NCF1 pSer345 antibody Ab
- Known as:
- NCF1 pSer345 (anti-) Antibody
- Catalog number:
- 1488278
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Acris antibodies
- Gene target:
- NCF1 pSer345 antibody
Related genes to: NCF1 pSer345 antibody Ab
- 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
Related products to: NCF1 pSer345 antibody Ab
Related articles to: NCF1 pSer345 antibody Ab
- Cerebral ischemia-reperfusion injury (CIRI) is a major contributor to poor outcomes after ischemic stroke, yet the mechanisms linking oxidative stress and inflammation remain incompletely understood. Neutrophil cytosolic factor 1 (NCF1), a key organizer subunit of the NOX2 NADPH oxidase complex, is involved in reactive oxygen species (ROS) generation and immune activation. Here, we investigated the expression pattern, pathological role, and mechanistic significance of NCF1 in CIRI. A public spatial transcriptomic dataset of ischemic mouse brain tissue was reanalyzed to assess the spatial distribution of Ncf1 after stroke. A transient middle cerebral artery occlusion (MCAO) model was established, and NCF1 expression was evaluated by spatial transcriptomics, immunofluorescence staining, RT-qPCR, and Western blotting. Loss-of-function experiments were performed using NCF1 knockdown, followed by neurological deficit scoring, TTC staining, ROS detection, and inflammatory gene analysis. We found that NCF1 was markedly upregulated in the ischemic brain after stroke and was enriched in infiltrating neutrophils. NCF1 knockdown significantly improved neurological outcomes and reduced infarct volume in MCAO mice. Mechanistically, silencing NCF1 suppressed NOX2 expression and ROS accumulation, indicating attenuation of oxidative stress. In addition, NCF1 knockdown decreased the expression of multiple pro-inflammatory mediators, including IL-1β, IL-2, IL6, HMGB1, TNF-α, and iNOS, while increasing the expression of the anti-inflammatory and reparative factors Arg-1 and IGF-1. These findings indicate that NCF1 aggravates cerebral ischemia-reperfusion injury by amplifying NOX2-dependent oxidative stress and inflammatory responses, and suggest that NCF1 may serve as a potential therapeutic target for ischemic stroke. - Source: PubMed
Publication date: 2026/07/04
Wang ZhuoYu CongHuang HengSong HuiqiongPeng XiaohongCheng Jiangxia - 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 - Understanding drivers of tuberculosis (TB) associated lung pathological damage is vital in identifying targets for host directed therapies (HDT). NETosis is a neutrophil specific cell death characterized by release of neutrophil extracellular traps (NETs). The role of NETosis in TB-associated lung damage and disease pathogenesis is still poorly understood. We analysed human lung TB granuloma samples using a proteomics approach, which revealed enrichment of neutrophil-associated proteins in necrotic regions of caseous and cavitary granulomas. Using immunohistochemistry (IHC), we validated the abundance of neutrophil-associated proteins, including myeloperoxidase (MPO), cytochrome b-245 beta chain (CYBB) and neutrophil cytosolic factor 1(NCF1), as well as NETosis markers, neutrophil elastase (NE) and citrullinated H3, in necrotizing caseum of human TB granulomas. MPO protein expression was also more abundant in the plasma of TB patients compared to healthy and latently infected (LTBI) participants. MPO directly correlated with an inflammatory disease marker, IP-10. In addition, MPO and IP-10 colocalized in caseous lesions. In-vitro drug inhibition assays were used to investigate potential drivers of NETosis, with pharmaceutical inhibition of MPO, NE and CYBB resulting in reduction of NETosis induced by Mycobacterium tuberculosis (Mtb). Using RT-qPCR we analysed the expression of 18 neutrophil associated genes in the blood of healthy (n = 20), latent TB infection (LTBI) (n = 20) and TB (n = 30) participants. We found that MPO, NCF1 and NCF2 were upregulated in the TB group. Furthermore, the NETosis-associated genes were induced in a human standardized antigen challenge model. Our data shows evidence of NETosis as an associate of lung pathological damage in TB and identifies key drivers of the neutrophil cell death that can be intercepted as potential HDT targets to reduce neutrophil driven lung pathological damage. - Source: PubMed
Publication date: 2026/06/02
Fisher Kimone LMpotje ThaboNargan KievershenMoodley DenelleRajkumar-Bhugeloo KerishkaBaiyegunhi Omolara ONaidoo ThrenesanMadansein RajhmunSathekge MikeLeslie AlasdairTomlinson GillianPollara GabrieleNoursadeghi MahdadSteyn Adrie J CNdung'u ThumbiMarakalala Mohlopheni J - Thyroid carcinoma (TC) presents a rising global incidence, with a subset of cases progressing aggressively despite standard therapies. The tumor microenvironment (TME), particularly the functional state of CD8⁺ T cells, is crucial in disease progression, yet a systematic, high-resolution understanding of the cellular interactions associated with immune exhaustion and tumor evolution in TC remains limited. - Source: PubMed
Publication date: 2026/05/30
Su HanZhang ZhengLi NuoZhang ZimoZhang RenjuLi ZiyiChen FenWang XinyueZhang ShuyuanZhang Chao - Neonatal lupus erythematosus (NLE) is a rare, passively acquired autoimmune disease. The manifestations of NLE are varied, and the outcomes of the majority of cases result in spontaneous resolution. However, severe cases are limited. Emerging evidence highlights the genetic heterogeneity of NLE. The missense variant p.Arg90His in has been demonstrated to be associated with autoimmune diseases, including systemic lupus erythematosus. Chromosomal abnormalities manifest as developmental and growth delays and facial anomalies, among other phenotypic characteristics. Whether the co-occurrence of the missense variant p.Arg90His in and (14)(4;14) translocation would raise critical questions about the individual remains a mystery. In this report, we first describe a female patient with NLE who is homozygous for the p.Arg90His mutation in the gene and also exhibits a (14)(4;14) translocation. Whole exome sequencing (WES) identified a homozygous missense variant of NM_000265.4:c.269G>A(p.Arg90His) in the proband. Sanger sequencing confined the variant and showed that both parents were heterozygous for this variant. G-banding karyotype showed a chromosome abnormality of 47,XX,+(14)(4;14)(p15.2;q11.1) in the proband and a balanced translocation of 46,XX,(4;14)(p15.2;q11.1) in her mother. The patient exhibited a refractory hematologic disease as a characteristic feature and was treated with glucocorticoids. She displayed unique facial features, developmental delay, and growth retardation during follow-up. This case offers a practical example to elucidate the genotype-phenotype correlations between chromosomal abnormalities, the variant, and the observed clinical manifestations. In addition, we propose that the homozygous p.Arg90His variant acts as a potent genetic modifier, exacerbating the severity of the clinical manifestations of NLE, with a predominant impact on the hematologic system. - Source: PubMed
Publication date: 2026/05/08
Yu XiaojingLou JiwuZhong YuliZhang Lan