Ask about this productRelated genes to: ApoBEC3D Blocking Peptide
- Gene:
- APOBEC3D NIH gene
- Name:
- apolipoprotein B mRNA editing enzyme catalytic subunit 3D
- Previous symbol:
- APOBEC3E
- Synonyms:
- ARP6, APOBEC3DE
- Chromosome:
- 22q13.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-12-12
- Date modifiied:
- 2017-05-11
Related products to: ApoBEC3D Blocking Peptide
Related articles to: ApoBEC3D Blocking Peptide
- 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 - The current research focuses on a systematic analysis of the expression patterns of the apolipoprotein B editing complex 3 () gene family in clear cell renal cell carcinoma (ccRCC) and their impact on disease progression, prognosis, and somatic gene mutations associated with ccRCC. - Source: PubMed
Zhang HanrongLuo HuiZhao LiYu ZhongyingLin ShanLin LianzhengLi Jinyu - Gemcitabine is a widely used chemotherapy that interferes with tumor growth by targeting DNA replication. Understanding why many tumors are unresponsive to gemcitabine is a clinical challenge. A new study reports that upregulation of the cytidine deaminases APOBEC3C and APOBEC3D facilitates gemcitabine resistance by protecting against DNA replication stress. - Source: PubMed
Maciejowski JohnMohamed Taha - Human APOBEC3 enzymes are a family of single-stranded (ss)DNA and RNA cytidine deaminases that act as part of the intrinsic immunity against viruses and retroelements. These enzymes deaminate cytosine to form uracil which can functionally inactivate or cause degradation of viral or retroelement genomes. In addition, APOBEC3s have deamination-independent antiviral activity through protein and nucleic acid interactions. If expression levels are misregulated, some APOBEC3 enzymes can access the human genome leading to deamination and mutagenesis, contributing to cancer initiation and evolution. While APOBEC3 enzymes are known to interact with large ribonucleoprotein complexes, the function and RNA dependence are not entirely understood. To further understand their cellular roles, we determined by affinity purification mass spectrometry (AP-MS) the protein interaction network for the human APOBEC3 enzymes and mapped a diverse set of protein-protein and protein-RNA mediated interactions. Our analysis identified novel RNA-mediated interactions between APOBEC3C, APOBEC3H Haplotype I and II, and APOBEC3G with spliceosome proteins, and APOBEC3G and APOBEC3H Haplotype I with proteins involved in tRNA methylation and ncRNA export from the nucleus. In addition, we identified RNA-independent protein-protein interactions with APOBEC3B, APOBEC3D, and APOBEC3F and the prefoldin family of protein-folding chaperones. Interaction between prefoldin 5 (PFD5) and APOBEC3B disrupted the ability of PFD5 to induce degradation of the oncogene cMyc, implicating the APOBEC3B protein interaction network in cancer. Altogether, the results uncover novel functions and interactions of the APOBEC3 family and suggest they may have fundamental roles in cellular RNA biology, their protein-protein interactions are not redundant, and there are protein-protein interactions with tumor suppressors, suggesting a role in cancer biology. Data are available via ProteomeXchange with the identifier PXD044275. - Source: PubMed
Publication date: 2024/03/27
Jang Gwendolyn MAnnan Sudarsan Arun KumarShayeganmehr ArzhangPrando Munhoz ErikaLao ReannaGaba AmitGranadillo Rodríguez MilaidLove Robin PPolacco Benjamin JZhou YuanKrogan Nevan JKaake Robyn MChelico Linda - Gemcitabine is a potent inhibitor of DNA replication and is a mainstay therapeutic for diverse cancers, particularly pancreatic ductal adenocarcinoma (PDAC). However, most tumors remain refractory to gemcitabine therapies. Here, to define the cancer cell response to gemcitabine, we performed genome-scale CRISPR-Cas9 chemical-genetic screens in PDAC cells and found selective loss of cell fitness upon disruption of the cytidine deaminases APOBEC3C and APOBEC3D. Following gemcitabine treatment, APOBEC3C and APOBEC3D promote DNA replication stress resistance and cell survival by deaminating cytidines in the nuclear genome to ensure DNA replication fork restart and repair in PDAC cells. We provide evidence that the chemical-genetic interaction between APOBEC3C or APOBEC3D and gemcitabine is absent in nontransformed cells but is recapitulated across different PDAC cell lines, in PDAC organoids and in PDAC xenografts. Thus, we uncover roles for APOBEC3C and APOBEC3D in DNA replication stress resistance and offer plausible targets for improving gemcitabine-based therapies for PDAC. - Source: PubMed
Publication date: 2024/03/06
Ubhi TajinderZaslaver OlgaQuaile Andrew TPlenker DennisCao PinjiangPham Nhu-AnBékési AngélaJang Gun-HoO'Kane Grainne MNotta FaiyazMoffat JasonWilson Julie MGallinger StevenVértessy Beáta GTuveson David ARöst Hannes LBrown Grant W