p47 phox (Phospho-Ser345) Antibody
- Known as:
- p47 phox (Phospho-Ser345) Antibody
- Catalog number:
- 11811
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Signalway
- Gene target:
- p47 phox (Phospho-Ser345) Antibody
Related genes to: p47 phox (Phospho-Ser345) Antibody
- Gene:
- NCF1 NIH gene
- Name:
- neutrophil cytosolic factor 1
- Previous symbol:
- -
- Synonyms:
- p47phox, NOXO2, NCF1A, SH3PXD1A
- Chromosome:
- 7q11.23
- Locus Type:
- gene with protein product
- Date approved:
- 1989-05-25
- Date modifiied:
- 2019-04-23
- Gene:
- NCF2 NIH gene
- Name:
- neutrophil cytosolic factor 2
- Previous symbol:
- -
- Synonyms:
- p67phox, NOXA2
- Chromosome:
- 1q25.3
- Locus Type:
- gene with protein product
- Date approved:
- 1989-05-25
- Date modifiied:
- 2019-04-23
- Gene:
- NCF4 NIH gene
- Name:
- neutrophil cytosolic factor 4
- Previous symbol:
- -
- Synonyms:
- p40phox, SH3PXD4
- Chromosome:
- 22q12.3
- Locus Type:
- gene with protein product
- Date approved:
- 1996-06-19
- Date modifiied:
- 2019-04-23
Related products to: p47 phox (Phospho-Ser345) Antibody
Related articles to: p47 phox (Phospho-Ser345) Antibody
- With the ongoing integration of offshore wind power and marine aquaculture, increasing attention has been paid to the potential biological effects of continuous low-frequency noise generated during wind farm operations on surrounding fish species. In this study, juvenile black scrapers (Thamnaconus modestus), a demersal species with low auditory sensitivity, were exposed to 500 Hz noise at low, medium, and high intensities (root-mean-square (RMS) sound pressure levels (SPLrms): 95 ± 5, 115 ± 5, and 135 ± 5 dB re 1 μPa) for 14 days to investigate physiological responses and molecular regulatory mechanisms. Low-intensity noise primarily suppressed the expression of feeding and digestion genes (Ghrl, Prss1) and activated oxidative stress and neuroprotective pathways. Medium-intensity noise caused dysregulation of lipid metabolism genes (Gba1, Degs2), significantly elevated malondialdehyde (MDA) content, and downregulated the expression of key genes in the neutrophil extracellular trap formation pathway (Ncf1, Ncf2, Ncf4). High-intensity noise disrupted the expression of circadian clock genes (Bmal1, Per2) and upregulated cholesterol synthesis pathway genes (Sqle, Cyp51a1, Dhcr24). Collectively, long-term low-frequency noise exposure during operation induced dose-dependent physiological stress on juvenile T. modestus, affecting digestive function, redox balance, lipid metabolism, immune responses, and circadian rhythm regulation. These findings contribute to understanding the potential impacts of low-frequency noise from offshore wind farms on marine fish and suggest that low-frequency noise should be incorporated as a key assessment criterion in the siting of marine ranching and fishery resource conservation. - Source: PubMed
Publication date: 2026/06/09
Song ShiqiShan Xiujuan - Chronic granulomatous disease (CGD) is an inborn error of immunity of caused by pathogenic variants of genes encoding components of the phagocyte NADPH oxidase complex, resulting in defective reactive oxygen species production and impaired microbial killing. We conducted a multicenter evaluation of 39 Colombian patients with CGD from 32 unrelated kindreds, describing their clinical, microbiological, and genetic characteristics. Genetic analyses were performed for 31/39 patients and identified variants of the following genes: ( = 22), ( = 3), ( = 1), ( = 1), and ( = 4). All but three of the patients had symptoms, the exceptions being individuals with p40 deficiency. BCG-related complications occurred in eight patients, pulmonary tuberculosis in four, and spp. bacteremia in 12 of 17 patients with infections. Colombian patients with CGD had clinical and microbiological profiles similar to those reported across Latin America. The genetic findings broaden the regional variant spectrum and emphasize the need for earlier diagnosis and better access to specialist testing. - Source: PubMed
Publication date: 2026/05/21
Rojas JulianArango-Franco Carlos AMoncada-Velez MarcelaArboleda Diana MarcelaFigueredo Edgar AlfonsoMolina ManuelaSánchez Juan PabloZapata Lina MarcelaDiaz Paula CatalinaÁlvarez Jesús ArmandoSerna-Arbelaez Maria SPérez Zapata Lizet JazminVélez GabrielSoudée CamilleAlzate Juan FCabarcas FelipeObando Gil CatalinaGarcés CarlosAlvarez-Olmos Martha IPérez-Camacho Paola MarcelaMedina-Valencia DiegoPatiño-Niño Jaime AlbertoRendón Juan PabloOrtega-López María ClaudiaCano Luz ElenaLópez Juan FranciscoEstupiñán Flor MarcelaChaparro MauricioNiño LauraEscobar Andrés FelipeCasanova Jean-LaurentBoisson-Dupuis StéphaniePuel AnneOlmos CarlosSosa Luis MiguelSarmiento-Wilches Patrick ElianaMuñoz CésarOrrego Julio CesarLópez Juan ÁlvaroOlaya-Hernández ManuelaBuiles NataliaVásquez-Echeverri EstefaníaVélez-Tirado NataliaFranco José LuisCastaño-Jaramillo Lina MaríaBustamante JacintaArias Andrés Augusto - Chronic granulomatous disease (CGD) is an inborn error of immunity caused by genetic defects in the nicotinamide adenine dinucleotide phosphate oxidase complex, resulting in recurrent severe infections and excessive inflammatory responses. CGD is inherited in X-linked recessive and autosomal recessive patterns. X-linked variants occur in the gene, whereas autosomal recessive variants are found in the , and genes. - Source: PubMed
Publication date: 2026/03/25
Thawabteh Fatima Az-ZahraAbu Rmilah SedrahSiaj AyaAbu Khdair RawanAdwan Rabee - Chronic granulomatous disease (CGD) is a rare inborn error of immunity caused by defects in components of the NADPH oxidase that impair the elimination of infectious microorganisms. Individuals affected by CGD become more susceptible to recurrent and severe infections. Six male patients from Southern Brazil were clinically and genetically analyzed through data collection from medical records and massively parallel sequencing by a panel for the following genes: CYBB, CYBA, NCF1, NCF2, and NCF4 and whole genome sequencing analysis. The gene-scan technique was used to identify the GT deletion in NCF1. The most common affected organs were the lungs, skin, and lymph nodes; the most common clinical manifestations were recurrent pneumonia, cutaneous involvement, lymph node manifestations, and failure to thrive. Four patients were identified with variants in CYBB: p.Cys257Ser, which is novel; p.Cys257Arg; p.Arg157Ter; and p.Trp483Ter. Both missense variants damage the loop E in gp91, a region with functional and structural relevance for the protein. Functional studies show the expression absence of the protein in patients with the variant p.Arg157Ter. The variant p.Trp483Ter is predicted to undergo nonsense mRNA-mediated decay. The GT deletion in NCF1 was identified in two siblings from consanguineous parents: one homozygous and the other apparently heterozygous for the deletion, both with a clinical diagnosis of CGD. Variant analysis in this gene is particularly challenging due to the presence of pseudogenes. A hypothesis for this genotypic discrepancy is the occurrence of a second type of pseudogene lacking the GT deletion, which may have arisen in one parent and been transmitted to the patient observed as heterozygous, being misinterpreted in the analyses as a functional NCF1 sequence. - Source: PubMed
da Rosa Leonardo Martinelloda Rosa Martha BraunWilson Mariana de Sampaio Leite JobimSchwartz Ida Vanessa DoederleinSperb-Ludwig Fernanda
- Source: PubMed