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CEM15 / APOBEC3G Antibody (C-Terminus)
Goat Polyclonal Antibody
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| WB, IHC-P, E |
|---|---|
| Primary Accession | Q9HC16 |
| Reactivity | Human |
| Host | Goat |
| Clonality | Polyclonal |
| Calculated MW | 46kDa |
| Dilution | ELISA (1:16000), IHC-P (2.5 µg/ml), WB (0.5-1.5 µg/ml) |
| Gene ID | 60489 |
|---|---|
| Other Names | 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 |
| Target/Specificity | Human APOBEC3G. |
| Reconstitution & Storage | Store at -20°C. Minimize freezing and thawing. |
| Precautions | CEM15 / APOBEC3G Antibody (C-Terminus) is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | APOBEC3G |
|---|---|
| Function | 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. |
| Cellular Location | Cytoplasm. Nucleus. Cytoplasm, P-body. Note=Mainly cytoplasmic. Small amount are found in the nucleus. During HIV-1 infection, virion-encapsidated in absence of HIV-1 Vif |
| 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. |
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Provided below are standard protocols that you may find useful for product applications.
Background
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.
References
Kao S.,et al.J. Virol. 77:11398-11407(2003).
Ota T.,et al.Nat. Genet. 36:40-45(2004).
Huang C.,et al.Submitted (SEP-1999) to the EMBL/GenBank/DDBJ databases.
Collins J.E.,et al.Genome Biol. 5:R84.1-R84.11(2004).
Dunham I.,et al.Nature 402:489-495(1999).
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