You are viewing an incomplete version of our website. Please click to reload the website as full version.

C-Abl Oncogene 1, Non-Receptor tyrosine Kinase (ABL1) (pTyr204) Peptide

Details for Product No. ABIN694198, Supplier: Log in to see
Protein Name
  • Abl
  • ABL
  • ABL1
  • ABLL
  • AI325092
  • bcr/abl
  • c-Abl
  • c-ABL
  • CABL
  • cb272
  • E430008G22Rik
  • JTK7
  • MTP
  • p150
  • v-abl
Protein Region
Peptide Type
Blocking Peptide (BP)
Log in to see
Supplier Product No.
Log in to see

Showcase your results, aid the scientific community, and receive a full refund.

Contribute a validation

Learn more

Specificity The synthetic peptide sequence used to generate the antibody AP3481a was selected from the region of human Phospho-ABL-Y204. A 10 to 100 fold molar excess to antibody is recommended. Precise conditions should be optimized for a particular assay.
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.
Restrictions For Research Use only
Storage 4
Storage Comment Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles
Expiry Date 6 months
Background publications 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).

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 ..." in: Genes, chromosomes & cancer, Vol. 43, Issue 1, pp. 37-44, 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).

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).

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).