Product Name: Abl1 (252-258)
Product Number: PE-01ACN01
Size: 200 µg      Price:7.00
1 mg      $US13.00
5 mg      36.00
Peptide Name: Abl1 (252-258)

Product Use: The peptide sequence is located in the protein kinase catalytic domain in and after subdomain I.

Peptide Production Method: Solid-phase peptide synthesis

Peptide Origin: Homo sapiens

Peptide Sequence: QYGEVYE

Peptide Modifications N Terminus: Free amino

Peptide Modifications C Terminus: βAla-Cys

Peptide Molecular Mass Calculated: 1061.09 Da

Peptide Purity Percent after Synthesis and Purification: >50

Peptide Appearance: White powder

Peptide Form: Solid

Storage Conditions: -20°C

Scientific Background: Abl1 is a protein-tyrosine kinase of the TK group and Abl family. This kinase is highly expressed and widely distributed in most tested human tissues and found in the cytoplasm and nucleus of cells. It has been implicated in the control of a wide range of cellular processes, including cell differentiation cell division cell adhesion and stress responses. Abl1 is activated by autophosphorylation as well as by Src-family kinase-mediated phosphorylation. The normal active form of Abl1 is nuclear, and it is sequestered into the cytoplasm by interaction with 14-3-3 through T735 phosphorylation. It localizes to the mitochondria under conditions of oxidative stress. It is a known oncoprotein (OP), although the wild-type form of Abl1 may function as a tumour-suppressor protein (TSP). The DNA-binding activity of Abl1 is regulated by CDK1-mediated phosphorylation. Some cancer-related mutations in human tumours point to a gain of function of the protein kinase. However, the most common mutations (T315 is near kinase Subdomain III; G250 and E255 are located around the ATP-binding kinase Subdomain I) are clustered within the kinase catalytic domain. It is likely that these common mutations may actually inactive Abl1's catalytic activity and reduce its tumour suppressing activity. The active form of the kinase normally acts to inhibit cell proliferation. Translocation t(9;22)(q34;q11) result in chimeric proteins from BCR and Abl1, and this is a cause of chronic myeloid leukemia (CML). BCR-Abl fusion protein results in constitutively active phosphotransferase activity by inhibiting 3BP1/Abl interaction. BCR-Abl1 is found in the cytoplasm and nucleus. BCR-Abl1 induces the Ras, PI3K, and Myc cell proliferation pathways. The abnormal phosphorylation of cytoplasmic proteins and receptors in the plasma membrane may result in a gain of function of Abl1 to stimulate cell proliferation. Abl1 is also activated by RIN1 binding to the SH2 and SH3 domains in Abl1, which normally stabilize it in its inactive form. Deletion of the SH3 domain of Abl turns its into an oncogene. Insertional mutagenesis studies in mice also support a role for this protein kinase in mouse cancer oncogenesis.