IFI35 monoclonal antibody (M01), clone 3H6
- Known as:
- IFI35 mab (anti-) (M01), clonality 3H6
- Catalog number:
- H00003430-M01
- Product Quantity:
- 100 ug
- Category:
- -
- Supplier:
- Abno
- Gene target:
- IFI35 monoclonal antibody (M01) clone 3H6
Ask about this productRelated genes to: IFI35 monoclonal antibody (M01), clone 3H6
- Gene:
- GTF2H2B NIH gene
- Name:
- general transcription factor IIH subunit 2B (pseudogene)
- Previous symbol:
- -
- Synonyms:
- DKFZP686M0199
- Chromosome:
- 5q13.2
- Locus Type:
- pseudogene
- Date approved:
- 2008-07-04
- Date modifiied:
- 2015-11-09
- Gene:
- IFI35 NIH gene
- Name:
- interferon induced protein 35
- Previous symbol:
- -
- Synonyms:
- IFP35
- Chromosome:
- 17q21.31
- Locus Type:
- gene with protein product
- Date approved:
- 1996-04-12
- Date modifiied:
- 2016-10-05
- Gene:
- POLR1A NIH gene
- Name:
- RNA polymerase I subunit A
- Previous symbol:
- -
- Synonyms:
- DKFZP586M0122, FLJ21915, RPO1-4, RPA1
- Chromosome:
- 2p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 2003-04-01
- Date modifiied:
- 2017-06-28
- Gene:
- TDRP NIH gene
- Name:
- testis development related protein
- Previous symbol:
- C8orf42
- Synonyms:
- INM01, TDRP1, TDRP2
- Chromosome:
- 8p23.3
- Locus Type:
- gene with protein product
- Date approved:
- 2005-07-28
- Date modifiied:
- 2015-08-26
Related products to: IFI35 monoclonal antibody (M01), clone 3H6
Related articles to: IFI35 monoclonal antibody (M01), clone 3H6
- Renqing Changjue (RQCJ) is a form of Tibetan medicine recognized for its immunomodulatory effects. However, the underlying mechanisms through which it exerts these effects remain to be elucidated. - Source: PubMed
Publication date: 2026/05/21
Jiang ZhaoKong XiumeiZhang XiaoyingLv YaxinWu SiqiJi XuZhao Qin - H5N6 highly pathogenic avian influenza virus (HPAIV) poses a serious threat to both poultry and public health due to its ability to cross species barriers. Although interferon-stimulated genes (ISGs) are key components of the host's antiviral defense, a systematic identification and functional characterization of duck ISGs has not yet been conducted. In this study, we identified 815 potential duck ISGs induced by type II interferon (IFN-γ) in duck embryo fibroblasts (DEFs). The majority of these type II ISGs were enriched in immune-related pathways, including "cytokine-cytokine receptor interaction" and "influenza A". Functional validation using siRNA-mediated knockdown demonstrated that six ISGs, including duIFI35, promote H5N6 AIV replication when silenced. Through TUNEL assay, flow cytometry, and apoptotic pathway analysis, Our analysis revealed that H5N6 AIV infection markedly upregulates apoptotic genes such as Fas, FADD, caspase-8, BAK, cytochrome c, APAF1, caspase-9, and caspase-3 (P < 0.05), thereby promoting apoptosis in DEFs. In investigating the antiviral mechanism of duIFI35, it was found that overexpression of duIFI35 further enhanced H5N6-induced apoptosis, as evidenced by increased transcription of these apoptotic genes, whereas duIFI35 knockdown had the opposite effect. Importantly, the antiviral effect of duIFI35 was significantly diminished upon treatment with the caspase inhibitor Z-VAD-FMK (20 μM) (P < 0.05), indicating that its antiviral activity is mediated through apoptosis induction. Collectively, this study provides the first systematic identification of type II ISGs in ducks and reveals duIFI35-mediated apoptosis as a critical antiviral mechanism, offering foundational insights into ISG-driven innate immunity against AIV in waterfowl. - Source: PubMed
Publication date: 2026/04/16
Zhang TaoYang NaMa LuluXu FengxiangLin XiaobingHuang JiangwuGao FeiLiao MingFeng MinDai Manman - Lupus nephritis (LN) represents the most severe renal manifestation of systemic lupus erythematosus (SLE), contributing to significant morbidity. While current assessments focus on glomerular pathology, tubulointerstitial lesions may offer critical insights into disease progression and treatment response. This study develops a clinical prediction model integrating tubulointerstitial molecular signatures. We performed bioinformatics analysis using two independent tubulointerstitial gene expression datasets (GSE113342 and GSE200306), applying batch effect correction and principal component analysis (PCA) to identify differentially expressed genes (DEGs). A protein‒protein interaction (PPI) network isolated hub genes, and least absolute shrinkage and selection operator (LASSO) regression defined the novel "Nscore" parameter predictive of treatment response. The Nscore, incorporating seven key genes (EGR1, IL6R, TFRC, CCL19, IFI16, IFI35, and Fra1), showed a significant positive correlation with 24-h proteinuria and effectively distinguished complete-response (CR)/partial-response (PR) from non-response (NR). Immune deconvolution using the CIBERSORT algorithm revealed an increased abundance of T follicular helper (Tfh) cells and M1 macrophages in NR samples. A clinical nomogram integrating Nscore and sex demonstrated excellent discrimination. This model combines molecular biomarkers with clinical parameters to improve personalized therapeutic stratification, advancing treatment strategies beyond traditional glomerulocentric paradigms and identifying immune cell signatures as potential targets for immunomodulatory interventions. - Source: PubMed
Publication date: 2026/04/02
Ke JialongGu GuanghongNi WenpengHe JialinZeng ZhouyuLin RunpeiPeng JianmingDeng KunyiWen LijuanChen YanhuiTan NanZhang Chilun - Hepatitis B virus (HBV) infection is a major health problem with hundreds of millions of people still chronically infected worldwide. Although it is known that cytokines can inhibit HBV replication in infected hepatocytes, much is still unknown about the underlying mechanisms or mediators. - Source: PubMed
Publication date: 2026/03/30
Kim NayeonShin Jae JinOh Jae WonWon JuheeLee Ah RamDezhbord MehrangizPark JeongwooLee Ki-YoungKim Dong-SikKim Kwang PyoKim Kyun-Hwan - Excessive activation of the immune system by damage-associated molecular patterns (DAMPs) contributes to COVID-19 severity. Interferon-induced protein 35 (IFI35) is a DAMP-related interferon-stimulated gene recently proposed as a biomarker of hyperinflammation. We investigated the association between IFI35 serum levels, gene expression, and COVID-19 severity in 430 hospitalized patients (214 critical and 216 severe) and 112 convalescent controls. Serum IFI35 levels were quantified using ELISA, and IFI35 mRNA expression in PBMCs was assessed using quantitative PCR (qPCR). IFI35 levels were significantly higher in critically ill patients (median 1,003.6 pg/mL) than in severe cases (867.6 pg/mL; = 0.001) and controls (798.3 pg/mL; < 0.0001). Gene expression analysis showed a similar pattern ( = 0.014). Higher IFI35 levels were also associated with adverse clinical outcomes, including mortality, invasive mechanical ventilation, acute kidney injury, and cardiac arrest (all < 0.05). In receiver operating characteristic analysis, adding IFI35 to a model including C-reactive protein and D-dimer improved discriminative performance for mortality. In survival analysis, IFI35 > 1,475 pg/mL was associated with reduced survival in this cohort ( = 0.0062). These findings identify IFI35 as a promising prognostic biomarker associated with COVID-19 severity and adverse outcomes. - Source: PubMed
Publication date: 2026/03/26
Freitas Mariana Ramosde França Chirles AraújoNunes Sávio Luiz PereiraBarbosa Milena Xavierde Souza Carlos Dornels Freireda Costa Armstrong AndersonCarmo Rodrigo Feliciano