Anti-APOBEC3G Antibody Picoband® Fluoro647 Conjugated

APOBEC3G (apolipoprotein B mRNA editing enzyme, catalytic polypeptide-like 3G) is a human enzyme encoded by the APOBEC3G gene. This gene is a member of the cytidine deaminase gene family. It is one of seven related genes or pseudogenes found in a cluster, thought to result from gene duplication, on chromosome 22. Members of the cluster encode proteins that are structurally and functionally related to the C to U RNA-editing cytidine deaminase APOBEC1. It is thought that the proteins may be RNA editing enzymes and have roles in growth or cell cycle control. The protein encoded by this gene has been found to be a specific inhibitor of human immunodeficiency virus-1 (HIV-1) infectivity.

DNA dC->dU-editing enzyme APOBEC-3G;3.5.4.-; APOBEC-related cytidine deaminase; APOBEC-related protein; ARCD; APOBEC-related protein 9; ARP-9; CEM-15; CEM15; Deoxycytidine deaminase; A3G; APOBEC3G; MDS019

Expressed in spleen, testes, ovary and peripheral blood leukocytes and CD4+ lymphocytes. Also expressed in non-permissive peripheral blood mononuclear cells, and several tumor cell lines; no expression detected in permissive lymphoid and non-lymphoid cell lines. Exists only in the LMM form in peripheral blood-derived resting CD4 T-cells and monocytes, both of which are refractory to HIV-1 infection. LMM is converted to a HMM complex when resting CD4 T-cells are activated or when monocytes are induced to differentiate into macrophages. This change correlates with increased susceptibility of these cells to HIV-1 infection. .

Antiviral Signaling, Chromatin Binding Proteins, Chromatin Modifying Enzymes, DNA/RNA Binding, Epigenetics and Nuclear Signaling, Host-Virus Interaction, Immune System Diseases, Immunology, Interspecies Interaction, Microbiology

DNA deaminase (cytidine deaminase) which acts as an inhibitor of retrovirus replication and retrotransposon mobility via deaminase-dependent and -independent mechanisms. Exhibits potent antiviral activity against vif-deficient HIV-1. After the penetration of retroviral nucleocapsids into target cells of infection and the initiation of reverse transcription, it can induce the conversion of cytosine to uracil in the minus-sense single-strand viral DNA, leading to G-to-A hypermutations in the subsequent plus-strand viral DNA. The resultant detrimental levels of mutations in the proviral genome, along with a deamination- independent mechanism that works prior to the proviral integration, together exert efficient antiretroviral effects in infected target cells. Selectively targets single-stranded DNA and does not deaminate double-stranded DNA or single-or double- stranded RNA. Exhibits antiviral activity also against simian immunodeficiency viruses (SIVs), hepatitis B virus (HBV), equine infectious anemia virus (EIAV), xenotropic MuLV-related virus (XMRV) and simian foamy virus (SFV) . May inhibit the mobility of LTR and non-LTR retrotransposons. .

1. Chelico L, Prochnow C, Erie DA, Chen XS, Goodman MF (2011) .Structural model for deoxycytidine deaminaton mechanism of the HIV-1 inactivation enzyme APOBEC3G. The Journal of Biological Chemistry 285 (21) : 16195–205. 2. Li X, Ma J, Zhang Q, Yin X, Zhai C, You X, Yu L, Guo F, Zhao L, Li Z, Zeng Y, Cen S (2011) . Functional analysis of the two cytidine deaminase domains in APOBEC3G. Virology 414 (2) : 130–136.

Cytoplasm. Nucleus. Cytoplasm, P-body. Mainly cytoplasmic. Small amount are found in the nucleus. During HIV-1 infection, virion-encapsidated in absence of HIV-1 VIF.