Polyclonal Rabbit APOBEC4 Antibody
- Known as:
- Polyclonal Rabbit APOBEC4 Antibody
- Catalog number:
- KA0248
- Product Quantity:
- 100ul
- Category:
- -
- Supplier:
- KareBay
- Gene target:
- Polyclonal Rabbit APOBEC4 Antibody
Related genes to: Polyclonal Rabbit APOBEC4 Antibody
- Gene:
- APOBEC4 NIH gene
- Name:
- apolipoprotein B mRNA editing enzyme catalytic polypeptide like 4
- Previous symbol:
- C1orf169
- Synonyms:
- MGC26594, FLJ25691, RP1-127C7.4
- Chromosome:
- 1q25.3
- Locus Type:
- gene with protein product
- Date approved:
- 2005-07-20
- Date modifiied:
- 2016-03-07
Related products to: Polyclonal Rabbit APOBEC4 Antibody
Related articles to: Polyclonal Rabbit APOBEC4 Antibody
- Cancer initiates as a consequence of genomic mutations and its subsequent progression relies in part on increased production of ribosomes to maintain high levels of protein synthesis for unchecked cell growth. Recently, cytidine deaminases have been uncovered as sources of mutagenesis in cancer. In an attempt to form a connection between these 2 cancer driving processes, we interrogated the cytidine deaminase family of proteins for potential roles in human ribosome biogenesis. We identified and validated APOBEC3A and APOBEC4 as novel ribosome biogenesis factors through our laboratory's established screening platform for the discovery of regulators of nucleolar function in MCF10A cells. Through siRNA depletion experiments, we highlight APOBEC3A's requirement in making ribosomes and specific role within the processing and maturation steps that form the large subunit 5.8S and 28S ribosomal (r)RNAs. We demonstrate that a subset of APOBEC3A resides within the nucleolus and associates with critical ribosome biogenesis factors. Mechanistic insight was revealed by transient overexpression of both wild-type and a catalytically dead mutated APOBEC3A, which both increase cell growth and protein synthesis. Through an innovative nuclear RNA sequencing methodology, we identify only modest predicted APOBEC3A C-to-U target sites on the pre-rRNA and pre-mRNAs. Our work reveals a potential direct role for APOBEC3A in ribosome biogenesis likely independent of its editing function. More broadly, we found an additional function of APOBEC3A in cancer pathology through its function in ribosome biogenesis, expanding its relevance as a target for cancer therapeutics. - Source: PubMed
Publication date: 2024/07/08
McCool Mason ABryant Carson JAbriola LauraSurovtseva Yulia VBaserga Susan J - Human apolipoprotein B mRNA editing enzyme, catalytic polypeptide (APOBEC) 3 cytidine deaminases are the prominent drivers of somatic mutations in cancers. However, the effect of functional polymorphisms on the development of renal cell carcinoma (RCC) remains unknown. Five genetic polymorphisms affecting the expression of APOBEC3A (A3A), APOBEC3B, and APOBEC4 and uracil DNA glycosylase (UNG) were genotyped in 728 RCC patients and 1500 healthy controls. The effects of tumor necrosis factor-α (TNFα) and interleukin-6 on the activity of the promoter with rs12157810-A or -C in four RCC cell lines (786-O, A498, Caki2, ACHN) and two colorectal cancer cell lines (HCT116, SW620) were evaluated using dual-luciferase assays. Transcriptional repressors to the promoter were identified by chromatin immunoprecipitation-quantitative PCR. The proapoptotic effect of on RCC cells was evaluated using cytometry. The prognostic values of A3A and ETS1 were evaluated by the Cox regression analysis. The expressions of A3A and ETS1 were evaluated in clear cell RCC (ccRCC) specimens with different polymorphic genotypes using quantitative RT-PCR and immunohistochemistry. Of those functional polymorphisms, CC genotype at rs12157810 in the promoter was significantly associated with a decreased risk of ccRCC, compared to the AA genotype (odds ratio adjusted for age and gender, 0.41, 95% confidence interval [CI], 0.28-0.57). Other polymorphic genotypes were not associated with the risk of RCC. The activity of the promoter with rs12157810-C was significantly higher than that with rs12157810-A in the four RCC cell lines and two colorectal cancer cell lines. The activity of the promoter with rs12157810-C was greatly up-regulated by TNFα and predominantly inhibited by a transcriptional repressor ETS1. The binding of ETS1 to the promoter with rs12157810-C was looser than that with rs12157810-A. Ectopic expression of significantly promoted apoptosis in ccRCC cells, rather than in colorectal cancer cells. Higher ETS1 expression predicted a favorable prognosis in ccRCC, with a hazard ratio of 0.58 (95% CI, 0.43-0.78). Rs121567810-C up-regulates the promoter activity, possibly due to higher response to TNFα and looser transcriptional repression by ETS1. Up-regulation of A3A increases apoptosis, thus decreasing ccRCC risk in those carrying rs121567810-C. - Source: PubMed
Publication date: 2021/09/15
Tan XiaojieZheng ShaolingLiu WenbinLiu YanKang ZhengchunLi ZishuaiLi PengSong JiahuiHou JianguoYang BoHan XueWang FuboJing ChunxiaCao Guangwen - The AID (activation-induced cytidine deaminase)/APOBEC (apolipoprotein B mRNA editing enzyme catalytic subunit) family with its multifaceted mode of action emerges as potent intrinsic host antiviral system that acts against a variety of DNA and RNA viruses including coronaviruses. All family members are cytosine-to-uracil deaminases that either have a profound role in driving a strong and specific humoral immune response (AID) or restricting the virus itself by a plethora of mechanisms (APOBECs). In this article, we highlight some of the key aspects apparently linking the AID/APOBECs and SARS-CoV-2. Among those is our discovery that shows high expression in cell types and anatomical parts targeted by SARS-CoV-2. Additional focus is given by us to the lymphoid structures and AID as the master regulator of germinal center reactions, which result in antibody production by plasma and memory B cells. We propose the dissection of the /s gene signature towards decisive determinants of the patient-specific and/or the patient group-specific antiviral response. Finally, the patient-specific mapping of the AID/APOBEC polymorphisms should be considered in the light of COVID-19. - Source: PubMed
Publication date: 2021/07/01
Meshcheryakova AnastasiaPietschmann PeterZimmermann PhilipRogozin Igor BMechtcheriakova Diana - To unravel the source of SARS-CoV-2 introduction and the pattern of its spreading and evolution in the United Arab Emirates, we conducted meta-transcriptome sequencing of 1067 nasopharyngeal swab samples collected between May 9th and Jun 29th, 2020 during the first peak of the local COVID-19 epidemic. We identified global clade distribution and eleven novel genetic variants that were almost absent in the rest of the world and that defined five subclades specific to the UAE viral population. Cross-settlement human-to-human transmission was related to the local business activity. Perhaps surprisingly, at least 5% of the population were co-infected by SARS-CoV-2 of multiple clades within the same host. We also discovered an enrichment of cytosine-to-uracil mutation among the viral population collected from the nasopharynx, that is different from the adenosine-to-inosine change previously reported in the bronchoalveolar lavage fluid samples and a previously unidentified upregulation of APOBEC4 expression in nasopharynx among infected patients, indicating the innate immune host response mediated by ADAR and APOBEC gene families could be tissue-specific. The genomic epidemiological and molecular biological knowledge reported here provides new insights for the SARS-CoV-2 evolution and transmission and points out future direction on host-pathogen interaction investigation. - Source: PubMed
Publication date: 2021/07/07
Liu RongWu PeiOgrodzki PaulineMahmoud SallyLiang KeLiu PengjuanFrancis Stephen SKhalak HanifLiu DenghuiLi JunhuaMa TaoChen FangLiu WeibinHuang XinyuHe WenjunYuan ZhaorongQiao NanMeng XinAlqarni BudoorQuilez JavierKusuma VinayLin LongJin XinYang ChongguangAnton XavierKoshy AshishYang HuanmingXu XunWang JianXiao PengAl Kaabi NawalFasihuddin Mohammed SaifuddinSelvaraj Francis AmirtharajWeber StefanAl Hosani Farida IsmailLiu SiyangZaher Walid Abbas - The APOBEC proteins play significant roles in the innate and adaptive immune system, probably due to their deaminase activities. Because APOBEC1 (A1) and APOBEC3 (A3) are absent in the chicken genome, we were interested in determining whether chicken APOBEC4 (A4) possessed more complex functions than its mammalian homologs. In this study, chicken A4 (chA4) mRNA was identified and cloned for the first time. Based on bioinformatics analyses, the conserved zinc-coordinating motif (HXE … PC(X)C) was identified on the surface of chA4 and contained highly conserved His97, Glu99, Pro130, Cys131 and Cys138 active sites. The highest expression levels of constitutive chA4 were detected in primary lymphocytes and bursa of Fabricius. Newcastle Disease (ND) is one of the most serious infectious diseases in birds, causing major economic losses to the poultry industry. In vitro, Newcastle Disease Virus (NDV) early infection induced significant increases in chA4 expression in the chicken B cell line, DT40, the macrophage cell line, HD11 and the CD4 T cell line, MSB-1, but not the fibroblast cell line, DF-1. In vivo, the expression levels of chA4 were up-regulated in several tissues from NDV-infected chickens, especially the thymus, testicles, duodenum and kidney. The high level expression of exogenous chA4 displayed inhibitory effects on NDV and reduced viral RNA in infected cells. Taken together, these data demonstrate that chA4 is involved in the chicken immune system and may play important roles in host anti-viral responses. - Source: PubMed
Publication date: 2020/01/25
Shi MengyuTan LeiZhang YaodanMeng ChunchunWang WeiSun YingjieSong CuipingLiu WeiweiLiao YingYu ShengqingRen TaoDing ZhuangLiu XiufanQiu XushengDing Chan