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Validated All-in-One™ qPCR Primer for JAK3(NM_000215.3) Search again
Product ID:
HQP101241
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
JAK-3, JAK3_HUMAN, JAKL, L-JAK, LJAK
Gene Description:
Janus kinase 3
Target Gene Accession:
NM_000215.3(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 Janus kinase (JAK) family of tyrosine kinases involved in cytokine receptor-mediated intracellular signal transduction. It is predominantly expressed in immune cells and transduces a signal in response to its activation via tyrosine phosphorylation by interleukin receptors. Mutations in this gene are associated with autosomal SCID (severe combined immunodeficiency disease).
Gene References into function
- The first demonstration that JAK3 mutations underlie autosomal recessive severe combined immunodeficiency
- JAK3 is associated with the Interleukin-2 receptor gamma-chain (IL2RG).
- JAK3 is phosphorylated in response to stimulation of lymphocytes with IL-2
- Cloning of human Jak3
- mutations in severe combined immune deficiency (SCID) due to JAK3 deficiency
- eleven novel mutations in patients with severe combined immunodeficiency-including the first patients with mutations in the kinase domain
- In the T cell line HUT-78, JAK3 was found to be highly phosphorylated. These results suggest that SHP-1 might be involved in maintaining the IL-2R/JAK3 signaling pathway under control and point towards a role of SHP-1 in the pathogenesis of the disease.
- JAK3 is associated with a pre-phosphorylated IL-4Ralpha and CD40. This novel "heterotrimer" (p-IL-4Ralpha, CD40/JAK3) is functional and controls STAT3 phosphorylation and CD40 expression.
- the JH2 domain contributes to both the uninduced and ligand-induced Jak-receptor complex, where it acts as a cytokine-inducible switch to regulate signal transduction
- newly described sequence corrects the previous published genomic sequence from Jak3 spanning introns 10 and 11 rather than identifying an insertion or translocation specific to these ALL
- 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.
- The Jak3 promoter is found 60 bp upstream of a large (roughly 3500 bp) intron in the nontranslated 5' protion of Jak3 mRNA; it is active in primary lymphocytes, Jurkat T cells, and NK3.3 cells, but not in COS or HeLa cells.
- A highly selective and potent JAK3 inhibitor is effective in a nonhuman primate model of transplant rejection
- mutations all resulted in abnormal B-cell Janus kinase 3 (JAK3)-dependent interleukin-2 (IL-2)-induced signal transducer and activator of transcription-5 (STAT5) phosphorylation.
- Findings support a model in which JAK3 signaling enhances IL-10 production in monocytes/macrophages leading to down-regulation of IL-1 beta converting enzyme (ICE) activation and suppression of IL-1 beta processing and release.
- Review. Jak3 mediates signal transduction via the gamma common chain of lymphokine surface receptors. Its structural and genetic features are discussed.
- CXCL12 signaling is independent of Jak2 and Jak3
- phosphate group on pTyr981 in the activation loop is in part coordinated by an arginine residue in the regulatory C-helix, suggesting a direct mechanism by which the active position of the C-helix is induced by phosphorylation of the activation loop
- We conclude that Jak3 activation is predominantly restricted to ALK-positive ALCL tumors. Most likely.
- Inhibition of JAK3 signaling in colon carcinoma tumors and cell lines induces apoptosis and cell cycle arrest of colon carcinoma cells.
- JAK3 is a highly significant, prognostic immunohistochemical marker in CRC. This study proves that cDNA microarrays, plotted by a small number of genes from a few samples, are both practical and useful.
- WHI-P154, an inhibitor of Janus protein tyrosine kinase (JAK3), Hck and Syk, prevented PDGF-induced neurite outgrowth.
- IL-9/Jak3 signaling plays a significant role in the pathogenesis of ALK+ anaplastic large-cell lymphoma
- The transforming activity of JAK3(V674A) was confirmed by its introduction into 32Dcl3-mCAT. Sequencing of the original JAK3 cDNA derived from the patient, however, failed to detect the V674A mutation.
- Loss of SHP1 enhances JAK3/STAT3 signaling and decreases proteosome degradation of JAK3 and NPM-ALK in ALK+ anaplastic large-cell lymphoma.
- Findings illustrate the biological importance of gain-of-function JAK3 mutations in leukemogenesis.
- evidence of VEGF production in cutaneous T-cell lymphoma, which is promoted by aberrant activation of Jak3 and the JNKs
- These results suggest that oncostatin M inhibits adiponectin expression by inducing dedifferentiation of adipocytes through signaling pathways involving JAK3 and MEK, but not JAK2.
- 4 types of JAK3 mutations were found in acute megakaryoblastic leukemia & transient myeloproliferative disorder patients, all in the pseudokinase domain or receptor-binding domain. I87T is in the common-gamma-subunit-binding domain.
- data suggest that both gain-, and loss-of function mutations of jak3 can be acquired in Down syndrome -transient myeloproliferative disorder /acute megakaryoblastic leukaemia (DS-TMD/AMKL)
- a novel pathway in intestinal enterocytes in which IL-2 enhances intestinal wound repair through mechanisms involving Jak3 and its interactions with villin.
- the effect of IL-15 and IL-21, which are closely related to IL-2 and share the usage of the common gamma chain and of its JAK3-associated pathway.
- 2 new Tyr phosphorylation sites within Jak3, Y904 & Y939, are conserved among Jak family proteins. Y904 and Y939 were required for optimal ATP usage by Jak3, while phosphorylation of Y939 preferentially promoted Stat5 activity in intact cells.
- review of roles of Jak2, Jak3, and MPL mutations in signal transduction and etiology of myeloid malignancies
- the JAK3 activating mutation is an early event during leukaemogenesis in Down syndrome
- Some of the JAK1 and JAK3 mutations may to be functional and contributes to cancer development, especially to T-ALL development.
- In a series of human AMKL samples from both Down syndrome and non-Down syndrome patients, mutations were identified within KIT, FLT3, JAK2, JAK3, and MPL genes, with a higher frequency in DS than in non-DS patients.