Product Name:

Abl1-pY139


Product Number:

ab-pk505

Price:

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$89.00
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$89.00

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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 phosphosite-specific antibody

Antibody Code: PK504

Antibody Target Type: Phosphosite-specific

Antibody Phosphosite: Y139

Protein UniProt: P00519

Protein SigNET: P00519

Antibody Type: Polyclonal

Antibody Host Species: Rabbit

Antibody Immunogen Source: Human Abl (Abl1) sequence peptide Cat. No.: PE-04AGC99

Antibody Immunogen Sequence: AAE(pY)LLS(bA)C

Antibody Immunogen Description: Corresponds to amino acid residues A136 to S142; In the SH2 domain.

Production Method: Corresponds to amino acid residues A136 to S142; In the SH2 domain.

Antibody Modification: Protein kinase phosphosite-specific antibody

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 Potency: Medium immunoreactivity of a target-sized protein by Western blotting in serum-starved A431 cells treated with for 10 minutes with 10% fetal calf serum.

Antibody Species Reactivity: Human

Antibody Positive Control: The observed molecular mass of the processed target protein on SDS-PAGE gels is reported to be around 140-142 kDa.

Antibody Specificity: High

Antibody Cross Reactivity: Prominent 75 and 80 kDa cross-reactive proteins are detected in FBS-treated A431 cells and forskolin-treated HEK-293 cells.

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.