Ask about this productRelated genes to: ApoBEC3B antibody
- Gene:
- APOBEC3B NIH gene
- Name:
- apolipoprotein B mRNA editing enzyme catalytic subunit 3B
- Previous symbol:
- -
- Synonyms:
- PHRBNL, FLJ21201
- Chromosome:
- 22q13.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-12-12
- Date modifiied:
- 2016-10-05
Related products to: ApoBEC3B antibody
Related articles to: ApoBEC3B antibody
- APOBECs are cytidine deaminases whose levels are increased in cells with high-risk HPV genomes and are responsible for most mutations in HPV associated cancers. APOBEC3B is a nuclear member of this family and is shown to be a positive regulator of HPV replication as well as expression. The proviral effects of A3B found in HPV positive cells contrast with its role as a restriction factor for many other viruses. Studies demonstrated that A3B can bind and regulate the formation of R-loops, which are trimeric nucleic acid structures consisting of an RNA paired with its complementary DNA strand, displacing one of the DNA strands. The present study demonstrates that A3B binds stably to both cellular and viral chromatin at sequences containing high R-loop levels, including the HPV URR and early polyadenylation sites. Importantly, A3B was found to play a critical role in the replication of HPV genomes and in regulating viral expression. Reduction of R-loop levels through overexpression of the R-loop specific RNase, RNase H1, impaired A3B binding to viral genomes as well as at multiple cellular sites. When A3B was depleted, total R-loop levels decreased by ~50%, leading to impaired viral transcription and an increase in the expression of immune genes, such as OASL, IL6, and IRF1. Mapping R-loop formation in A3B depleted cells revealed that A3B regulated a subset of R-loops that form on the transcriptional start (TSS) and termination sites (TTS) of cellular genes, including at the HPV URR. Furthermore, A3B depletion resulted in over a 50% reduction of DNA breaks along with altered expression of DNA damage repair proteins. This study demonstrates that A3B is an inducer of R-loop formation and DNA damage in HPV positive cells, thereby regulating cellular and viral gene expression along with HPV replication. - Source: PubMed
Publication date: 2026/03/23
Templeton Conor WGulik Jasmine SLaimins Laimonis A - The apolipoprotein B mRNA editing catalytic polypeptide-like (APOBEC) family was first defined as an innate antiviral defense system, but the APOBEC3 subfamily (APOBEC3s) is now recognized as a major endogenous source of somatic mutagenesis in cancer. APOBEC3s enzymes, particularly APOBEC3A and APOBEC3B, generate characteristic mutation patterns that promote genomic instability, clonal evolution, and adaptation to therapy. Beyond driving tumor evolution, APOBEC3 activity reshapes antitumor immunity in solid cancers. APOBEC3-induced mutations increase tumor mutational burden and create neoantigens that can enhance CD8 T-cell infiltration and interferon signaling. However, sustained APOBEC activation may also reinforce immunosuppressive circuits: through chronic inflammation and PD-1/PD-L1-interferon signaling, tumors can induce T-cell dysfunction, immune escape, and resistance to immune checkpoint blockade. This functional ambivalence has sparked debate over whether APOBEC3s should be inhibited to limit genomic instability, leveraged to enhance tumor immunogenicity, or modulated dynamically in a context-dependent manner. This review outlines the immune landscape and biochemical characteristics of the APOBEC3 family and situates these features within broader cancer-related disease contexts. APOBEC3-mediated mutagenesis is discussed as a mechanistic link between genomic instability and tumor-immune crosstalk in solid tumors, with emphasis on its relationships to immunoediting, immune checkpoint pathways, and therapeutic responses. Context-dependent associations of APOBEC3 activity with immune activation or immune evasion are also considered, together with their implications for strategies that modulate this pathway. - Source: PubMed
Publication date: 2026/02/11
Li QiaoxiWan WenyuZhu ZihanLin XuanduoWang FeiLi MengmengGuo HaoYang Yang - This study systematically investigated the genomic alterations in driven by Replication Factor A (RFA) dosage insufficiency using a promoter-replacement strategy combined with mutation accumulation and whole-genome sequencing. Our findings reveal that transcriptional suppression of or leads to severe growth inhibition. RFA deficiency induces a distinct mutational spectrum characterized by a high frequency of monosomy and terminal deletions, indicative of severe replication stress. Furthermore, loss of heterozygosity is significantly enriched at centromeres and high-GC regions, underscoring the role of RFA in stabilizing intrinsic genomic barriers. Utilizing an APOBEC3B-induced mutagenesis assay, we demonstrate that RFA insufficiency leads to the extensive accumulation of exposed ssDNA with a distinct bias towards the lagging strand template. Notably, we observed that cells spontaneously inactivate Mismatch Repair (MMR) genes, such as and , to survive RFA-induced stress. This hypermutant phenotype grants a certain degree of growth recovery on Low Galactose (LG) medium. Overall, these findings demonstrate that RFA dosage is a key determinant of genomic integrity and elucidate how repair pathway modulation drives adaptive evolution under replication stress. - Source: PubMed
Publication date: 2026/01/30
Zhang RunbiaoTian LiyanHe MinLi Kejing - Hepatitis B virus (HBV) covalently closed circular DNA (cccDNA) constitutes a viral persistence reservoir that sustains chronic infection. Although the DNA damage response (DDR) facilitates cccDNA biogenesis, its role in regulating cccDNA stability remains unclear. By intersecting published cccDNA-associated proteomic datasets with known DDR-related host factors, we identified heterogeneous nuclear ribonucleoprotein A2/B1 (hnRNPA2B1) as a novel restriction factor that binds cccDNA and suppresses HBV replication by promoting cccDNA degradation. Mechanistically, hnRNPA2B1 interacted with the G-quadruplex (G4) structure of cccDNA, with preference for G4-1, G4-7, and G4-10, and leads to the recruitment of the cytidine deaminase APOBEC3B by its prion-like domain (PrLD), thereby inducing C>T and G>A hypermutations and initiating cccDNA decay. Notably, HBV counteracts this defense mechanism through HBx-mediated hnRNPA2B1 polyubiquitination and proteasomal degradation, revealing a viral evasion strategy that perpetuates cccDNA persistence. These findings reveal a G4-dependent surveillance axis wherein hnRNPA2B1 directs APOBEC3B-mediated cytidine deamination to destabilize cccDNA while identifying HBx-induced hnRNPA2B1 ubiquitination as a viral countermeasure. This mechanistic duality not only elucidates a critical virus-host interaction governing cccDNA persistence but also provides a promising therapeutic target for the treatment of HBV infection. - Source: PubMed
Fu ZhendongWang LiyuanSun YangRen CaiyueDou YutongWang KaiFan YuchenYue XuetianLi ChunyangGao LifenLiang XiaohongMa ChunhongWu Zhuanchang - Oestrogen receptor (ER) activation leads to the formation of DNA double strand breaks (DSB), promoting genomic instability and tumour heterogeneity. The single-stranded DNA cytosine deaminase APOBEC3B (A3B) serves as a co-activator of ER and is implicated in inducing DSBs at transcriptional enhancers regulated by ER. Using whole-genome sequencing in an engineered cell model lacking base excision repair (BER) function, we demonstrate that A3B preferentially targets transcriptionally active regulatory regions in an R-loop-dependent manner. Strand-specific DNA:RNA immunoprecipitation sequencing (ssDRIP-seq) and ssDNA-associated protein immunoprecipitation sequencing (SPI-seq) confirm that A3B binds to and deaminates ssDNA within R-loops, a process facilitated by ER transactivation. Furthermore, BER-mediated processing of A3B-induced uracil bases contributes to the formation of R-loop-associated DSBs, which are essential for ER-regulated gene activation. These findings establish a role for A3B in R-loop homeostasis and transcriptional regulation, with implications for understanding ER-driven genomic instability and potential therapeutic targeting of A3B. - Source: PubMed
Publication date: 2026/02/18
Zhang ChiLu Yu-JingChen BingjieBai ZhiyanZeng QiaoxiHervieu AlexiaLicciardello Marco PMitsopoulos KonstantinosAl-Lazikani BissanTortorici MarcelloRossanese Olivia WWorkman PaulClarke Paul A