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Validated All-in-One™ qPCR Primer for NFKB2(NM_001077494.3) Search again
Product ID:
HQP067180
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
CVID10, H2TF1, LYT-10, LYT10, NF-kB2, p100, p49/p100, p52
Gene Description:
nuclear factor kappa B subunit 2
Target Gene Accession:
NM_001077494.3(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
NFKB has been detected in numerous cell types that express cytokines, chemokines, growth factors, cell adhesion molecules, and some acute phase proteins in health and in various disease states.
Gene References into function
- Genetic evidence for the essential role of beta-transducin repeat-containing protein in the inducible processing of NF-kappa B2/p100
- interaction with S9 19S proteasome subunit
- BAFF-induced NEMO-independent processing of NF-kappa B2 in maturing B cells
- NF-kappa B2 p100 has I kappa B-independent apoptotic activity and a unique tumour suppressor role
- LT-beta receptor agonists and LPS induce NF-kappaB/p100 processing to p52 at the level of the ribosome.
- p52 NF-kappaB subunit associates with histone deacetylase 1 when p53 represses cyclin D1 transcription through down regulation of Bcl-3
- p50 and p52 homodimers can transactivate the bcl-2 promoter through association with Bcl-3; in breast cancer and leukemic cells (CLL), high NF-kappaB2/p100 expression was associated with high Bcl-2 expression
- RelB has an effect on p100 processing, which is possibly regulated in a signal-dependent manner
- Constitutive processing of C-terminal truncation mutants of p100 is associated with their active nuclear translocation. , Mutation of the nuclear localization signal (NLS) of p100 abolishes its processing.
- p100HB is a new mutant form of p100/NF-kappa B2 associated with deregulated NF-kappa B/Rel functions
- LMP1 activation of these two NF-kappa B pathways, NFKB2 and I kappa B alpha, is shown here to require distinct regions of the LMP1 C-terminal cytoplasmic tail.
- The mechanism of processing of the NFKB2 precursor is regulated by a unique pathway.
- Induction of p100 processing by NF-kappaB-inducing kinase involves docking IkappaB kinase alpha (IKKalpha) to p100 and IKKalpha-mediated phosphorylation
- beta-transducin repeat-containing protein-dependent and -independent mechanisms contribute to Tax-deregulated p100 processing
- the mechanism by which the different sequences within p100 work in concert to regulate its processing
- IkappaB kinase alpha has an essential role in the constitutive processing of NF-kappaB2 p100
- Enhanced expression of NF-kappaB2/p52 and RelB-containing NF-kappaB DNA-binding activity in Epstein-Barr virus-negative Reed Sternberg cells.
- (p52)2/Bcl-3P ternary complex, which is specifically induced in CD30-stimulated anaplastic large cell lymphoma, can modulate expression of apoptosis-related genes regulated by NF-kappaB.
- studies define one important mechanism of NF-kappaB-inducing kinase (NIK) regulation and the central role of NIK stabilization in the induction of NF-kappaB2 precursor protein p100 processing
- mutants of p53 may induce loss of drug sensitivity is via the NF-kappaB2 pathway
- These data suggest that p100 processing involves its phosphorylation at specific terminal serines, which form a binding site for beta-TrCP thereby regulating p100 ubiquitination.
- Stat3-mediated p100 processing to p52 requires activation of Stat3 by the acetyltransferase activity of cAMP-response element-binding protein (CREB)-binding protein (CBP)/p300
- Data demonstrate an important role of NF-kappaB-1 and -2 pathways in mediating resistance to apoptosis and distinctive antiapoptotic downstream target gene profiles responsible for this effect.
- HBx and NF-kappaB2/BCL3 mediated-cyclin D1 up-regulation might play an important role in the HBx-mediated HCC development and progression
- p52 can regulate p53 function and influence p53-regulated decision-making following DNA damage and oncogene activation.
- Novel interactions reveal of IKKepsilon in the regulation of the alternative NF-kappaB activation pathway involving p52 and p65 are reported.
- We herein report that STP-A11 activates non-canonical NF-kappaB pathway, resulting in p100 processing to p52.
- Monarch-1 inhibits CD40-mediated activation of NFKB and processing of NFKB2 to p52. This inhibition stems from the ability of Monarch-1 to associate with and induce proteasome-mediated degradation of NF-kappaB inducing kinase.
- Study reports that androgenic stimulation of LNCaP cells with the androgen analogue R1881 appears to positively regulate the non-canonical NF-kappaB pathway as p52 accumulates both in the cytoplasm and nucleus after 48-72 h of stimulation.
- C-terminally truncated NF-kappaB2 precursors are endoproteolytically processed at kappaB-containing promoters
- cell adhesion-mediated proteolysis of the NF-kappaB precursor, p100 (NF-kappaB2) resulted in the generation of active p52, which translocated to the nucleus in complex with p65 and RelB
- NF-kappaB2/p100 acts as a late-acting negative-feedback signaling molecule in the TCR-mediated NF-kappaB pathway.
- activation of NF-kappaB2/p100 plays a crucial role in the Tax1-mediated transformation of T cells
- The findings demonstrate a key role for NF-kappaB2 in the regulation of RelA activation and suggest overlap in the function of NF-kappaB members in canonical and noncanonical pathway signaling.
- These unique protein-protein contacts explain why RelB prefers p52 as its dimeric partner for transcriptional activity and is retained in the cytoplasm as an inhibited complex by p100.
- NF-kappaB2 gene rearrangement may be a factor in the constitutive activation of NF-kappaB in ATL, and thereby playing a role in the ATL pathogenesis.
- NFkappaB2 gene duplication is associated with fetal pyelectasis in partial trisomy 10q (10q24.1 --> qter).
- RIG-1 - MAVS interacts with cytoplasmic 100-kDa NF-kappa B2 complexes via a novel retinoic acid-inducible gene-I - NF- kappa B-inducing kinase signaling pathway
- Overexpression of NF-kappaB2/p52 protects androgen sensitive human prostate cancer cells from apoptotic cell death and cell cycle arrest induced by androgen-deprivation.
- The X-ray structure of the nuclear factor-kappaB p52:RelB:kappaB DNA complex reveals a new recognition feature not previously seen in other NF-kappaB:kappaB DNA complexes. Arg 125 of RelB is in contact with an additional DNA base pair.