NCF1 pSer304 antibody Ab
- Known as:
- NCF1 pSer304 (anti-) Antibody
- Catalog number:
- 1488085
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Acris antibodies
- Gene target:
- NCF1 pSer304 antibody
Related genes to: NCF1 pSer304 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 pSer304 antibody Ab
Related articles to: NCF1 pSer304 antibody Ab
- Chronic Granulomatous Disease (CGD) is a defect or abnormality in the immune system that produces severe and persistent signs and symptoms in affected individuals. Phenotypic diversity and genetic heterogeneity exist among patients with inborn errors of immunity (IEI). Symptoms may vary even when the mutations are identical; conversely, patients with different mutations may have similar clinical features. The expression of phenotype may be determined by the gene sequence, epigenetic changes, and sometimes environmental factors. Some of these outcomes are influenced by the individual's past immunological exposure. This study discusses two CGD cases, a father and son; after the diagnosis of CGD in the child and confirmation of the genetic mutation, the same mutation was also identified in the father. Therefore, physicians should have more awareness that a single genetic mutation can have different clinical manifestations. - Source: PubMed
Publication date: 2026/04/22
Yazdizadeh SarvinSaberi MohammadKarimi AbdollahSharafian SaminRafiei Tabatabaei SedighehSeraj SaharSadat Seyedmehdi MaryamFallah Shahrzad - establishes infection in hosts by deploying effector proteins that reprogram cytokine-driven immunity. While protozoan parasite-encoded macrophage migration inhibitory factor (MIF) homologs exemplify cytokine mimicry, whether targets additional host cytokine axes remains unclear. Here, we identify a 3-ketoacyl-CoA reductase (KCR) as a noncanonical cytokine modulator that engages the granulocyte-macrophage colony-stimulating factor (CSF2) receptor alpha chain (CSF2Rα). In HEK293T cells, forward and reverse co-immunoprecipitation (Co-IP) assays demonstrated a specific interaction between KCR and murine CSF2Rα. The recombinant KCR triggered rapid activation of canonical CSF2 signaling in RAW264.7 macrophages, inducing phosphorylation of JAK2 and STAT5 to levels comparable to murine CSF2. Functionally, KCR enhanced NADPH oxidase-dependent oxidative responses, increasing intracellular reactive oxygen species (ROS) and upregulating transcripts encoding core oxidase subunits, including CYBB, CYBA, NCF1, and NCF2. KCR also promoted phagocytic capacity, elevating FITC-dextran uptake and inducing expression of complement, Fc, and scavenger receptor genes, including CR3, CD16, CD64, MSR1, and MARCO. Notably, KCR pretreatment attenuated CSF2-induced JAK2/STAT5 phosphorylation, ROS production, and phagocytosis, consistent with competitive interference with endogenous CSF2-CSF2R signaling. Together, these findings reveal KCR as a previously unrecognized factor that targets the CSF2/CSF2R axis to recalibrate macrophage effector functions, expanding the repertoire of parasite strategies for cytokine pathway modulation and highlighting CSF2-CSF2R signaling as a potential interface for mechanistic and therapeutic investigation in toxoplasmosis. - Source: PubMed
Publication date: 2026/05/09
Mei JiePu XianglinZhang MengkaiLiu YueMeng ChuangXu LixinSong XiaokaiYan RuofengLi XiangruiLu Mingmin - Bacterial effector proteins manipulate host signalling cascades, including immune responses, to facilitate infection. While most effectors of Gram-negative bacteria rely on a secretion system for intracellular delivery, some possess intrinsic cell-penetrating capabilities. Here, we characterize the Shigella flexneri LPX effector IpaH7.8, which combines autonomous cell entry with enzymatic modulation of immunomodulatory host signaling pathways through distinct structural domains. We show that recombinant IpaH7.8 (rIpaH7.8) enters human cells independent of Shigella's type III secretion system (T3SS) via lipid raft-mediated endocytosis and escapes the endosome through a conserved N-terminal domain composed of two α-helices. In the cytosol, the C-terminal E3 ubiquitin ligase domain of the cell-penetrating effector protein targets the pore-forming protein gasdermin D (GSDMD), suppressing inflammasome-induced IL-1β release. Beyond inflammasome inhibition, integrated transcriptomic and kinome profiling in primary human monocytes revealed that IpaH7.8 induces a coordinated reprogramming of host signaling networks. Cluster-resolved gene expression analysis demonstrated selective suppression of immune effector pathways alongside induction of regulatory programs and interference with vesicular trafficking. These transcriptional changes converged with kinase activity remodeling, characterized by attenuation of PKC- and PKA-dependent signaling pathways. Notably, both datasets identified the NOX2 complex as a central target of IpaH7.8 activity. The NOX2 subunit NCF1 was downregulated at the transcriptional level and showed reduced phosphorylation at regulatory sites, indicating impaired activation. Consistently, IpaH7.8 significantly reduced reactive oxygen species production in primary human monocytes, demonstrating functional suppression of oxidative burst responses. Together, our findings reveal that IpaH7.8 acts as a multi-layered regulator of host immunity that integrates ubiquitination and kinase signaling to suppress both inflammatory and antimicrobial responses. By converging on the NOX2 axis, this effector uncovers a central vulnerability in host defense and highlights bacterial effector proteins as modulators of complex signaling networks with potential therapeutic relevance. - Source: PubMed
Publication date: 2026/04/29
Karagöz TheresaNgueya Yango IvanNorkowski StefanieTeschke YannickKörner BrittaFernandes Joyleen MaryannBörgeling YvonneDersch PetraRüter Christian - Invasive pulmonary aspergillosis (IPA) poses a serious threat to immunocompromised hosts, with limited therapeutic options highlighting the need for novel strategies. Franch. (CCF), a traditional Chinese herb containing antimicrobial alkaloids like berberine, was investigated for its therapeutic efficacy and immunological effects in a murine IPA model. Immunosuppressed female KM mice infected with AF293 were treated with CCF or amphotericin B (AmB). CCF significantly improved survival, reduced fungal burden, and alleviated lung pathology, without inducing hepatotoxicity or nephrotoxicity. Transcriptomic profiling revealed a time-dependent immune response. Complement-related pathways were enriched at 2 days post-infection, whereas neutrophil recruitment and NET-related pathways became more prominent by day 4. Hub gene analysis identified Syk, Rac2, Ncf1, and Cybb as key nodes associated with the NADPH oxidase complex. Western blot and inhibitor experiments further supported the involvement of this pathway in CCF-mediated protection. Additionally, 16S rDNA sequencing indicated enrichment of species in the gut microbiota of CCF-treated mice, which was positively correlated with the expression of NADPH oxidase-related genes, suggesting a potential gut-lung association. In conclusion, these findings support the antifungal efficacy of CCF in IPA and suggest that its protective effects may involve coordinated changes in complement-related responses, NADPH oxidase-associated neutrophil activity, and gut microbiota composition. - Source: PubMed
Publication date: 2026/04/20
Jiang ZhuqiaoZhou LingmeiWang JinpingSun HaoCai LiwenYin HanqiZhu HuiLi MingWang Zhuoya - We assessed the role of a systemic lupus erythematosus causal, hypofunctional variant, neutrophil cytosolic factor 1 (NCF1)-p.Arg90His (p.R90H) substitution, in Sjögren's disease (SjD). - Source: PubMed
Publication date: 2026/04/17
Yuan XinranQin XiaodongWu XinjieChen YiWang YujiaoZhang YuluXie DongLiu YaoZhao JianGuthridge Joel MJames Judith ALessard Christopher JShen NanSun LingyunTsao Betty P