Ask about this productRelated genes to: ApoBEC3F antibody
- Gene:
- APOBEC3F NIH gene
- Name:
- apolipoprotein B mRNA editing enzyme catalytic subunit 3F
- Previous symbol:
- -
- Synonyms:
- ARP8, BK150C2.4.MRNA, KA6
- Chromosome:
- 22q13.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-12-12
- Date modifiied:
- 2016-10-05
Related products to: ApoBEC3F antibody
Related articles to: ApoBEC3F antibody
- Cytosine base editors (CBEs) mediate precise C-to-T conversion and hold considerable therapeutic promise, yet their editing function and utility in oncology remain underexplored. Here, we integrate evolutionary scale modeling (ESM) with structure-guided mutagenesis to remodel human APOBEC3F (A3F), yielding a panel of high-performance CBEs. Our high-efficiency A3F-CBEs achieve up to 1.9- and 3.3-fold higher on-target editing within the canonical editing window than A3A- and Anc689-BE4max, respectively. The high-accuracy A3F-CBEs deliver up to 3.0-fold improvement over haA3A-G at the majority of surveyed loci without compromising specificity. To demonstrate therapeutic potential, we deploy a dual-AAV platform packaging A3F-BE4max and dual gRNAs co-targeting KRAS and MYC in pancreatic ductal adenocarcinoma (PDAC) models. It elicits robust oncogene silencing and inhibited PDAC cell proliferation both in vitro and patient-derived organoids (PDOs). In a PDAC mouse model, it markedly suppresses tumor burden and extends survival. Our work establishes ESM-guided A3F-based CBEs as a versatile, precise platform for cancer genetic therapy. - Source: PubMed
Publication date: 2026/03/07
Fang QingxiaoZhang JinWang KeshanWang ZheLv ZongjingZhang XiaopingBi ChanghaoZhang XueliYu JunFeng YukuanZhou TianxingHao JihuiYang Chao - Immunogenic cell death (ICD) plays a critical role in the host’s antitumor immune response, and its dysregulation is linked to poor prognosis in colorectal cancer (CRC). Identifying ICD-related genes and developing prognostic models can enhance the prediction of patient outcomes and facilitate personalized treatments. Utilizing data from CRC patients in the Cancer Genome Atlas, we employed weighted gene co-expression network analysis, LASSO regression analysis, and multivariate Cox regression screening to identify immunogenic cell death-related prognostic genes (IPGs) in CRC patients. An IPGs scoring system was constructed, allowing for the stratification of patients into high-risk and low-risk groups based on the best cutoff ICD-RiskScore, with the Gene Expression Omnibus dataset serving as a validation cohort. We then examined the correlations between the high-risk and low-risk groups concerning clinicopathological features, immune infiltration, immunotherapy responses, and tumor mutational burden. Additionally, we analyzed the cellular landscape and cell-cell interactions in colorectal cancer at a single-cell resolution. A prognostic model comprising 12 immune-related prognostic genes (IPGs)—CAV2, NOXA1, TGFB2, WRNIP1, CCL22, ICAM2, APOBEC3F, COTL1, CTSD, IDO1, NFATC1, and RUNX3—was established, demonstrating a high area under the curve value in survival analysis, which indicates robust predictive performance. In comparison to the low-risk group, the high-risk group exhibited lower survival rates, higher mutation rates of genes, and was associated with more advanced tumor stages. Single-sample gene set enrichment analysis revealed that the low-risk group possessed a stronger immune surveillance function. Additionally, single-cell analysis uncovered a lower abundance of immune cells and an increased proportion of epithelial cells within tumor samples. The frequency of interactions among epithelial cells, endothelial cells, and fibroblasts was found to be elevated in tumor samples. Subsequently, validation of the prognostic genes revealed that COTL1 expression was significantly elevated in CRC tissues compared to adjacent normal tissues (P < 0.05). This study presents a prognostic model for colorectal cancer that integrates 12 immune-related genes. The model holds potential clinical value in predicting patient prognosis and guiding personalized treatment strategies. These findings also provide insights into the molecular mechanisms of immune cell dynamics in colorectal cancer and highlight potential therapeutic targets. - Source: PubMed
Publication date: 2026/01/21
Dong XianwenYang WenjuanGong ChunxiangWang ChangrongWan QijunYang Ti - Porcine reproductive and respiratory syndrome virus (PRRSV) is a major pathogen that causes substantial economic losses to the global swine industry. Apolipoprotein B mRNA-editing enzyme catalytic polypeptide-like 3 F (APOBEC3F), a key constituent of cytoplasmic processing bodies (P-bodies) and a member of the deaminase protein family, possesses intrinsic antiviral activity. This study systematically investigates the effects of APOBEC3F and its functional domains on PRRSV replication. This study systematically investigated the effects of APOBEC3F and its functional domains on PRRSV replication. We found that overexpression of APOBEC3F and its C-terminal deaminase domain (CD2) markedly suppressed PRRSV replication (including transcription, protein expression, and viral titers) in susceptible porcine cells. Conversely, APOBEC3F knockdown enhanced viral replication. Notably, several PRRSV proteins-NSP1α, NSP1β, NSP5, NSP7, GP4, GP5, and N-were found to downregulate endogenous APOBEC3F mRNA expression in host cells. Moreover, IP-MS analysis identified several potential candidate interactors, including DEAD-box helicases (such as DDX6 and MOV10) and other host factors, suggesting that APOBEC3F may associate with P-body components to exert its antiviral function. These results offer new insights into the molecular mechanisms of APOBEC3F-mediated antiviral defense against PRRSV and underscore its potential as a therapeutic target. - Source: PubMed
Publication date: 2026/01/02
Wang PengchengHu XuanTian LangLu XiaoyuXiong QianLiang KangliDeng QiaomuWen GuilanCheng Anchun - The anti-HIV-1 activity of the double-domain cytidine deaminases APOBEC3G (A3G) and APOBEC3F (A3F) depends on their encapsidation into progeny virions. While A3G requires AA-dinucleotide recognition by its N-terminal deaminase domain (CD1) for packaging, the mechanism for A3F encapsidation has remained unclear. Here, we present the structure of an A3F CD1 variant, revealing AA-binding pocket residues nearly identical to those of A3G CD1. Modeling further shows that A3F's C-terminal deaminase domain (CD2) harbors a similarly conserved AA-binding pocket. Both A3F CD1 and CD2 preferentially bind AA/GA-containing RNA, and mutations in the AA-binding pocket of either domain in full-length A3F do not impair virion packaging or antiviral activity, indicating functional redundancy. Consistently, double-domain chimeras with A3F CD1 or CD2 at either terminus are efficiently packaged and restrict HIV-1 through both deaminase-dependent and -independent mechanisms. In contrast, A3G exhibits strict domain-position dependence: only constructs with A3G CD1 at the N-terminus support packaging, and HIV-restriction activity varies with the particular domain at the C-terminus. A3G CD1 at the C-terminus is inactive, but the A3G CD2 at the C-terminus is active with either the A3F CD1 or A3F CD2 at the N-terminus. These findings highlight the mechanistic flexibility of A3F, in which either domain can mediate RNA recognition, virion encapsidation, and antiviral activity. - Source: PubMed
Publication date: 2025/11/07
Pacheco JosueYousefi MariaYang HanjingLi ShuxingChelico LindaChen Xiaojiang S - Survivors of childhood cancers are at risk of second malignant neoplasms (SMNs). Exposure to radiation therapy and different chemotherapy agents are known risk factors for SMN development. However, there remains interindividual variability that could be attributed to genetic variations. Our study aims to identify rare genetic variants associated with SMN risk and assess the influence of treatment on the associated risk of these variants. - Source: PubMed
Publication date: 2025/09/17
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