Product Name: Abl1
Product Number: AB-NK001-3
Size: | 25 µg | | Price: | 89.00 |
| | | $US | |
Target Full Name: Abelson murine leukemia viral oncogene homologue 1
Target Alias: Abelson murine leukemia viral oncogene 1; Abl; C-Abl; JTK7; P150; v-abl Abelson murine leukemia viral oncogene 1; ENSG00000097007; Q13688; Q13914; Q59FK4
Product Type Specific: Protein kinase pan-specific antibody
Antibody Code: NK001-3
Antibody Target Type: Pan-specific
Protein UniProt: P00519 Protein SigNET: P00519 Antibody Type: Polyclonal
Antibody Host Species: Rabbit
Antibody Immunogen Source: Human Abl (Abl1) sequence peptide Cat. No.: PE-01ARQ80
Antibody Immunogen Sequence: CISTRVSLRKTRQPP
Antibody Immunogen Description: Corresponds to amino acid residues I1006 to P1019; In the proline-rich segment in the C-terminal region of the kinase.
Production Method: The immunizing peptide was produced by solid phase synthesis on a multipep peptide synthesizer and purified by reverse-phase hplc chromatography. Purity was assessed by analytical hplc and the amino acid sequence confirmed by mass spectrometry analysis. This peptide was coupled to KLH prior to immunization into rabbits. New Zealand White rabbits were subcutaneously injected with KLH-coupled immunizing peptide every 4 weeks for 4 months. The sera from these animals was applied onto an agarose column to which the immunogen peptide was thio-linked. Antibody was eluted from the column with 0.1 M glycine, pH 2.5. Subsequently, the antibody solution was neutralized to pH 7.0 with saturated Tris.
Antibody Modification: Unconjugated. Contact KInexus if you are interest in having the antibody biotinylated or coupled with fluorescent dyes.
Antibody Concentration: 1 mg/ml
Storage Buffer: Phosphate buffered saline pH 7.4, 0.05% Thimerasol
Storage Conditions: For long term storage, keep frozen at -40°C or lower. Stock solution can be kept at +4°C for more than 3 months. Avoid repeated freeze-thaw cycles.
Product Use: Western blotting | Antibody microarray
Antibody Dilution Recommended: 2 µg/ml for immunoblotting
Antibody Species Reactivity: Human; Mouse; Rat
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.
