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Validated All-in-One™ qPCR Primer for JAK1(NM_002227.3) Search again
Product ID:
HQP101233
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
AIIDE, JAK1A, JAK1B, JTK3
Gene Description:
Janus kinase 1
Target Gene Accession:
NM_002227.3(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
Janus kinase 1 (JAK1), is a member of a new class of protein-tyrosine kinases (PTK) characterized by the presence of a second phosphotransferase-related domain immediately N-terminal to the PTK domain. The second phosphotransferase domain bears all the hallmarks of a protein kinase, although its structure differs significantly from that of the PTK and threonine/serine kinase family members. JAK1 is a large, widely expressed membrane-associated phosphoprotein. JAK1 is involved in the interferon-alpha/beta and -gamma signal transduction pathways. The reciprocal interdependence between JAK1 and TYK2 activities in the interferon-alpha pathway, and between JAK1 and JAK2 in the interferon-gamma pathway, may reflect a requirement for these kinases in the correct assembly of interferon receptor complexes.
Gene References into function
- role in regulating oncostatin M receptor surface expression
- requirement in interferon-gamma-mediated inhibition in human chondrocytes
- interaction with cytokine receptors and role in activation of cytokine and growth factor signaling pathways
- Measles virus suppresses interferon-alpha signaling pathway: suppression of Jak1 phosphorylation
- Data suggest there is no defect in the JAK/STAT pathway in the tested melanoma cell lines, and that interferon resistance must be mediated through other components.
- In the IFN signaling pathway leading to STAT activation, both JAK1 and TYK2 are essential, whereas NF-kappaB activation requires only TYK2.
- the SH2 domain is structurally important for cytokine receptor binding and surface expression of the oncostatin m receptor
- Data show that medroxyprogesterone acetate treatment of mammary tumor cells up-regulated Stat3 protein expression and induced rapid, nongenomic Stat3, Jak1, and Jak2 tyrosine phosphorylation.
- JAK1 and JAK2 must work cooperatively and not independently and that their actions are dependent on having normal kinase activity to trigger downstream signals leading to Interleukin-3 independent proliferation
- Two different heterozygous mutations in the Janus kinase 1 (JAK1) gene result in complete loss of the protein in several different prostate cancer cell lines.
- mutations in the JAK1 and Tyk2 genes may be identified as initial molecular defects in human cancers and autoimmune diseases
- JAK1/2 are client proteins of Hsp90 alpha and beta; Hsp90 and CDC37 play a critical role in types I and II interferon pathways
- These results suggest that the JAK1-JH7-3 domains are required for interleukin-3 receptor common beta subunit interaction and abolish wild type JAK1 and JAK2-mediated signaling.
- IFN-alpha-induced apoptosis in the MM cell lines U266 and H929 was completely blocked by a specific inhibitor of Jak1
- Functional cross-talk between Ras/extracellular signal-regulated kinase (Erk) and IL-4/Janus kinase 1 (JAK1)/STAT6 contributes to the regulation of IL-4 transcription in T cells.
- The results indicate that Adenovirus down-regulates host epithelial cell Jak1 to assure inhibition of the antiviral effects of multiple mediators to subvert airway defense responses and establish a productive infection.
- Mealse virus V protein can block the direct phosphorylation of STAT1 by Jak1 to escape IFN alpha/beta signaling.
- Small interference RNAs specific for Jak1, was identified that reproducibly reduce viral RNA and viral protein levels in hepatitis C virus replicon-bearing cells
- two independent and indispensable signaling pathways-1) JAK1-associated PI3K signaling and 2) Act1/TRAF6/TAK1-mediated NF-kappaB activation-are stimulated by IL-17A to regulate gene induction in human airway epithelial cells.
- identified 2 novel somatic mutations in highly conserved residues of the JAK1 gene (T478S, V623A), in 2 separate patients
- The structural integrity of both the FERM domain and of the kinase domain of JAK1 is essential for both receptor binding and catalytic function/autoinhibition
- Theses findings illustrate the biologic significance of JAK1, 2/STAT3 signaling in colorectal cancer (CRC) progression and provide novel evidence that the JAK/STAT3 pathway may be a new potential target for therapy of CRC.
- These findings implicate dysregulated JAK1 function in acute lymphoblastic leukemia.
- The C-28 methyl ester of the oleane triterpenoid 2-cyano-3,12-dioxooleana-1,9-dien-28-oic acid (CDDO-Me) inhibits activation of the JAK1-->STAT3 pathway by forming adducts with both JAK1 and STAT3.
- murine OSMR initiates STAT5 activation directly via the receptor bound Janus kinases. Intriguingly, the murine receptor preferentially recruits JAK2, whereas the human receptor seems to have a higher affinity for JAK1.
- Some of the JAK1 and JAK3 mutations may to be functional and contributes to cancer development, especially to T-ALL development.
- JAK/STAT-1 signaling pathway was necessary and sufficient to mediate the down-regulation of FcRn gene expression by IFN-gamma
- Iron chelators and hypoxia mimetics inhibit IFNgamma-mediated Jak-STAT signaling
- TCPTP is a negative regulator of SFK, JAK1 and STAT3 signalling during the cell cycle.