IFI16 Mouse Monoclonal Antibody
- Known as:
- IFI16 Mouse Monoclonal Antibody
- Catalog number:
- BIN-003428-M06
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- IFI16 Mouse Monoclonal Antibody
Related genes to: IFI16 Mouse Monoclonal Antibody
- Gene:
- IFI16 NIH gene
- Name:
- interferon gamma inducible protein 16
- Previous symbol:
- -
- Synonyms:
- IFNGIP1, PYHIN2
- Chromosome:
- 1q23.1
- Locus Type:
- gene with protein product
- Date approved:
- 1993-09-29
- Date modifiied:
- 2016-10-05
Related products to: IFI16 Mouse Monoclonal Antibody
Related articles to: IFI16 Mouse Monoclonal Antibody
- Following the publication of the above article, a concerned reader drew the Editor's attention to the fact that the figures presented in this paper appeared to contain the following anomalies: In Fig. 4D, the 'Met 5 mM' and 'Met 10 mM' data panels were overlapping; in Fig. 8F, the 'IF116 si' and 'IF116 si + Met' data panels were overlapping; in Fig 5A, the 'Un' and 'Ctr' rows of data were overlapping; and in Fig. 7A, the 'Ctr' and 'IF116 Si' rows of data were overlapping. In addition, after having performed an independent analysis of the data in this paper in the Editorial office, it came to light that the 'Met 0 mM' panel in Fig. 4D contained an overlapping section with the Control panel in Fig. 8F. Given that these issues have come to light, the Editor of has decided that this article should be retracted from the publication on the grounds of an overall lack of confidence in the presented data. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a satisfactory reply. The Editor sincerely apologizes to the readership for any incovenience caused, and we thank the reader for drawing this matter to our attention. [International Journal of Molecular Medicine 41: 1365‑1376, 2018; DOI: 10.3892/ijmm.2017.3346]. - Source: PubMed
Publication date: 2026/04/24
Hao BiaoXiao YanSong FangLong XiangshuHuang JingTian MaoboDeng ShiyanWu Qiang - Biomarkers predicting response to trifluridine/tipiracil (FTD/TPI) with or without bevacizumab (BEV) in refractory metastatic colorectal cancer (mCRC) remain unclear. We identified candidate biomarkers in preclinical models and evaluated their clinical relevance. - Source: PubMed
Publication date: 2026/04/17
Suenaga MMashima TKawata NDan SSeimiya HYamaguchi K - Keloids represent a pathological fibroproliferative disorder with high recurrence rates and limited therapeutic options. This study integrates multi-dataset transcriptomics (GSE158395, GSE188952, GSE92566, GSE173900) and machine learning algorithms (XGBoost, Random Forest, LASSO) to systematically investigate the role of lactylation modification in keloid pathogenesis. We identified 26 lactylation-related differentially expressed genes (15 upregulated, 11 downregulated) enriched in oxidative stress, immune response, and extracellular matrix pathways. Machine learning convergence revealed five lactylation hub genes (PRDX1, CSRP1, IFI16, CALD1, VIM), with PRDX1 exhibiting the highest diagnostic efficacy (AUC = 0.85). Immune infiltration analysis demonstrated significant correlations between hub genes and dysregulated immune cells. Experimental validation confirmed reduced PRDX1 expression in keloid tissues; its knockdown in fibroblasts elevated ROS levels and enhanced proliferation and migration. Regulatory network analysis predicted shared transcription factors (KLF12, NFKB1, MYC) governing hub genes, while drug screening prioritized three clinically actionable compounds (acetaminophen, valproic acid, vorinostat) targeting PRDX1. These findings establish lactylation as a critical regulator of keloid pathogenesis and identify PRDX1 as a promising therapeutic target. - Source: PubMed
Publication date: 2026/04/17
He RuizheSun MengzheLiu TiantianPeng YinboPeng LinboFang Yong - Inflammasomes are an essential component of the innate immune response against pathogen infections. However, the molecular mechanism regulating the inflammasome signaling in response to gangrenous () infection remains elusive. We herein report the unexpected discovery that IFI204 (the murine homolog of human IFI16)-dependent STING protects against gas gangrene via enhancing NLRP3 inflammasome signaling. In the gas gangrene model, compared with wild-type (WT) mice, deficiency ( ) mice displayed an increased susceptibility to soft tissue infection, with more bacterial colonization, severe muscle damage, and higher mortality rates. Obviously, deficiency leads to the defect of inflammasome signaling activation and bacterial killing and clearance. STING promotes inflammasome signaling activation in an IFI204-dependent manner. Crucially, the IFI204-STING axis enhances NLRP3 inflammasome signaling activation, which, in turn, facilitates pathogen elimination and host defense. Our findings highlight STING acts as a positive regulator in defense of infection and present it as a potential target for anti-infection drug development. - Source: PubMed
Publication date: 2026/03/31
Zhang Ming-YueLi Jia-QiXu QianZhuang Zi-JianLiang JingHe Ao-BoZhang Shu-XinZhao YiChen XueLi Zhen-YuSheng PingLiu YangYu Shui-Xing - Oncolytic adenovirus (OAd) therapy is one of the effective treatment strategies for solid malignant tumors, and E1A is a requirement for adenovirus replication. Thus, it is very important to study how E1A regulates adenovirus replication. The p300 and E1A expression were detected by Western blot. The viral replication of OAd was detected by virus replication assay. The interaction between E1A and p300 was analyzed by immunofluorescence and immunoprecipitation assays. The therapeutic effect of OAd-shp300 was analyzed by MTT assay and animal experiments. The results indicated that OAd infection or E1A overexpression could reduce p300 expression, implying that OAd might reduce p300 expression via E1A, and p300 knockdown could enhance viral replication and cell cytotoxicity of OAd. Furthermore, E1A promoted viral replication of OAd via mediating p300 ubiquitination degradation to inhibit the IFI16/STING/IRF3/IFN-β signaling pathway. Additionally, OAd-shp300 induced highly efficient viral replication and potent antitumor activity both in vitro and in vivo. In this study, OAd can reduce p300 expression by promoting its ubiquitination via E1A, thereby enhancing viral replication and cell cytotoxicity. Therefore, this study can provide a biomarker for screening patients who are sensitive to OAd and new ideas for clinical tumor treatment. - Source: PubMed
Publication date: 2026/03/18
Xiao BoduanYang QingzheHu ShichuanHu JianchuanQi ZhongbingZhang YaoQin YuCheng Ping