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Validated All-in-One™ qPCR Primer for RELB(NM_006509.3) Search again
Product ID:
HQP108590
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
I-REL, IMD53, IREL, REL-B
Gene Description:
RELB proto-oncogene, NF-kB subunit
Target Gene Accession:
NM_006509.3(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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Gene References into function
- Rel activity plays role in regulation of apoptosis in hepatocellular carcinoma through activation of downstream target genes
- During dendritic cell maturation, rapidly activated dimers (e.g., RelA) bound to a subset of target promoters are gradually replaced by slowly activated dimers (e.g., RelB).
- RelB has an effect on p100 processing, which is possibly regulated in a signal-dependent manner
- RelB mediates TNF-induced up-regulation of the human polymeric Ig receptor.
- RelB overexpression promoted, whereas endogenous RelB inhibition (by p100DeltaN) blocked, precursor cell development along this DC subset pathway.
- induced by cytomegalovirus (CMV) immediate-early 1 protein via activation of JNK and AP-1
- RelB expression during dendritic cells differentiation is controlled by protein kinase CbetaII-mediated regulation of transcriptional initiation and elongation
- Plays an important role in redox regulation of the cell and protects aggressive prostate cancer cells against radiation-induced cell death.
- The roles of RAC1 and RAC1b in the RelB mediated transciption in 3 tumor cell lines are reported.
- IKKalpha regulates growth pathway involving the p52/RelB-dependent transcriptional regulation of the skp2 gene.
- RelB can repress proinflammatory gene expression and may play a role in the endotoxin-tolerant phenotype in the blood leukocytes of sepsis patients.
- RelB plays a previously unrecognized negative regulatory role upon specific Langerhans cell activation.
- Data demonstrate that CD40 signals B cell survival in part via transcriptional activation of the RelB NF-kappaB subunit.
- aryl hydrocarbon receptor with NF-kappaB RelB signaling pathways represent a new mechanism of cross talk between the two transcription factors
- The interaction of AhR with RelB binding on a novel type of NF-kappaB binding site represents a new regulatory function of the AhR.
- RelB is differentially regulated by IkappaB Kinase-alpha in B cells and mouse lung by cigarette smoke
- The authors conclude that RelB functions as a dual transcription regulator during LPS tolerance and human severe systemic inflammation by activating and repressing innate immunity genes.
- identification of aryl hydrocarbon nuclear translocator(ARNT) as a CD30-interacting protein that modulated activity of the RelB subunit of NF-kappaB; findings indicate ARNT functions in concert with RelB in a CD30-induced negative feedback mechanism