ADAR1 (E6X9R) XP® Rabbit mAb #81284
- WB
- IP
- IHC
- IF
- F
Supporting Data
| REACTIVITY | H Mk |
| SENSITIVITY | Endogenous |
| MW (kDa) | 110, 150 |
| Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
- IP-Immunoprecipitation
- IHC-Immunohistochemistry
- IF-Immunofluorescence
- F-Flow Cytometry
Species Cross-Reactivity Key:
- H-Human
- Mk-Monkey
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
| Immunoprecipitation | 1:50 |
| Immunohistochemistry (Paraffin) | 1:100 - 1:400 |
| Immunofluorescence (Immunocytochemistry) | 1:800 - 1:1600 |
| Flow Cytometry (Fixed/Permeabilized) | 1:100 - 1:400 |
Storage
For a carrier free (BSA and azide free) version of this product see product #95404.
Protocol
Specificity / Sensitivity
ADAR1 (E6X9R) XP® Rabbit mAb recognizes endogenous levels of total ADAR1 protein.
Species Reactivity:
Human, Monkey
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Leu419 of human ADAR1 protein.
Background
Post-transcriptional processing of RNAs, such as RNA editing, is an important mechanism by which diversity in RNA and protein is achieved that is not otherwise encoded by the genome (1,2). The most common form of RNA editing is the conversion of adenosine (A) into inosine (I) on double-stranded RNA by the adenosine deaminase acting on RNA (ADAR) family of proteins (1-3). Since inosine base pairs with cytidine, it is interpreted as a guanosine by the splicing and translational machinery, leading to alteration in the protein sequence, as well as generation of splicing isoforms (1,4-6). A-to-I editing can also influence RNA sequence recognition by RNA-binding proteins and non-coding RNA, such as miRNAs, affecting subsequent RNA processing, stability, and protein expression levels (2).
ADAR1 is ubiquitously expressed with two known isoforms, ADAR1L (p150) and ADAR1S (p110), resulting from transcription using alternative promoters and start codons. ADAR1S is constitutively expressed in the nucleus, while ADAR1L is interferon-inducible and present in both the nucleus and the cytoplasm. The induction of ADAR1L in response to cellular stress and viral infection suggests a role for RNA editing in the innate immune response (1,7). In addition, ADAR1 is essential in mammalian development, particularly in hematopoiesis and suppression of interferon signaling to protect hematopoietic stem cells from destruction in fetal liver and adult bone marrow (8,9).
- Zinshteyn, B. and Nishikura, K. (2009) Wiley Interdiscip Rev Syst Biol Med 1, 202-9.
- Nishikura, K. (2006) Nat Rev Mol Cell Biol 7, 919-31.
- Bass, B.L. (2002) Annu Rev Biochem 71, 817-46.
- Reenan, R.A. (2001) Trends Genet 17, 53-6.
- Maas, S. et al. (2006) RNA Biol 3, 1-9.
- Rueter, S.M. et al. (1999) Nature 399, 75-80.
- Patterson, J.B. and Samuel, C.E. (1995) Mol Cell Biol 15, 5376-88.
- Iizasa, H. and Nishikura, K. (2009) Nat Immunol 10, 16-8.
- Hartner, J.C. et al. (2009) Nat Immunol 10, 109-15.
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