德泰生物DNA dC->dU-editing enzyme APOBEC-3A Protein, APOBEC3A, 多种规格可供选择. 货号: DTD0078, 表达宿主: HEK293, 纯度:>90%. 10年蛋白表达经验, 品质保证, 值得信赖.
英文名称:Cricetulus longicaudatus Probable DNA dC dU editing enzyme APOBEC3 APOBEC3Cricetulus longicaudatus Probable DNA dC dU editing enzyme APOBEC3 APOBEC3 is available 4 times 来自 M,中文名称:长喙魟很可能DNA dC dU编辑酶APOBEC3
DNA dC->dU-editing enzyme APOBEC-3G Basic informationMore.. Product Name:DNA dC->dU-editing enzyme APOBEC-3G Synonyms:ANTI-CEM15(N-TERMINAL) antibody produced in rabbit;APOBEC3G;APOBEC-related cytidine deaminase;APOBEC-related protein 9;CEM-15;DNA dC->dU-editing enzyme APOBEC-3G ...
Probable DNA dC→dU-editing enzyme APOBEC-3D Synonyms:Anti-APOBEC3D antibody produced in rabbit;APOBEC3D;Probable DNA dC→dU-editing enzyme APOBEC-3D;Anti-Apolipoprotein B mRNA editing enzyme, catalytic polypeptide-like 3D (putative) CAS:
The different local targeting specificities of APOBEC1 and AID argue strongly that both proteins are involved directly in deaminating dC residues in DNA, generating dU/dG lesions. Given this likely mode of action, one would expect that the stimulation of mutation by APOBEC1 (like that by AID ...
Crystal structure of APOBEC3A bound to single-stranded DNA reveals structural basis for cytidine deamination and specificity 2017, Nature Communications The double-domain cytidine deaminase APOBEC3G is a cellular site-specific RNA editing enzyme 2016, Scientific Reports Crystal structures of APOBEC3G N-do...
3; cytidine deaminase; hypermutation; cancer genomics; 3DPCR Erroneous identification of APOBEC3-edited chromosomal DNA in cancer genomics R Suspe` ne1, V Caval1, M Henry1, M S Bouzidi1, S Wain-Hobson1 and J-P Vartanian*,1 1Molecular Retrovirology Unit, Institut Pasteur, 28 rue du Dr....
The bottom half of the matrix depicts individual pairwise APOBEC3 expression scatterplots, with regression lines plotted. Top half of the matrix indicates the one-tailed Pearson’s coefficient (r) for each pairwise combination. c, Induction of A3A, A3B, A3C, and A3D mRNA levels following ...
The revolution in cancer genomics shows that the dominant mutations are CG->TA transitions. The sources of these mutations are probably two host cell cytidine deaminases APOBEC3A and APOBEC3B. The former in particular can access nuclear DNA and monoto
[135–141]. All APOBEC3 proteins inhibit LINE-1 retrotransposition to varying degrees, with A3A and A3B being most effective. AID and APOBEC1 proteins both inhibit cell culture L1 and LTR element retrotransposition [142–145]. AID may also promote methylation of TEs in the nuclei of ...