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Validated All-in-One™ qPCR Primer for CYBB(NM_000397.3) Search again
Product ID:
HQP003741
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
AMCBX2, CGD, CGDX, GP91-1, GP91-PHOX, GP91PHOX, IMD34, NOX2, p91-PHOX
Gene Description:
cytochrome b-245 beta chain
Target Gene Accession:
NM_000397.3(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
Cytochrome b (-245) is composed of cytochrome b alpha (CYBA) and beta (CYBB) chain. It has been proposed as a primary component of the microbicidal oxidase system of phagocytes. CYBB deficiency is one of five described biochemical defects associated with chronic granulomatous disease (CGD). In this disorder, there is decreased activity of phagocyte NADPH oxidase; neutrophils are able to phagocytize bacteria but cannot kill them in the phagocytic vacuoles. The cause of the killing defect is an inability to increase the cell's respiration and consequent failure to deliver activated oxygen into the phagocytic vacuole. [provided by RefSeq].
Gene References into function
- novel mutations in X-linked chronic granulomatous disease
- p22(phox), gp91(phox), p47(phox), p67(phox), and p40(phox) existed as a functional complex in the cytoskeletal fraction.
- PU.1, HAF-1 trans activation of gp91(phox) promoter
- analyzed DNA from two unusual X-CGD patients and established the genetic basis for their phenotype
- In nonatherosclerotic aortic intima, gp91phox expression is restricted to 28.4+/-1.4% of intimal smooth muscle cells; in fatty streaks, macrophages and macrophage-derived foam cells express high amounts of gp91phox.
- gp91(phox) protein with a Y41D mutation and modest superoxide activity in chronic granulomatous disease
- histidine 115 is required for proton conduction by both full-length gp91 (phox) and the N-terminal 230-amino-acid fragment of gp91 (phox).
- adenosine pretreatment of fMLF-stimulated neutrophils results in decreased plasma membrane/secretory granule content of the flavocytochrome b components p22phox and gp91phox of the NADPH oxidase, which correlates with inhibition of ROS production
- promoter activity repressed by SATB1 and P300 complex; the repressed activity is partially released by CDP binding to the CCAAT element directly downstream of the AT-rich region
- Cells expressed gp91phox homologs Nox1, Nox2, and Nox4. Keratinocytes expressed Nox distinct from phox isoform of phagocytes. Source of superoxide that may regulate cell proliferation and host defense in skin and oral mucosa.
- DNA phasing generated by TA dinucleotide polymorphisms may influence the expression level of gp91 phox of NADPH oxidase and protect against severe falciparum malaria.
- The N-terminus of Nox2 is present in the mature protein and is located to the cytoplasmic side of the plasma membrane.
- Platelet CD40L expression occurs via arachidonic acid-mediated gp91phox activation.
- NAD(P)H oxidase activity is associated with increased protein levels of p22phox, p47phox, and p67phox, and increased p22phox and nox2 (gp91phox) mRNA expression. The NAD(P)H oxidase is predominantly nox2-based in saphenous veins.
- a woman with a novel mutation in CYBB (CCG[90-92]-->GGT), predicting Tyr30Arg31-->stop, Val in gp91phox, who presented with clinical symptoms at the age of 66
- significantly reduced at the Anaplasma phagocytophilum phagosome
- The presence of outward proton currents in COS-7 cells expressing gp91phox provides further support for our proposed role for gp91phox as the NADPH oxidase-associated proton channel
- 11 different mutations in the CYBB gene were identified, and 7 of them were novel. The types of mutations were intronic, single-nucleotide substitution resulting in nonsense or missense codons and 1 or 2 nucleotide deletions resulting in frameshifts.
- His119, in addition to His115, is required for the conduction of protons through Nox2.
- ANP is a novel endogenous activator of endothelial Nox/Nox2.
- CYBB is a common target gene repressed by HoxA10 and activated by HoxA9, and Meis1 and Nup98-hoxA9 have roles in repressing myeloid-specific gene transcription
- the alpha-helical loop of the C-terminal of Nox2 is probably involved in the correct assembly of the NADPH oxidase complex occurring during activation, permitting cytosolic factor translocation and electron transfer from NADPH to FAD
- mRNA expression and localization of NOX2 in human umbilical vein endothelial cells.
- monoclonal antibody CL5 was used to probe for the presence of gp91phox in membrane preparations from neutrophils of patients with nine genetically distinct forms of X-linked chronic granulomatous disease
- NOX2 and NOX4 have roles as redox messengers in the activation of intracellular signaling pathways leading (or contributing) to mitochondriogenesis, cell survival, and differentiation in hematopoietic stem cells
- IQGAP1 may function to link Nox2 to actin at the leading edge, thereby facilitating reactive oxygen species production at the site of injury, which may contribute to endothelial cell migration
- These results suggest that APP-dependent microglia activation and subsequent reactive oxygen species generation by the phagocyte NADPH oxidase play a crucial role in neuronal killing in a cellular model of Alzheimer's disease
- Rac1 facilitated the recruitment of Nox2 into the endosomal compartment and subsequent redox-dependent recruitment of TRAF6 to the MyD88/IL-1R1 complex.
- chronic granulomatous disease arose due to a splice-supporting mutation in the last position of a cryptic exon towards the middle of intron 6 of the CYBB (gp91-phox) gene
- NOX2 plays a critical role in conferring DCs the ability to function as specialized phagocytes adapted to process antigens rather than kill pathogens.
- analysis of the p22phox subunit of flavocytochrome b558: identification of regions critical for gp91phox maturation and NADPH oxidase activity
- In endothelial cells, NOX2 and NOX4, but not NOX1, equally contributed to ROS generation and proliferation under basal conditions, indicating that a complex relation between NOX homologues controls endothelial function.
- analysis of the integral membrane protein flavocytochrome b(558) by mass spectrometry
- In a three-dimensional model of the C-terminal tail of Nox2, Leu505 appears to have a strategic position just at the entry of the NADPH binding site and at the end of the alpha-helical loop (residues 484-504), a potential cytosolic factor binding region.
- De novo null mutations affecting the CYBB gene that encodes the gp91 protein were found in both cases in the heterozygous state of CGD.
- Endothelial-targeted Nox2 overexpression is sufficient to increase vascular NADPH oxidase activity, activate downstream signaling pathways, and potentiate hemodynamic response to angiotensin II, despite increases in vascular antioxidant enzymes.
- study shows HIV-1 Tat signaling, leading to concurrent but separate Nox4-dependent Ras/ERK activation, and Nox2-dependent JNK activation; Tat signaling, therefore, provides an example of Nox-specific differential control of MAP kinase pathways
- Src homology-containing tyrosine phosphatase 2 activation blocks IFN consensus sequence-binding protein (ICSBP) induced CYBB transcription.
- Aged transgenic mice overexpressing the Swedish mutation of amyloid precursor protein and lacking the catalytic subunit Nox2 of NADPH oxidase do not develop oxidative stress, cerebrovascular dysfunction, or behavioral decline.
- Comparison of CYBB coding sequences among mammals evidences the action of long-term purifying selection, which is stronger on the C-terminal cytosolic domain than on the N-terminal transmembrane domain of gp91-phox
- None of the CYBB SNPs serve as good surrogates for the microsatellite alleles, previously associated with mild malaria.
- PCR-sequencing of the entire coding regions of CYBB identified nonsense mutations, 271C>T (R91X) in exon 4 and 456T>A (Y152X) in exon 5, in probands of each family.
- CYBB analysis revealed a novel complex mutation atggacg --> ttca in exon 12 (base pairs 1532-1538). As a result, 3 amino acids Tyr 511, Gly 512 and Arg 513 were deleted and replaced by 2 amino acids, Phe and Gln.
- a previously unrecognized dual role of NOX2 in the regulation of NF-kappaB in response to RSV and Sendai virus in human airway epithelial cells.
- Nox2 and Nox4 exhibit distinctive patterns of acute activation by angiotensin II, TNFalpha, and insulin and regulate the activation of distinct protein kinases.
- Nox2 and Nox4-generated ROS modulate glucose uptake in a leukaemic cell line
- NF-kappaB is necessary for CYBB and NCF1 gene expression and activation of the phagocyte NADPH oxidase normal and anhidrotic ectodermal dysplasia leukocytes.
- NOX2 activity participates in the regulation of the phagosomal and endosomal pH in human dendritic cells, and is required for efficient antigen cross-presentation.
- a novel mutation in the CYBB gene and an extremely skewed X-inactivation event resulted in the rare expression of the chronic granulomatous disease phenotype in a carrier female.
- p67(phox)-SH3(N) specifically functions in gp91(phox)/Nox2 activation probably via facilitating oxidase assembly.