APOBEC3G (CEM15) Blocking Peptide | APOBEC3G blocking peptide

APOBEC3G (CEM15) Antibody (Center E133) Blocking peptide

• Gene Names: APOBEC3G; A3G; ARCD; ARP9; ARP-9; CEM15; CEM-15; MDS019; bK150C2.7; dJ494G10.1
• Synonyms: APOBEC3G (CEM15); APOBEC3G (CEM15) Antibody (Center E133) Blocking peptide; DNA dC->dU-editing enzyme APOBEC-3G; 354-; APOBEC-related cytidine deaminase; APOBEC-related protein; ARCD; APOBEC-related protein 9; ARP-9; CEM-15; CEM15; Deoxycytidine deaminase; A3G; APOBEC3G; APOBEC3G blocking peptide

• Specificity: The synthetic peptide sequence used to generate the antibody was selected from the Center region of human CEM15. A 10 to 100 fold molar excess to antibody is recommended. Precise conditions should be optimized for a particular assay.
• Form/Format: The synthetic peptide was lyophilized with 100% acetonitrile and is supplied as a powder. Reconstitute with 0.1 ml deionized water for a final concentration of 1 mg/ml.
• Sequence Length: 384

• 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.
• Preparation and Storage: Maintain refrigerated at 2-8 degree C for up to 6 months. For long term storage store at -20 degree C.

Related Product Information for APOBEC3G blocking peptide

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.

NCBI and Uniprot Product Information

• NCBI GI #: 44887683
• NCBI GeneID: 60489
• UniProt Accession #: Q9HC16; Q45F02; Q5TF77; Q7Z2N1; Q7Z2N4; Q9H9H8; B2RDR9
• Molecular Weight: 9,386 Da
• NCBI Official Full Name: DNA dC->
• NCBI Official Synonym Full Names: apolipoprotein B mRNA editing enzyme catalytic subunit 3G
• NCBI Official Symbol: APOBEC3G
• NCBI Official Synonym Symbols: A3G; ARCD; ARP9; ARP-9; CEM15; CEM-15; MDS019; bK150C2.7; dJ494G10.1
• NCBI Protein Information: DNA dC->dU-editing enzyme APOBEC-3G
• UniProt Protein Name: DNA dC->dU-editing enzyme APOBEC-3G
• Protein Family: DNA dC->dU-editing enzyme
• UniProt Gene Name: APOBEC3G
• UniProt Synonym Gene Names: APOBEC-related protein; ARCD; ARP-9; CEM15; A3G
• UniProt Entry Name: ABC3G_HUMAN

NCBI Description

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. [provided by RefSeq, Jul 2008]

Uniprot Description

APOBEC3G: 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. May also prevent the transposition of a subset of retroelements. Binds a variety of RNAs, but does not display detectable APOB, NF1 and NAT1 mRNA editing. Belongs to the cytidine and deoxycytidylate deaminase family. 2 isoforms of the human protein are produced by alternative splicing.

Protein type: RNA-binding; RNA processing; EC 3.5.4.-; Hydrolase

Chromosomal Location of Human Ortholog: 22q13.1-q13.2

Cellular Component: apolipoprotein B mRNA editing enzyme complex; cytoplasm; cytosol; ribonucleoprotein complex

Molecular Function: cytidine deaminase activity; dCTP deaminase activity; deoxycytidine deaminase activity; protein binding; RNA binding; zinc ion binding

Biological Process: base conversion or substitution editing; cytidine deamination; defense response to virus; innate immune response; negative regulation of retroviral genome replication; negative regulation of viral genome replication; negative regulation of viral reproduction; positive regulation of defense response to virus by host