA stability. These genes have an intron immediately upstream of the initiator Met codon, which separates the site of transcription initiation from protein coding sequence. This feature is characteristic of tryptases but is unusual in other genes. The alleles of this gene exhibit an unusual amount of sequence variation, such that the alleles were once thought to represent two separate genes, alpha and beta 1. Beta tryptases appear to be the main isoenzymes expressed in mast cells; whereas in basophils, alpha tryptases predominate. Tryptases have been implicated as mediators in the pathogenesis of asthma and other allergic and inflammatory disorders. [provided by RefSeq].
Gene References into function
- mitogenic effects in human airway smooth muscle cells
- stability and catalytic properties mediated by residues at the S1 pocket
- structure of Bowman-Birk inhibitor derived peptides
- Proliferative action is mediated by PAR2, COX2, prostaglandins, and PPARgamma : possible relevance to human fibrotic disorders.
- Beta-tryptase activates peripheral blood mononuclear cells isolated from healthy donors as well as multiple sclerosis (MS) patients, inducing release of TNF-alpha, IL-6, and IL-1 beta, and is most probably an important mediator of inflammation in MS.
- Results indicate a key role for heparin in the activation of human betaI- and beta2-tryptase.
- Tryptase and chymase and protein levels were determined in mast cells in fibrosarcoma.
- Mast cell tryptase cleaves protease-activated receptor 2 (PAR2) on colonocytes to increase paracellular permeability of the intestine during stress and inflammation.
- crystal structures of both the single and the double mutant forms of recombinant human alphaI-tryptase in complex with the peptide inhibitor leupeptin, as well as the structure of the non-inhibited single mutant
- mast cell beta-tryptase selectively cleaves asthmatic airway smooth muscle (ASM)-derived eotaxin and RANTES and abrogates their chemotactic activities, thus providing an explanation for the eosinophil paucity in asthmatic ASM bundles
- Bikunin was found to localize on the cell membrane, while tryptase was in the secretary granules of the mast cells from psoriatic lesions.
- Mast cell tryptase secretion into rheumatoid arthritis synovial fluid is higher than Osteoarthritis synovial fluid and stimulates the proliferation of Synovial fibrobalst-like cells.
- The disease severity and plasma tryptase levels were not affected by the number of alpha or beta tryptase alleles in mastocytosis patients.
- These results suggest that the characteristic neovascularization observed in pterygium may be sustained, at least in part, by mast cells angiogenic mediators, in particular tryptase.
- siHTbeta is for the most part an inactive species and any active monomer is a consequence of heparin binding to siHTbeta under dilute conditions where unfavorable thermodynamics and/or kinetics restrict formation of active tetramer.
- Up-regulates interleukin-8 expression in airway smooth muscle cells through a protease-activated receptor(PAR)-2-independent proteolytic mechanism.
- Tryptase activates TGFbeta via a PAR2-independent proteolytic mechanism in human ASM cells and may help understanding the role of tryptase in asthma.
- Tryptase stimulation of human small airway epithelial cells increased membrane-associated, calcium-independent phospholipase A(2)gamma (iPLA(2)gamma) activity, resulting in increased arachidonic acid and PGE(2) release.
- alternative mRNA splicing in multiple human tryptase genes has a role in regulating tetramer formation
- Positive correlation between serum tryptase concentration and hemoglobin, hematocrit, red blood cell count, and hepatic cell damage in kidney transplantation.