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Validated All-in-One™ qPCR Primer for NFKBIA(NM_020529.2) Search again
Product ID:
HQP011810
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
EDAID2, IKBA, MAD-3, NFKBI
Gene Description:
NFKB inhibitor alpha
Target Gene Accession:
NM_020529.2(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
NFKB1 (MIM 164011) or NFKB2 (MIM 164012) is bound to REL (MIM 164910), RELA (MIM 164014), or RELB (MIM 604758) to form the NFKB complex. The NFKB complex is inhibited by I-kappa-B proteins (NFKBIA or NFKBIB, MIM 604495), which inactivate NF-kappa-B by trapping it in the cytoplasm. Phosphorylation of serine residues on the I-kappa-B proteins by kinases (IKBKA, MIM 600664, or IKBKB, MIM 603258) marks them for destruction via the ubiquitination pathway, thereby allowing activation of the NF-kappa-B complex. Activated NFKB complex translocates into the nucleus and binds DNA at kappa-B-binding motifs such as 5-prime GGGRNNYYCC 3-prime or 5-prime HGGARNYYCC 3-prime (where H is A, C, or T; R is an A or G purine; and Y is a C or T pyrimidine).[supplied by OMIM].
Gene References into function
- IkappaBalpha x p53 complex plays an important role in responses involving growth regulation, apoptosis, and hypoxic stress
- A novel in vitro assay for deubiquitination of I kappa B alpha
- NF-kappa Beta activation in BAL cells may play in important role in initiation and progression of silica-induced pulmonary inflammation, cellular damage, and fibrosis
- results demonstrate that SLPI prevents LPS-induced NF-kappaB activation by inhibiting degradation of IkappaBalpha without affecting the LPS-induced phosphorylation and ubiquitination of IkappaBalpha
- Lipid-induced insulin resistance in human muscle is associated with changes in diacylglycerol, protein kinase C and Ikappab-alpha
- The protein IkappaBalpha is a novel substrate of recombinant c-Abl in HEK cells. c-Abl-mediated phosphorylation at tyrosine 305 is associated with an increase of the IkappaBalpha protein stability.
- A membrane-transducing mutant of I kappa B alpha has been generated that efficiently enters cells, associates with NF-kappa B p65 subunit, and inhibits NF-kappa B-mediated transcription and binding to its consensus sequence.
- Increased nuclear accumulation of I kappa B alpha in neutrophils is associated with the inhibition of NF-kappa B activity and the induction of apoptosis in these cells.
- NFkB, I-kB and I-kB kinase are present in platelets; upon platelet activation, the NF-kappaB/I-kappaBalpha complex is dissociated by phosphorylation of I-kB and proteolysis.
- polymorphism associated with an increased risk of multiple myeloma
- These data suggest that the subcellular location of I(kappa)B(alpha) is a critical determinant in ionizing radiation-induced nuclear factor-kappaB activation.
- IkappaBalpha attenuates NF-kappaBeta transcriptional activity which is an important process that restores the latent state in post-induced cells
- found in mitochondria; regulates mitochondrial gene expression
- Our data suggest that the serine and tyrosine phosphorylation of IkappaB-alpha may play a role in determining the radiosensitivity of malignant glioma cells.
- IkappaBalpha and p65 have roles in regulating the cytoplasmic shuttling of nuclear corepressors
- data suggest that NO may play a major role in the regulation of IkappaBalpha levels in aortic endothelial cells and that the application of low shear flow increases NF-kappaB activity by attenuating NO generation and thus IkappaBalpha levels.
- Data show that increased nuclear factor-kappaB (NF-kB) activity in the amnion during labor is associated with an increase in the expression of NF-kBp65 and of the NF-kB binding proteins IkBa, IkBb-1 and IkBb-2.
- Induced stabilization of IkappaBalpha can facilitate its re-synthesis and prevent sequential degradation.
- H2O2 induces NF-kappaB activation, not through serine phosphorylation or degradation of IkappaBalpha, but through Syk-mediated tyrosine phosphorylation of IkappaBalpha
- results indicate that protein kinase CKII may control IkappaBalpha and p27Kip1 degradation and thereby G1/S phase transition through the phosphorylation of threonine 10 within CKBBP1 protein
- IKBA is degraded by HSP27 through the 26s proteasome
- Okadaic acid induces degradation of the nuclear IKBA in neutrophils.
- Inhibitor kappa B-alpha promoter polymorphisms is associated with pulmonary sarcoidosis
- IkappaBalpha regulates the transcriptional activity of homeodomain-containing proteins positively through cytoplasmic sequestration of HDAC1 and HDAC3
- single nucleotide polymorphisms in the 3'-UTR were significantly increased only in Crohn's disease patients without a variation in the CARD15 gene.
- IkappaBalpha was markedly degraded at 1 h, and NF-kappaB-DNA-binding activity markedly increased 2 h after beta(2) integrin aggregation
- Down-regulation of PTEN by NIK/NF-kappaB results in activation of the PI3K/Akt pathway. This effect is associated with a lack of an inhibitor of kappaB (IkappaB)-alpha autoregulatory loop.
- PCR measure of I kappa B-alpha mRNA levels is a rapid, sensitive, and powerful method to quantify the transcriptional power of NF-kappa B.
- nuclear factor-kappa B and I kappa B alpha proteins have roles in development of prostatic adenocarcinomas
- I kappa B-NF kappa B participates on ERK2-mediated survival mechanisms
- IkappaBalpha is inhibited by ultraviolet rays and activates NFkappaB
- Calpain plays an important role in IkB alpha degradation, a crucial event in T cell activation.
- results indicate that the PKC pathway leading to SOD2 induction proceeds at least in part through NF-kappaB and that inhibition of IkappaBalpha synthesis might serve as a potential pharmacological approach to up-regulate MnSOD
- IkappaBalpha mutation can result in different clinical syndromes within one family
- demonstrated that TRAIL mediates the recruitment of PI-3K/Akt and NF-B/IB pathways in leukaemic cells, namely Jurkat T cells
- IkappaBalpha is recruited to the promoter regions of the Notch-target gene, hes1
- IkappaB-alphaS32/36A, a proteolysis-resistant inhibitor of NF-kappaB, potently inhibits the growth of HIV-1 and SIVmac239 in cell cultures.
- Results indicate that polymyxin B induces a partial maturation of human dendritic cells through increased adhesion and activation of the IkappaB-alpha/NF-kappaB pathway, and that increased ERK1/2 activation inhibits maturation.
- gene transactivation by the transcription factor NF-kappaB is subject to the regulation of a dynamic balance between the coactivators and corepressors in the IkappaB alpha promoter
- IkappaB-alpha is involved in the proliferation of human Burkitt lymphoma Daudi cells, possibly through the MAP kinase pathway.
- Galpha13-induced VASP phosphorylation that involves activation of RhoA and MEKK1, phosphorylation and degradation of IkappaB, release of PKA catalytic subunit from the complex with IkappaB and NF-kappaB, and subsequent phosphorylation of VASP
- p65 phosphorylated on serine 536 is not associated with or regulated by IkappaBalpha, but it has a distinct set of target genes and may represent a noncanonical NF-kappaB pathway that is independent of IkappaBalpha regulation
- IkappaB kinase and IkappaBalpha have NF-kappaB-dependent as well as NF-kappaB-independent pathways of HAS1 activation
- Herpes simplex virus disrupts NF-kappaB regulation by blocking its recruitment on the IkappaBalpha promoter
- ST2 negatively regulates LPS-induced IL-6 production via the inhibition of IkappaB degradation in THP-1 cells
- Significant differences in the frequency of particular polymorphisms across the NFKBIA gene were noted between patients and controls, and analysis may lead to associations with disease progression and survival and thus more personalized therapy.
- TLR8-mediated MEKK3-dependent IKKgamma phosphorylation might play an important role in the activation of IKK complex, leading to IkappaBalpha phosphorylation
- Surface plasmon resonance (SPR) data showed that the IkappaBalpha and NF-kappaB associate rapidly but dissociate very slowly, leading to an extremely stable complex.
- glucose intake induces an immediate increase in intranuclear NF-kappaB binding, a fall in IkappaBalpha, an increase in IKKalpha, IKKbeta, IKK activity, and messenger RNA expression of TNF-alpha in MNCs in healthy subjects.
- Results indicate that 14-3-3 proteins facilitate the nuclear export of IkappaBalpha-p65 complexes and are required for the appropriate regulation of NFkappaB signaling.
- heat shock increases IkappaBalpha gene expression primarily by increasing Ikappa Balpha mRNA stability and this effect is partially dependent on p38 MAP kinase.
- Human HIF asparaginyl hydroxylase, factor inhibiting HIF (FIH), also efficiently hydroxylates specific asparaginyl (Asn)-residues within proteins of the IkappaB family.
- DSCR1 attenuates NF-kappaB-mediated transcriptional activation by stabilizing its inhibitory protein, IkappaBalpha
- IkappaBalpha conformational flexibility and regions of IkappaBalpha folding upon binding to NF-kappaB are important attributes for its regulation of NF-kappaB transcriptional activity
- The IkappaBalpha-826 T and -550 A alleles are associated with susceptibility to rheumatoid arthritis .
- Immature intestinal epithelial cells have increased IKKbeta expression & phosphorylation compared with adult IEC.
- I-kappa B alpha, the inhibitory subunit of NF-kappa B (a transcription factor activated by oxidative stress), was upregulated following wounding.
- Polymorphisms in NFKBIA gene associated with type 1 diabetes.
- IkappaBalpha acts as a sensor of viral infection.
- Chinese individuals >or=50 years of age carrying the AG genotype of NFKBIA may be at an increased risk of developing colorectal cancer, and the GG genotype of NFKBIA may be considered as a prognostic factor for Swedish patients.
- NFKBIA polymorphisms associate with susceptibility to pneumococcal disease.
- Polymorphisms in NF-kappaB1 and NF-kappaBIalpha genes is associated with melanoma
- Hyaluronan of intrinsic molecular weight suppresses LPS-stimulated production of proinflammatory cytokines via ICAM-1 through down-regulation of NF-kappaB and IkappaB
- Berberine suppressed Il-1beta/TNF-alpha production in lung inflammation models. Suppression was dependent on inhibition of IkappaB-alpha phosphorylation and degradation.
- NFKB and NFKBI polymorphisms have roles in susceptibility of tumour and other diseases [review]
- Tyrosine nitration of IKBA reveals a novel mechanism for NF-kappaB activation.
- IkappaB-alpha negatively regulates the HIV-1 expression and replication in an NF-kappaB-independent manner by directly binding to Tat
- reduction of phosphorylation leads to nuclear retention of p65, which might be partly responsible for altered transcriptional behavior of p65 serine mutants
- IkappaBalpha -826 T nucleotide promoter polymorphism may be a risk factor for the development of systemic lupus erythematosus in Taiwanese.
- cytoplasmic pI kappaB-alpha expression in non-small cell lung cancer that independently predict overall survival have been identified.
- The canonical IKK2/IkappaBalpha pathway of NF-kappaB activation mediates the up-regulation of RGS4 expression in response to IL-1beta.
- NF-kappaB, IkappaB-alpha, IkappaB-beta mRNA decreased significantly after weight loss.
- H(2)O(2) prolongs NF-kappaB activation in co-stimulated cells by suppressing the negative regulatory functions of Cezanne and IkappaBalpha.
- These data demonstrate clearly that the coupled folding and binding of IkappaBalpha is critical for its precise control of NF-kappaB transcriptional activity.
- Interleukin (IL) 1beta induction of IL-6 is mediated by a novel phosphatidylinositol 3-kinase-dependent AKT/IkappaB kinase alpha pathway targeting activator protein-1
- Cys(189) of IkappaB alpha is a target for S-glutathionylation.
- promoter polymorphisms is associated with susceptibility to primary Sjogren's syndrome in Taiwan
- Transfection of IkappaBalpha can inhibit NF-kappaB activity, thus inhibit cell invasion of A549, which may be through the down-regulation of MMP-2 and MMP-9 expressions.
- Blocking NF-kappaB with IKKbeta- or RelA siRNA substantially sensitized Adriamycin-induced cytotoxicity
- NFKBIA 3'UTR GG genotype associated with an increased risk for extensive colitis in Hungarian inflammatory bowel disease patients
- tumor suppressor protein SMAR1 can modulate NF-kappaB transactivation and inhibit tumorigenesis by regulating NF-kappaB target genes
- These data suggest a mechanism for maintaining NF-kappaB activity in human T cells through the binding of the Caspase-3-generated carboxy-terminal fragment of p65/RelA to IkappaBalpha in order to protect wild-type p65/RelA from IkappaBalpha inhibition.