APOBEC3C (C_term)
- Known as:
- APOBEC3C (C_term)
- Catalog number:
- Y213998
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- APOBEC3C (C_term)
Related genes to: APOBEC3C (C_term)
- Gene:
- APOBEC3C NIH gene
- Name:
- apolipoprotein B mRNA editing enzyme catalytic subunit 3C
- Previous symbol:
- -
- Synonyms:
- APOBEC1L, PBI, bK150C2.3, ARDC2, ARDC4, ARP5
- Chromosome:
- 22q13.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-12-12
- Date modifiied:
- 2016-10-05
Related products to: APOBEC3C (C_term)
Related articles to: APOBEC3C (C_term)
- Hepatitis B virus (HBV) infects human hepatocytes, causing acute or chronic liver infection. Chronic HBV infection leads to progressive liver damage, potentially resulting in cirrhosis or hepatocellular carcinoma. One promising antiviral strategy involves activating cytidine deaminases of the APOBEC/AID family, which could induce mutational degradation of HBV. Using a CRISPRa-based transcriptional activation system with modified sgRNAs, we investigated antiviral and oncogenic effects of the activating genes encoding APOBEC3C, APOBEC3D, and APOBEC3H. - Source: PubMed
Karandashov Ivan VBrezgin Sergey APonomareva Natalia ITikhonov Andrey SChulanov Vladimir PKostyushev Dmitry SKostyusheva Anastasiya P - Prostate cancer (PCa) is a prevalent malignancy with a rising incidence. Advanced PCa, often resistant to therapy, remains a major clinical challenge, underscoring the need to identify novel molecular drivers. Utilizing transcriptomic data from the TCGA and GEO databases, we identified as a key candidate through WGCNA, differential expression analysis, and LASSO regression. Its clinical relevance was assessed via Kaplan-Meier survival analysis. Then, we validated expression patterns using immunohistochemistry and Western blot in normal and malignant prostate cell lines. The functional effects of on proliferation, migration, and invasion and mechanisms of such were evaluated through in vitro gain- and loss-of-function assays (CCK-8, Ki67 staining, wound healing, Transwell, Western blot, etc.). was significantly downregulated in PCa, and this low expression strongly correlated with adverse clinicopathological features, including advanced T stage, higher Gleason scores, and worse survival. Bioinformatically, high expression was associated with an activated anti-tumor immune microenvironment, characterized by enhanced CD8+ T cell infiltration, reduced M2 macrophage abundance, and upregulation of the immune checkpoint . In vitro, overexpression effectively suppressed PCa cell proliferation, migration, and invasion, while its knockdown promoted these malignant phenotypes. Mechanistically, enhances the expression of the and its downstream related molecules , , and ; upregulates DNA damage-protective genes ( and ); and enhances the expression of cell cycle regulator . This study establishes as a suppressor in PCa, which impedes tumor progression by regulating key molecules involved in cellular inflammation, cell cycle arrest, and DNA damage response. - Source: PubMed
Publication date: 2026/01/03
Pang ZhongqiWang JiansheXu YidanJi BoRen MinghuaDing Beichen - Genomic instability is a hallmark of cancer, encompassing both sequence and structural alterations that drive tumor evolution and heterogeneity. The APOBEC3 family of deoxycytidine deaminases has emerged as a major source of mutagenic activity in cancers. R-loops are RNA-DNA hybrids and structural barriers that interfere with replication and transcription. Among the APOBEC3 family, APOBEC3C (A3C) is particularly worthy of attention for its upregulation, driving the DNA replication stress tolerance in response to replication stress-inducing drug gemcitabine. However, the molecular mechanisms of gemcitabine resistance and regulatory circuitries mediated by A3C remain largely unknown, especially in checkpoint-deficient tumors. Initially, we screened that A3C was a putative transcriptional target of p53, and p53-deficient H1299 cells harboring A3C elicited a chemoresistant phenotype upon gemcitabine treatment both in vitro and in vivo. A3C expression enhanced Chk1-dependent S-phase checkpoint activation, thus slowing down replication fork progression and facilitating DNA repair. Pull-down assay and proteomic analysis identified that A3C had a specific interaction with the RNA helicase DDX5, which coordinately played critical roles in R-loop resolution. In contrast to A3C, DDX5 expression attenuated Chk1-dependent S-phase checkpoint activation. Knockdown of DDX5 in A3C-proficient H1299 cells attenuated gemcitabine-induced Chk1 activation and enhanced the therapeutic index of gemcitabine by promoting R-loop accumulation. Therefore, we conclude that A3C/DDX5/R-loop complex may impair the sensitivity of gemcitabine by modulating Chk1 dynamics and DNA replication/damage response machinery. - Source: PubMed
Publication date: 2026/01/07
Tao LiZhao YangJiang ZhuangzhaungKong ShujingDing YanlinNi TengyangWang WeiminLiu Yanqing - Previous reports revealed immune dysfunction, chromosomal abnormalities, cytokine deregulation, and telomere alterations after prolonged spaceflight. However, the stress of space on hematopoietic stem and progenitor cells (HSPCs) and the resilience properties maintaining lifelong hematopoiesis and immunity were not studied. We performed HSPC functionally organized multi-omics aging and resilience (HSPC-FOMA-R) analyses in 9 astronauts before, during, and after three short-duration International Space Station (ISS) missions. Whole-genome sequencing (with telomere length analysis and mitochondrial and clonal mutational profiling), whole-transcriptome sequencing (with RNA editing and retrotransposon analyses), single-cell RNA sequencing, cytokine arrays, and fluorescence-activated cell sorting (FACS) analyses assessed HSPC and immune subpopulation survival dynamics. We show that spaceflight is associated with partially reversible changes in HSPC survival and self-renewal, adenosine deaminase associated with RNA1 (ADAR1), telomere maintenance, mobilization, cell cycle, and "fight or flight" gene expression. Combined with clonal hematopoietic mutations, apolipoprotein B mRNA editing catalytic polypeptide-like (APOBEC3C) activation, and retrotransposon deregulation, HSPC-FOMA-R analyses are needed before extended missions. - Source: PubMed
Publication date: 2025/11/24
Pham JessicaNandi Shuvro PBalaian LarisaEngstrom ClaireChang PatrickMack Karlavan der Werf IngeKlacking EmmaSneifer JennaKatragadda NehaWirtjes KendaleRuiz AntonioChilin-Fuentes DaisyMolina ElsaMesci PinarStoudemire JanaMorris Sheldon RWhisenant ThomasAlexandrov Ludmil BJamieson Catriona H M - Prostate adenocarcinoma (PRAD) poses a significant global health burden. Apolipoprotein B mRNA editing enzyme catalytic polypeptide-like 3C (APOBEC3C) exhibits context-dependent roles in cancer but its function in PRAD remains unclear. This study aims to resolve APOBEC3C's functional duality in PRAD and identify immune-related hub genes using integrated bioinformatics and experimental validation. - Source: PubMed
Publication date: 2025/09/25
Zhao YaMa Chaoqun