Full length protein corresponding to Human APOBEC3G aa 1-384. (AAH24268.1)Sequence: MKPHFRNTVERMYRDTFSYNFYNRPILSRRNTVWLCYEVKTKGPSRPPLD AKIFRGQVYSELKYHPEMRFFHWFSKWRKLHRDQEYEVTWYISWSPCTKC TRDMATFLAEDPKVTLTIFVARLYYFWDPDYQEALRSLCQKRDGPRATMK IMNYDEFQHCWSKFVYSQ
Conjugate
Unconjugated
Applications
Application Notes
WB: 1 μg/ml.
Target
Alternative Names
APOBEC3G; apolipoprotein B mRNA editing enzyme, catalytic polypeptide-like 3G; DNA dC->dU-editing enzyme APOBEC-3G; bK150C2.7; CEM15; dJ494G10.1; FLJ12740; MDS019; DNA dC-> dU-editing enzyme APOBEC-3G; APOBEC-related protein 9; dU editing enzyme; phorboli
DNA deaminase (cytidine deaminase) that mediates a form of innate resistance to retroviral infections (at least to HIV-1 infection) by triggering G-to-A hypermutation in the newly synthesized viral DNA. The replacements C-to-U in the minus strand DNA of HIV-1 during reverse transcription, leads to G-to-A transitions in the plus strand. The inhibition of viral replication is either due to the degradation of the minus strand before its integration or to the lethality of the hypermutations. Modification of both DNA strands is not excluded. This antiviral activity is neutralized by the virion infectivity factor (VIF), that prevents the incorporation of APOBEC3G into progeny HIV-1 virions by both inhibiting its translation and/or by inducing its ubiquitination and subsequent degradation by the 26S proteasome. APOBEC3G binds a variety of RNAs, but does not display detectable APOB, NF1 and NAT1 mRNA editing.
Pathway
APOBEC3G mediated resistance to HIV-1 infection; Disease; HIV Infection; Host Interactions of HIV factors; Vif-mediated degradation of APOBEC3G;
Citations
Publication ()
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