C-Abl Oncogene 1, Non-Receptor tyrosine Kinase (ABL1) (pTyr272) antibody

Antigen: C-Abl Oncogene 1, Non-Receptor tyrosine Kinase (ABL1)

Synonyms: ABL, JTK7, p150, c-ABL, v-abl, bcr/abl, Abl, c-Abl, AI325092, MGC117749, E430008G22Rik, ABL1, ARG, ABLL, FLJ22224, FLJ31718, FLJ41441, Arg, Abll, AA536808, MGC169395, ABL2, CABL, cb272

Binding Site: pTyr272

Clonality: Polyclonal

Host: Rabbit

Reactivity: Human

Conjugate: Un-conjugated

Application: Immunohistochemistry (IHC), Dot Blot (Dot), ELISA

Certificates: ISO 9001:2008

Catalog no.: ABIN389504

Additional Information

Alternative name: ABL1

Gene ID: 25

UniProt: P00519

Immunogen: This Phospho-ABL1-Y272 antibody is generated from rabbits immunized with a KLH conjugated synthetic phosphopeptide corresponding to amino acid residues surrounding Y272 of human ABL1.

Isotype: Ig

Description: Other names: Proto-oncogene tyrosine-protein kinase ABL1, p150, c-ABL, Abelson murine leukemia viral oncogene homolog 1, ABL1, ABL, JTK7,

Characteristics: Peptide Affinity Purified Rabbit Polyclonal Antibody (Pab)

Specificity: This Phospho-ABL1-Y272 antibody is generated from rabbits immunized with a KLH conjugated synthetic phosphopeptide corresponding to amino acid residues surrounding Y272 of human ABL1.

Molecular Weight: 122873 DA

Comments:

Background: ABL1 is a cytoplasmic and nuclear protein tyrosine kinase that has been implicated in processes of cell differentiation, cell division, cell adhesion, and stress response. Activity of c-Abl protein is negatively regulated by its SH3 domain, and deletion of the SH3 domain turns ABL1 into an oncogene. The t(9,22) translocation results in the head-to-tail fusion of the BCR and ABL1 genes present in many cases of chronic myelogeneous leukemia. The DNA-binding activity of the ubiquitously expressed ABL1 tyrosine kinase is regulated by CDC2-mediated phosphorylation, suggesting a cell cycle function for ABL1.

Application Details

Application Notes: The suggested dilution is: ELISA~~1:1,000 Immunohistochemistry~~1:50~100 Dot Blot 1:500

Concentration: 0.25 mg/ml

Purification: Purified

Buffer: Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is first purified by protein G affinity chromatography. Then, the antibody fraction is peptide affinity purified in a 2-step procedure with control and phosphorylate

Storage: Maintain refrigerated at 2-8 deg C for up to 6 months. For long term storage store at -20 deg C in small aliquots to prevent freeze-thaw cycles

Research Area: Apoptosis/Necrosis, Phospho-specific antibodies, Cell Signaling, Protein Modifications, Cancer, Cell Cycle, Cell Structure

Restrictions: For Research Use only

Images

Dot blot analysis of anti-Phospho-ABL1-Y272 Antibody (ABIN389504) on nitrocellulose membrane. 50ng of Phospho-peptide or Non Phospho-peptide per dot were adsorbed. Antobodies working concentration was 0.5ug per ml.

Formalin-fixed and paraffin-embedded human cancer tissue reacted with the primary antibody, which was peroxidase-conjugated to the secondary antibody, followed by AEC staining. This data demonstrates the use of this antibody for immunohistochemistry. clinical relevance has not been evaluated. BC = breast carcinoma. HC = hepatocarcinoma.

Publications

Product: Aichberger, Mayerhofer, Krauth et al.: "Identification of mcl-1 as a BCR/ABL-dependent target in chronic myeloid leukemia (CML): evidence for cooperative antileukemic effects of imatinib and mcl-1 antisense oligonucleotides." in: Blood, Vol. 105, Issue 8, pp. 3303-11, 2005 (PubMed).

Wei, Li, Liu: "Insights into selective activation of p53 DNA binding by c-Abl." in: The Journal of biological chemistry, Vol. 280, Issue 13, pp. 12271-8, 2005 (PubMed).

Robinson, Martineau, Harris et al.: "Derivative chromosome 9 deletions are a significant feature of childhood Philadelphia chromosome positive acute lymphoblastic leukaemia." in: Leukemia : official journal of the Leukemia Society of America, Leukemia Research Fund, U.K, Vol. 19, Issue 4, pp. 564-71, 2005 (PubMed).

Kim, Cho, Yoon et al.: "Interpretation of submicroscopic deletions of the BCR or ABL gene should not depend on extra signal-FISH: problems in interpretation of submicroscopic deletion of the BCR or ABL gene with extra signal-FISH." in: Genes, chromosomes & cancer, Vol. 43, Issue 1, pp. 37-44, 2005 (PubMed).

Barnes, McIntosh, Whetton et al.: "Chronic myeloid leukaemia: an investigation into the role of Bcr-Abl-induced abnormalities in glucose transport regulation." in: Oncogene, Vol. 24, Issue 20, pp. 3257-67, 2005 (PubMed).