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APOBEC3G Antibody
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Application 
| WB, E, IHC-P |
|---|---|
| Primary Accession | Q9HC16 |
| Other Accession | NP_068594, 13399304 |
| Reactivity | Human |
| Host | Rabbit |
| Clonality | Polyclonal |
| Isotype | IgG |
| Calculated MW | 46408 Da |
| Concentration (mg/ml) | 1 mg/mL |
| Conjugate | Unconjugated |
| Application Notes | APOBEC3G antibody can be used for detection of APOBEC3G by Western blot at 5 µg/mL. Antibody can also be used for immunohistochemistry starting at 1 µg/mL. |
| Gene ID | 60489 |
|---|---|
| Other Names | APOBEC3G Antibody: A3G, ARCD, ARP9, ARP-9, CEM15, CEM-15, MDS019, bK150C2.7, dJ494G10.1APOBEC-related cytidine deaminase, APOBEC-related protein, apolipoprotein B mRNA editing enzyme, catalytic polypeptide-like 3G |
| Target/Specificity | APOBEC3G; APOBEC3G antibody will also detect the APOBEC3F isoform. |
| Reconstitution & Storage | APOBEC3G antibody can be stored at 4℃ for three months and -20℃, stable for up to one year. As with all antibodies care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures. |
| Precautions | APOBEC3G Antibody is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | APOBEC3G {ECO:0000303|PubMed:14557625, ECO:0000312|HGNC:HGNC:17357} |
|---|---|
| Function | DNA deaminase (cytidine deaminase) which acts as an inhibitor of retrovirus replication and retrotransposon mobility via deaminase- dependent and -independent mechanisms (PubMed:12808465, PubMed:16527742, PubMed:17121840, PubMed:18288108, PubMed:18849968, PubMed:19153609, PubMed:21123384, PubMed:22791714, PubMed:25542899). Exhibits potent antiviral activity against Vif-deficient HIV-1 (PubMed:12167863, PubMed:12859895, PubMed:14557625, PubMed:20219927, PubMed:21835787, PubMed:22807680, PubMed:22915799, PubMed:23097438, PubMed:23152537, PubMed:31397674). 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 (PubMed:12808465, PubMed:12808466, PubMed:12809610, PubMed:12970355, PubMed:14528300, PubMed:22807680). 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 (PubMed:12808465, PubMed:12808466, PubMed:12809610, PubMed:12970355, PubMed:14528300). Selectively targets single-stranded DNA and does not deaminate double-stranded DNA or single- or double-stranded RNA (PubMed:12808465, PubMed:12809610, PubMed:12970355, PubMed:14528300). 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) (PubMed:15031497, PubMed:16378963, PubMed:18448976, PubMed:19458006, PubMed:20335265). May inhibit the mobility of LTR and non-LTR retrotransposons (PubMed:16527742). |
| Cellular Location | Cytoplasm. Nucleus Cytoplasm, P-body. Note=Mainly cytoplasmic (PubMed:16527742, PubMed:16699599, PubMed:21835787). Small amount are found in the nucleus (PubMed:18667511). During HIV-1 infection, virion-encapsidated in absence of HIV-1 Vif (PubMed:12859895) |
| Tissue Location | 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. |
For Research Use Only. Not For Use In Diagnostic Procedures.
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
APOBEC3G Antibody: The Apoliprotein B mRNA-editing, enzyme-catalytic, polypeptide-like (APOBEC) 3 is a multi-isoform member of the cytidine deaminase family of enzymes that act on monomeric nucleoside and nucleotide substrates. Similar to TRIM5α which targets incoming retroviral capsids, APOBEC3 plays a major role in cellular defense against retroviral infection as at least two isoforms, APOBEC3G and to a lesser extent APOBEC3F, can be incorporated HIV-1 virions and induce hypermutation in the newly synthesized viral DNA and thus destabilize the viral genome. This innate mechanism of retroviral resistance is counteracted by the HIV-1 Vif protein by inducing the ubiquitization and degradation of APOBEC3G; a single amino acid substitution (D128K) blocks APOBEC3G depletion without affecting its inhibitory activity.
REFERENCES
Jarmuz A, Chester A, Bayliss J, et al. An anthropoid-specific locus of Orphan C to U RNA-editing enzymes on chromosome 22. Genomics 2002; 79:285-96.
Stremlau M, Owens CM, Perron MJ, et al. The cytoplasmic body component TRIM5a restricts HIV-1 infection in Old World monkeys. Nature 2004; 427:848-53.
Bieniasz PD. Intrinsic immunity: a front-line defense against viral attack. Nat Immunol. 2004; 5:1109-15.
Sheehy AM, Gaddis NC, Choi JD, et al. Isolation of a human gene that inhibits HIV-1 infection and is suppressed by the viral Vif protein. Nature 2002; 418:646-50.
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