APOBEC3C (C_term) Antibody
- Known as:
- APOBEC3C (C_term) Antibody
- Catalog number:
- AF1079a
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- APOBEC3C (C_term) Antibody
Related genes to: APOBEC3C (C_term) Antibody
- 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) Antibody
Related articles to: APOBEC3C (C_term) Antibody
- Prostate cancer (PCa) is one of the most common malignancies in men and remains particularly challenging as it progresses to the castration-resistant stage. Increasing evidence indicates that dysregulated RNA editing plays an active role in PCa progression and resistance to therapy. Among these modifications, adenosine-to-inosine editing catalyzed by adenosine deaminase acting on RNA 1 (ADAR1) alters transcripts, such as androgen receptor (AR) and antizyme inhibitor 1, promoting androgen-independent growth, metastasis, and immune evasion. Conversely, cytidine-to-uridine editing mediated by apolipoprotein B mRNA editing catalytic polypeptide-like 3 (APOBEC3) enzymes contributes to genomic instability. For example, APOBEC3B induces mutagenesis and resistance to AR-targeted therapy, and APOBEC3C functions as a context-dependent tumor suppressor that is transcriptionally repressed by the AR in advanced disease. Clinically, RNA editing signatures, including APOBEC3C expression levels, have shown promise as biomarkers for risk stratification, disease monitoring, and prognosis. Therapeutically, inhibition of ADAR1 or APOBEC3B, restoration of APOBEC3C activity, and site-specific corrective RNA editing using the CRISPR-ADAR2 platform represent emerging precision strategies. Ongoing development of small-molecule inhibitors, oligonucleotide-based modulators, and liquid biopsy-based detection methods further highlights the translational relevance of RNA editing in PCa. Future research should focus on improving editing specificity, minimizing off-target effects, and validating these biomarkers and therapeutic targets in clinical settings to fully realize the diagnostic and therapeutic potential of RNA editing in the precise management of prostate cancer. - Source: PubMed
Publication date: 2026/05/04
Li ShoukangLi AnshuHuang YongmingWang YoujiaFan MeiyinJiang XiaoyingBing KaijianLiang JiaqianWang KeshanXu ZhiWang Liyang - Prostate adenocarcinoma (PRAD) is a highly prevalent malignant tumor in males and exhibits substantial heterogeneity. Identifying key associated genes is therefore critical for improving disease diagnosis and therapeutic strategies. - Source: PubMed
Publication date: 2026/04/26
Hu JimengZhou MinWu XiaoboHu Mengbo - Graves' disease (GD) is a classical autoimmune disorder caused by interactions between genetic susceptibility and immune dysregulation. However, the transcriptomic mechanisms underlying disease relapse and remission, particularly those involving alternative splicing (AS), remain poorly understood. - Source: PubMed
Publication date: 2026/05/13
Wu YangLiu JieYang YuChen KunHua FeiWang Kun - 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