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5.B.1.1.1
The gp91phox/p22phox NADPH oxidase-associated, cytochrome b558, Nox2. TMS2 is important for stability and electron transfer (Picciocchi et al., 2011). The integral membrane flavocytochrome of Nox 2 transfers an electron from intracellular NADPH to extracellular O2, generating superoxide anion, O2- (Fisher 2009).

Accession Number:P13498
Protein Name:Cytochrome b-245 light chain
Length:195
Molecular Weight:21013.00
Species:Homo sapiens (Human) [9606]
Number of TMSs:4
Location1 / Topology2 / Orientation3: Membrane1
Substrate Electron

Cross database links:

Genevestigator: P13498
eggNOG: NOG39609
HEGENOM: HBG715705
Entrez Gene ID: 1535   
Pfam: PF05038   
KEGG: hsa:1535   

Gene Ontology

GO:0043020 C:NADPH oxidase complex
GO:0030141 C:secretory granule
GO:0009055 F:electron carrier activity
GO:0020037 F:heme binding
GO:0046982 F:protein heterodimerization activity
GO:0017124 F:SH3 domain binding
GO:0017004 P:cytochrome complex assembly
GO:0022900 P:electron transport chain
GO:0050665 P:hydrogen peroxide biosynthetic process
GO:0006954 P:inflammatory response
GO:0045087 P:innate immune response
GO:0045730 P:respiratory burst
GO:0014895 P:smooth muscle hypertrophy
GO:0042554 P:superoxide anion generation
GO:0006810 P:transport

References (20)

[1] “Primary structure and unique expression of the 22-kilodalton light chain of human neutrophil cytochrome b.”  Parkos C.A.et.al.   3368442
[2] “The sequence and analysis of duplication-rich human chromosome 16.”  Martin J.et.al.   15616553
[3] “The status, quality, and expansion of the NIH full-length cDNA project: the Mammalian Gene Collection (MGC).”  The MGC Project Teamet.al.   15489334
[4] “Human neutrophil cytochrome b light chain (p22-phox). Gene structure, chromosomal location, and mutations in cytochrome-negative autosomal recessive chronic granulomatous disease.”  Dinauer M.C.et.al.   2243141
[5] “Characterization of two monoclonal antibodies against cytochrome b558 of human neutrophils.”  Verhoeven A.J.et.al.   2469497
[6] “Novel human homologues of p47phox and p67phox participate in activation of superoxide-producing NADPH oxidases.”  Takeya R.et.al.   12716910
[7] “Site-specific inhibitors of NADPH oxidase activity and structural probes of flavocytochrome b: characterization of six monoclonal antibodies to the p22phox subunit.”  Taylor R.M.et.al.   15585859
[8] “Identification of a novel partner of duox: EFP1, a thioredoxin-related protein.”  Wang D.et.al.   15561711
[9] “The NADPH oxidase Nox3 constitutively produces superoxide in a p22phox-dependent manner: its regulation by oxidase organizers and activators.”  Ueno N.et.al.   15824103
[10] “Functional analysis of Nox4 reveals unique characteristics compared to other NADPH oxidases.”  Martyn K.D.et.al.   15927447
[11] “Phosphorylation of p22phox on threonine 147 enhances NADPH oxidase activity by promoting p47phox binding.”  Lewis E.M.et.al.   19948736
[12] “Cytochrome b558-negative, autosomal recessive chronic granulomatous disease: two new mutations in the cytochrome b558 light chain of the NADPH oxidase (p22-phox).”  de Boer M.et.al.   1415254
[13] “Point mutation in the cytoplasmic domain of the neutrophil p22-phox cytochrome b subunit is associated with a nonfunctional NADPH oxidase and chronic granulomatous disease.”  Dinauer M.C.et.al.   1763037
[14] “Identification of allele-specific p22-phox mutations in a compound heterozygous patient with chronic granulomatous disease by mismatch PCR and restriction enzyme analysis.”  Hossle J.-P.et.al.   8168815
[15] “156Pro-->Gln substitution in the light chain of cytochrome b558 of the human NADPH oxidase (p22-phox) leads to defective translocation of the cytosolic proteins p47-phox and p67-phox.”  Leusen J.H.et.al.   7964505
[16] “Molecular analysis of 9 new families with chronic granulomatous disease caused by mutations in CYBA, the gene encoding p22(phox).”  Rae J.et.al.   10910929
[17] “Genetic studies of three Japanese patients with p22-phox-deficient chronic granulomatous disease: detection of a possible common mutant CYBA allele in Japan and a genotype-phenotype correlation in these patients.”  Yamada M.et.al.   10759707
[18] “Statistical and mutational analysis of chronic granulomatous disease in Japan with special reference to gp91-phox and p22-phox deficiency.”  Ishibashi F.et.al.   10914676
[19] “Characterization of six novel mutations in CYBA: the gene causing autosomal recessive chronic granulomatous disease.”  Teimourian S.et.al.   18422995
[20] “Three common polymorphisms in the CYBA gene form a haplotype associated with decreased ROS generation.”  Bedard K.et.al.   19388116
Structure:
1WLP     

External Searches:

  • Search: DB with
  • BLAST ExPASy (Swiss Institute of Bioinformatics (SIB) BLAST)
  • CDD Search (Conserved Domain Database)
  • Search COGs (Clusters of Orthologous Groups of proteins)
  • 2° Structure (Network Protein Sequence Analysis)

Analyze:

Predict TMSs (Predict number of transmembrane segments)
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FASTA formatted sequence
1:	MGQIEWAMWA NEQALASGLI LITGGIVATA GRFTQWYFGA YSIVAGVFVC LLEYPRGKRK 
61:	KGSTMERWGQ KYMTAVVKLF GPFTRNYYVR AVLHLLLSVP AGFLLATILG TACLAIASGI 
121:	YLLAAVRGEQ WTPIEPKPRE RPQIGGTIKQ PPSNPPPRPP AEARKKPSEE EAAVAAGGPP 
181:	GGPQVNPIPV TDEVV