R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.
APOBEC3A/B/G (5210-87-13) Rabbit mAb #81001
Filter:
- WB
Supporting Data
| REACTIVITY | H |
| SENSITIVITY | Endogenous |
| MW (kDa) | 35 |
| Source/Isotype | Rabbit |
Application Key:
- WB-Western Blotting
Species Cross-Reactivity Key:
- H-Human
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
| Simple Western™ | 1:10 - 1:50 |
Storage
Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/mL BSA, 50% glycerol, and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody.
Protocol
Specificity / Sensitivity
APOBEC3A/B/G (5210-87-13) Rabbit mAb recognizes endogenous levels of total APOBEC3B protein. This antibody cross-reacts with APOBEC3A and APOBEC3G proteins. Based on the sequence of the peptide antigen, this antibody is not expected to detect APOBEC3C, APOBEC3D, APOBEC3F, or APOBEC3H proteins.
Species Reactivity:
Human
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues near the carboxy terminus of human APOBEC3B protein.
Background
Members of the APOBEC3 subfamily of cytosine deaminases (APOBEC3A, APOBEC3B, APOBEC3C, APOBEC3D, APOBEC3F, APOBEC3G, and APOBEC3H) function in innate immunity by preventing viral DNA replication, including that of human immunodeficiency virus-1 (HIV-1) (1,2). APOBEC3B mutation and aberrant expression in cancer is thought to result in mutation of genomic DNA, and to drive tumorigenesis. APOBEC3B is highly expressed in human breast cancer, glioma, and other human cancers (3-5).
APOBEC3A expression is upregulated in several human cancers, and is a major source of mutation in breast cancer (6). APOBEC3A contributes to chromosomal instability and disease progression in pancreatic cancer (7), and upregulates PD-L1 expression in cancer cells (8).
APOBEC3G suppresses the replication of HIV-1 in T cells (9,10). The HIV-1 virion infectivity factor (Vif) inhibits APOBEC3G activity and targets it for proteasomal ubiquitination degradation (11).
APOBEC3A expression is upregulated in several human cancers, and is a major source of mutation in breast cancer (6). APOBEC3A contributes to chromosomal instability and disease progression in pancreatic cancer (7), and upregulates PD-L1 expression in cancer cells (8).
APOBEC3G suppresses the replication of HIV-1 in T cells (9,10). The HIV-1 virion infectivity factor (Vif) inhibits APOBEC3G activity and targets it for proteasomal ubiquitination degradation (11).
- Olson, M.E. et al. (2018) Cell Chem Biol 25, 36-49.
- Siriwardena, S.U. et al. (2016) Chem Rev 116, 12688-12710.
- Cescon, D.W. and Haibe-Kains, B. (2016) Genome Biol 17, 202.
- Zou, J. et al. (2017) Cell Biosci 7, 29.
- Schmitt, C. et al. (2018) Oncol Rep 40, 2742-2749.
- Cortez, L.M. et al. (2019) PLoS Genet 15, e1008545.
- Wörmann, S.M. et al. (2021) Nat Cancer 2, 1338-1356.
- Zhao, K. et al. (2021) Mol Cancer Res 19, 1571-1582.
- Sheehy, A.M. et al. (2002) Nature 418, 646-50.
- Harris, R.S. et al. (2003) Cell 113, 803-9.
- Sheehy, A.M. et al. (2003) Nat Med 9, 1404-7.
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