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Western blotAntibody data
- Antibody Data
- Antigen structure
- References [4]
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- Product number
- ABIN317534 - Provider product page
- Provider
- antibodies-online
- Product name
- anti-Activation-Induced Cytidine Deaminase (AICDA) (AA 1-54), (N-Term) antibody
- Antibody type
- Monoclonal
- Antigen
- Recombinant human AID (1-54 aa) purified from E. coli
- Description
- Protein-G affinity chromatography
- Reactivity
- Human
- Host
- Mouse
- Epitope
- AA 1-54,N-Term
- Isotype
- IgG
- Antibody clone number
- 2D3
- Vial size
- 0.1 mL
- Concentration
- 1.0 mg/mL
- Storage
- Store the antibody undiluted at 2-8°C for one month or (in aliquots) at -20°C for longer. Avoid repeated freezing and thawing.Shelf life: one year from despatch.
Submitted references AID associates with single-stranded DNA with high affinity and a long complex half-life in a sequence-independent manner.
Activation-induced cytidine deaminase (AID) promotes B cell lymphomagenesis in Emu-cmyc transgenic mice.
The AID enzyme induces class switch recombination in fibroblasts.
Activation-induced cytidine deaminase (AID) deficiency causes the autosomal recessive form of the Hyper-IgM syndrome (HIGM2).
Larijani M, Petrov AP, Kolenchenko O, Berru M, Krylov SN, Martin A
Molecular and cellular biology 2007 Jan;27(1):20-30
Molecular and cellular biology 2007 Jan;27(1):20-30
Activation-induced cytidine deaminase (AID) promotes B cell lymphomagenesis in Emu-cmyc transgenic mice.
Kotani A, Kakazu N, Tsuruyama T, Okazaki IM, Muramatsu M, Kinoshita K, Nagaoka H, Yabe D, Honjo T
Proceedings of the National Academy of Sciences of the United States of America 2007 Jan 30;104(5):1616-20
Proceedings of the National Academy of Sciences of the United States of America 2007 Jan 30;104(5):1616-20
The AID enzyme induces class switch recombination in fibroblasts.
Okazaki IM, Kinoshita K, Muramatsu M, Yoshikawa K, Honjo T
Nature 2002 Mar 21;416(6878):340-5
Nature 2002 Mar 21;416(6878):340-5
Activation-induced cytidine deaminase (AID) deficiency causes the autosomal recessive form of the Hyper-IgM syndrome (HIGM2).
Revy P, Muto T, Levy Y, Geissmann F, Plebani A, Sanal O, Catalan N, Forveille M, Dufourcq-Labelouse R, Gennery A, Tezcan I, Ersoy F, Kayserili H, Ugazio AG, Brousse N, Muramatsu M, Notarangelo LD, Kinoshita K, Honjo T, Fischer A, Durandy A
Cell 2000 Sep 1;102(5):565-75
Cell 2000 Sep 1;102(5):565-75
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