Ask about this productRelated genes to: NCF4 antibody
- 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: NCF4 antibody
Related articles to: NCF4 antibody
- Renal cell carcinoma (RCC) is a prevalent and heterogeneous malignancy with clear cell RCC (ccRCC) as the most common subtype. Despite advances in surgical, targeted, and immunotherapeutic approaches, prognosis for advanced and metastatic RCC remains poor, and the effectiveness of current immunotherapies is limited by immune tolerance, tumor heterogeneity, and adverse effects. The identification of tumor-associated antigens (TAAs) and tumor-specific antigens (TSAs) is crucial for the development of personalized and effective antigen-directed therapies, including vaccines, antibodies and adoptive cell therapies. This review summarizes epidemiological data, molecular features of RCC, and the role of the von Hippel Lindau - Hypoxia Inducible Factor (VHL-HIF) signaling pathway in pathogenesis, alongside recent progress in characterizing possible antigen targets for vaccination such as TOP2A, NCF4, FMNL1, DOK3, MUC1, CAIX, CD70, and 5T4. Preclinical models, including genetically engineered mouse models, zebrafish, and various patient-derived xenograft (PDX) systems, are discussed as tools for studying tumor biology and testing immunotherapeutic strategies. Clinical trial data on RCC vaccines, including autologous renal tumor cell vaccination, peptide-based, dendritic cell-based, and viral vector platforms, demonstrate immunogenicity but have not yet yielded clear survival benefits in phase III trials. Future directions emphasize integrating antigen discovery with immune profiling, refining preclinical modeling, and developing personalized vaccines to enhance therapeutic efficacy, particularly for immunologically favorable patient subtypes and for certain applications such as reducing metastasis after surgery. In particular, we discuss carrier-based vaccine approaches for overcoming tolerance and increasing the immunogenicity of vaccines. - Source: PubMed
Publication date: 2026/03/27
Kagirova EvelinaEnikeeva KadriiaMukhamadeev RadmirAsadullina DilaraSharifyanova YuliyaShmelkova PolinaGainullina DianaTrifonova DariaGattinger PiaDocena GuillermoDubovets AlexandraTulaeva InnaKaraulov AlexanderValenta RudolfPavlov Valentin - 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 - Kidney transplant rejection (KTR) poses significant challenges to long-term graft survival, with involvement from ubiquitination-related genes (URGs) in immune modulation. This study aimed to identify key URGs linked to KTR and develop a predictive model for rejection risk. mRNA array data from the Gene Expression Omnibus were analyzed to find differentially expressed genes in GSE98320, which were intersected with URGs to yield 16 DE-URGs. Gene Ontology and KEGG enrichment analysis highlighted the NF-kappa B and TNF signaling pathways. A URGScore model stratified patients and revealed significant differences in immune cell infiltration, especially among Treg cells, demonstrating strong predictive performance in the discovery cohort (AUC = 0.774, 95% CI 0.747–0.800). Six signature genes (,,,,,) were identified, and their expression displayed a subtype-dependent gradient, increasing from antibody-mediated rejection to T cell-mediated rejection and reaching the highest levels in mixed rejection. These genes were incorporated into a nomogram, which achieved an AUC of 0.771 (95% CI 0.745–0.798). Validation in independent datasets confirmed the model’s reliability. In the two transplant rejection cases, and showed higher expression than the other biopsy samples, while generalized high expression of all marker genes was observed in an IgA nephropathy patient. Together, these findings demonstrate the clinical relevance of URG-based biomarkers in KTR and provide molecular insight into immune-mediated rejection. - Source: PubMed
Publication date: 2026/02/10
Shan ZhengfeiYu ShengqiangWang JiantaoCui JianxinWei HaijianFu XiaohuaZhang ChenZhang Chengjun - 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 - The involvement of intestinal microbiota in the process of neutrophil-mediated colorectal cancer liver metastasis (CRCLM) is not yet fully understood. Here, we show that Escherichia coli (E. coli) is prevalent in CRC tissues with LM using 2bRAD-M-Seq and is linked to the release of neutrophil extracellular traps (NETs). Utilizing multi-omics and molecular techniques, we establish that E. coli recruits RIPK2, which promotes the binding of HNRNPK to the Atf3/Relb promoters in neutrophils, thereby enhancing their transcription. This process results in the upregulation of Ncf4, which triggers p-MLKL-mediated NET formation. NETs, in turn, increase the expression of TRPC1 and NFATC3 in CRC cells, promoting the calcium-dependent assembly of the STAT3/S100A8/9 heterotrimer. This trimer stabilizes STAT3-enhancer-promoter loops (EPLs), thereby reinforcing the Tns1 transcription and facilitating CRCLM. Our findings elucidate the mechanism by which E. coli-induced NETs promote CRCLM through epigenetic modifications, offering an insight into the role of EPLs in immune regulation and tumor progression. - Source: PubMed
Publication date: 2026/02/03
Pan BanglunYao YuxinZhang ZhuYe DongjieWu HaoZhang XinyuWang XiaoqianTang Nanhong