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Validated All-in-One™ qPCR Primer for BTK(NM_000061.2) Search again
Product ID:
HQP017988
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
AGMX1, AT, ATK, BPK, IGHD3, IMD1, PSCTK1, XLA
Gene Description:
Bruton tyrosine kinase
Target Gene Accession:
NM_000061.2(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 plays a crucial role in B-cell development. Mutations in this gene cause X-linked agammaglobulinemia type 1, which is an immunodeficiency characterized by the failure to produce mature B lymphocytes, and associated with a failure of Ig heavy chain rearrangement.
Gene References into function
- Btk deficiency results in significantly impaired hydrogen peroxide-induced calcium signaling and reduced tyrosine phosphorylation of phospholipase Cgamma2 in cultured cells.
- mutational analysis in Spanish X linked agammaglobulinemia patients
- Direct stimulation of Bruton's tyrosine kinase by G protein alpha subunits
- mutations in Turkish patients with presumed X-linked agammaglobulinemia
- changes in the local concentration of Btk itself, or co-localization with exogenous signaling molecules that have high affinity for either proline sequence or the SH3 domain, can significantly alter species composition and regulate Btk kinase activity
- Interaction of Bruton's tyrosine kinase and protein kinase Ctheta in platelets
- Interaction between Btk TH and SH3 domain
- A total of 391 genes were found to be differentially expressed in BTK(-)cells, including kinases and transcriptions factors. Furthermore, one expressed sequence tag and eight complementary DNA clones with unknown function were down-regulated.
- Review article on X-linked agammaglobulinemia. The BTK gene is the primary defect in this disease.
- Flow cytometry revealed deficient expression of BTK protein in 10 of the 13 families, and this is the first report of the diagnosis of XLA by analysis of mutations of the BTK gene in Brazilian patients.
- the presence of wild-type BTK transcripts can be one of the many factors that influence the clinical and immunological phenotype in X-linked agammaglobulinemia.
- CD40 is a surface receptor through which the activity of Btk can be stimulated in human B cells.
- Btk is a Toll/interleukin-1 receptor domain-binding protein that is important for NFkappaB activation by TLR4
- Mutations were identified in BTK including a novel sequence deletion.
- Data show that overexpression of Bruton's tyrosine kinase results in the stabilization of tumor necrosis factor alpha mRNA via the 3' untranslated region.
- Defective expression of Bruton's tyrosine kinase in acute lymphoblastic leukemia in infants.
- results indicate that, contrary to Src and Abl, Btk might not require an assembled conformation for the regulation of its activity
- Conclusion of Btk transgene study is that autophosphorylation at residue Y223 is not essential for Btk function in vivo except for regulation of lambda light chain usage; and Btk partially acts as an adapter molecule independent of its catalytic activity
- Twenty-two novel mutations including one large deletion comprising the coding sequence from exon 11 to 18 in European X-linked agammaglobulinemia patients.
- Conservation and covariance in mutations of BTK domain sequences causing agammaglobulinemia were studied.
- Btk is essential in regulating thresholds for human B cell tolerance.
- 2 insertions, an SVA element and an AluY sequence, occurred 12 bp before the end of exon 9. Both had the typical hallmarks of a retrotransposon insertion including target site duplication and a long poly A tail.
- required for the signaling pathway activated by TLR4, which culminates in phosphorylation of p65 on serine 536 promoting transactivation by NFkappaB
- Ca2+-independent activation of Bruton's tyrosine kinase is required for store-mediated Ca2+ entry in human platelets
- lack of BTK expression or expression of dominant-negative splice variants in B cell precursor leukemia cells can (i) inhibit differentiation beyond the pre-B cell stage and (ii) protect from radiation-induced apoptosis
- Review summarizes how activated Btk transmits survival signals that are essential for the transforming activity of oncogenic Abl tyrosine kinase.
- Mal phosphorylation has an effect on tyrosine during signaling by TLR2 and TLR4 and Btk is the kinase involved
- data provide evidence for a common requirement for Btk in toll-like receptor 2 (TLR2)- and TLR4-mediated induction of two important proinflammatory cytokines, TNF and IL-1beta
- Btk is not essential for early lipopolysaccharide signaling in human monocytes.
- splice mutations of the BTK gene may have roles in X-linked agammaglobulinemia
- analysis of BTK activation mechanism and steady state kinetics
- A first report of an X-linked Agammaglobulinemia patient with a polymorphism in Btk SH3 domain has been identified after sequencing of the entire gene.
- Most of mutations were located at the kinase domain of Btk and, less frequently, they were found in PH and SH2 domains. Protein expression was also affected since most of the patients did not express or express very low Btk.
- Btk as a key signaling molecule that interacts with and acts downstream of TLR8 and TLR9.
- Plasmacytoid dendritic cells express a signalosome consisting of Lyn, Syk, Btk, Slp65 (Blnk) and PLCgamma2.
- Of 9 CVID patients from a single Taiwanese tertiary care hospital, we identified 2 cousins with decreased Btk expression who had a mutated (Asp521Val) kinase domain of Btk (1694A>T in exon 15)
- results suggest that none of the X-linked agammaglobulinaemia-associated Btk mutants with significant protein expression have a dominant negative effect over wild type Btk function
- Bruton's tyrosine kinase is not essential for Bcr-Abl-mediated transformation of lymphoid or myeloid cells.
- Btk mutation is associated with myelodysplastic syndrome in X-linked agammaglobulinemia.
- Mutations were categorized as mild or severe and patients were evaluated for the clinical severity of disease
- The crystal structure of the Btk PH domain in complex with dibutylyl-phosphatidylinositol-3,4,5-triphosphate was determined.
- Btk-regulated eicosanoid and ROS production occurs downstream of PI3K.