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Validated All-in-One™ qPCR Primer for S100A9(NM_002965.3) Search again
Product ID:
HQP016548
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
60B8AG, CAGB, CFAG, CGLB, L1AG, LIAG, MAC387, MIF, MRP14, NIF, P14, S100-A9
Gene Description:
S100 calcium binding protein A9
Target Gene Accession:
NM_002965.3(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
The protein encoded by this gene is a member of the S100 family of proteins containing 2 EF-hand calcium-binding motifs.
Gene References into function
- S100A8/A9 accounts for the entire arachidonic acid-binding capacity of the neutrophil cytosol, indicating that S100A8/A9 plays an essential role in arachidonic acid-dependent enzymes and arachidonic acid-consuming pathways.
- investigagion of serum levels in organ transplantation (procalcitonin)--marker of inflammation
- crystal structure of the calcium-bound form, analyzed at 2.1 A resolution
- These data indicate that calprotectin (MRP8 and MRP14) has higher specific activity to induce apoptosis than the individual subunits, and that the mechanism is exclusion of zinc from target cells.
- identifies regulatory elements within the promoter that drive the cell type-specific and differentiation-dependent protein expression
- Proinflammatory myeloid-related protein S100A9 induces a dose- and time-dependent activation of the HIV-1 long terminal repeat promoter region that can be blocked by specific polyclonal antibody and by physical denaturation of the protein.
- S100A8 and S100A9 calcium-binding proteins: localization within normal and cyclosporin A-induced overgrowth gingiva, in spino-cellular layer and extracellularly in desmosomes, in cytoplasm and nuclei.
- the localization of the arachidonic acid-binding site within the unique C-tail of S100A9 correlates with the fact that fatty acid binding has not yet been reported for other S100 proteins
- S100A9 stimulates shedding of L-selectin, up-regulates and activates Mac-1/CD11b, induces neutrophil adhesion to fibrinogen in vitro, and is involved in neutrophil migration to in vivo inflammatory sites.
- plays a prominent role in leukocyte trafficking and arachidonic acid metabolism; elevated levels of S100A9 and S100A8 in body fluids of inflamed tissues strengthen the view that these molecules are important players in fighting inflammation [review]
- increased levels in fetal disease, premature rupture of membranes, and preterm labor
- MRP8/MRP14 dimer behaves as a positive mediator of phagocyte NADPH oxidase regulation
- Abrogation of MRP-14 activity with a specific antibody reduced the IL-8-stimulating potential of bronchial secretions, suggesting it was a stimulus to IL-8 production in the lung and may amplify neutrophilic inflammation in bronchial disease
- MRP8/MRP14 complex inhibited proliferation and differentiation of myoblasts and induced apoptosis via activation of caspase-3 in a time- and dose-dependent manner. Activated macrophages can destroy and regenerate myocytes via MRP8/MRP14.
- Since MRP-8/MRP-14 exhibit direct effects on leukocyte adhesion to the vascular endothelium, their extensive expression in the epidermis indicates an active role for these S-100 proteins in the initial phase of this systemic autoimmune disease.
- protein expression profiles in HL-60 cells with ATRA treatment revealed a protein remarkably expressed in the differentiated cells, which was identified as S100A9
- Results of this study suggest that reduction of MRP14 expression is a frequent event in Chinese human esophageal cancer.
- decreased expression of MRP8 and MRP14 might play an important role in the pathogenesis of human esophageal squamous cell carcinoma, being particularly associated with poor differentiation of tumor cells.
- S100A8/A9 might induce apoptosis in tumor cells through a dual mechanism: one is zinc exclusion from the target cells, and the other represents an as yet undefined mechanism, possibly in a ligand-receptor dependent fashion.
- Fibronectin adhesive capacity and integrin expression of monocytes of type 1 and type 2 diabetic patients is related to the subjects' serum levels of MRP14.
- expression of MRP8/MRP14 closely correlated with the inflammatory activity in systemic vasculitis
- S100A8/A9 promotes phagocyte NADPH oxidase activation by supplying the enzyme with its cofactor arachidonic acid
- Correlated with degree of differentiation. Absent in undifferentiated basalioma and strongly expressed in carcinoma in situ, keratoacanthoma, and differentiated squamous cell carcinoma. Expressed in superficial, differentiated region of normal epithelium
- MRP-14 is a potential mediator of p38 MAP kinase-dependent functional responses in human neutrophils.
- data suggest that enhanced expression of S100A8, S100A9, and RAGE is an early event in prostate tumorigenesis and may contribute to development and progression or extension of prostate carcinomas
- S100A8 and S100A9 in atherosclerotic plaque and calcifying matrix vesicles may significantly influence redox- and Ca2+-dependent processes during atherogenesis
- This study indicates a potential role for pro-inflammatory S100A9 and S100A12 in pathogenesis caused by inflammation and protein complex formation in Alzheimer's disease
- heterodimeric S100 calcium binding protein A8/S100 calcium binding protein A9 might play a hitherto unknown role in triggering atherosclerosis in diabetes and renal failure
- S100A8/A9 heterodimer, secreted extracellularly from activated tissue macrophages, may amplify proinflammatory cytokine responses in rheumatoid arthritis.
- MRP-14 expression increases before ST-segment-elevation myocardial infarction (STEMI), and increasing plasma concentrations of MRP-8/14 among healthy individuals predict the risk of future cardiovascular events.
- calcium-dependent formation of (S100A8/S100A9)2 tetramers is an essential prerequisite for biological function.
- MRP-8/14 was mainly detected in human cervical mucus and showed a positive correlation with proinflammatory cytokines
- MRP-8/MRP-14 are exclusively secreted by granulocytes in patients with acute Kawasaki disease, and intravenous immune globulin treatment suppresses their gene expression.
- Zinc-binding, like calcium, induces (S100A8/S100A9)(2)-tetramers.
- S100A8 and S100A9 are involved in the innate defense of the bronchial epithelium
- Excessive release of cytotoxic MRP8/MRP14 by activated phagocytes might therefore present an important molecular pathomechanism contributing to endothelial damage during vasculitis and other inflammatory diseases
- Authors hypothesize that L1AG might become internalized nonspecifically into target cells, perhaps by pinocytosis. This predicts cell survival of cultured stomach tumor cells as a function of L1AG concentration.
- poly(ADP-ribose)polymerase-1 and Ku70/Ku80 are transcriptional regulators of S100A9 gene expression
- In contrast, neutrophil adhesion to fibronectin was completely inhibited by anti-beta2 integrins, suggesting that S100A9-induced specific activation of beta2 integrin is essential to neutrophil adhesion.
- data suggest unidentified natural ligands for CD69 and/or CD69 autoantibodies possibly affect joint-composing cell types through increased production of S100A9 in neutrophils, providing insight into functions of CD69 on neutrophils in rheumatoid arthriti
- The pattern of S100A4 expression differed significantly from that of the proinflammatory proteins S100A9 and S100A12, which were restricted to phagocytes and granulocytes.
- HaCaT keratinocytes overexpressing the S100 proteins S100A8 and S100A9 show increased NADPH oxidase and NF-kappaB activities.
- Report showed S100A9 was expressed human bone and cartilage cells and may contribute to calcification of the cartilage matrix and its replacement with trabecular bone, and to regulation of redox in bone resorption.
- Data suggest that S100 proteins calprotectin and S100A12 are related to radiographic changes rather than disease activity in psoriatic arthritis with low disease activity.
- Serum calprotectin (S100A8/S100A9)and S100A12 are increased in children with inflammatory bowel disease and indicate disease activity.
- MRP8/14 may be involved in the pathogenesis of sarcoid granulomas. The measurement of serum MRP8/14 levels is useful for the diagnosis of sarcoidosis.
- The homo-oligomeric forms of S100A8 and S100A9 are readily degraded by proteases, and the preferred hetero-oligomeric S100A8/A9 complex displays a high resistance even against proteinase K degradation.
- presence of a positive feedback loop for growth stimulation involving S100A8/A9 and cytokines in human epidermal keratinocytes
- These data indicate that S100A8/A9-induced cell death involves Bak, selective release of Smac/DIABLO and Omi/HtrA2 from mitochondria, and modulation of the balance between pro- and anti-apoptotic proteins.
- S100A8/A9-promoted cell growth occurs through RAGE signaling and activation of NF-kappaB.
- It is suggested that S100A8 is S100A9-dependently expressed and acquires the protein stability by S100A8/A9 heterocomplex formation; S100A8 and S100A9 overexpression should be considered marker of poor prognosis in invasive ductal carcinoma
- S100A9 expression was significantly decreased in CRS without nasal polyps
- RAGE, carboxylated glycans and S100A8/A9 play essential roles in tumor-stromal interactions, leading to inflammation-associated colon carcinogenesis.
- analysis of calgranulin B (S100A9) levels in bronchoalveolar lavage fluid of patients with interstitial lung diseases
- annexin A6 contributes to the calcium-dependent cell surface exposition of the membrane associated-S100A8/A9 complex
- S100A9 is gene with moderate CpG-density that show a less stringent relationship between DNA methylation and gene expression
- This study revealed S100A8/A9 genes as candidate markers for metastatic potential of breast epithelial cells.
- Overexpression of S100A9 is associated with barrett's esophagus-associated high-grade dysplasia.
- These data suggested that upregulation of S100A9 mediated by P. gingivalis is an important event in the development of aortic intimal hyperplasia.
- Data indicate that both S100A8 and S100A9 are required for their fully active antifungal effect and that oxidation regulates S100A8/A9 antifungal activity through mechanisms that remain to be elucidated and evaluated.
- S100A9 was induced in human monocytes and macrophages, by polyinosinic:polycytidylic acid, a dsRNA mimetic