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Abl an ubiquitously expressed and highly conserved proto-oncogenic, non-receptor tyrosine kinase. Shuttles between the nucleus and the cytoplasm, where it localizes to the cytosol, endoplasmic reticulum, and mitochondria. Negatively regulated by its SH3 domain, and deletion of the SH3 domain turns ABL1 into an oncogene. It has been implicated in regulation of cell proliferation, differentiation, apoptosis, cell adhesion and stress response. The Philadephia chromosome translocation t(9;22)(q34;q11) creates a Bcr-Abl fusion protein, responsible for 90% of chronic myelogenous leukemia (CML) and ~25% of acute lymphoblastic leukemia (ALL). Is inhibited by active-site binding small molecules such as imatinib (Gleevec), Dasatinib, Nilotinib, Bosutinib, Ponatinib, and Bafetinib. Compounds such as GNF-2 that bind the myristate-binding pocket of Abl allosterically inhibit Abl kinase activity. Two alternatively-spliced human isoforms have been described: one that is N-terminally myristoylated and the other not due to an alternative splicing of the first exon. Note: This description may include information from UniProtKB.
Protein type: Abl family; EC; Kinase, protein; Oncoprotein; Protein kinase, TK; Protein kinase, tyrosine (non-receptor); TK group
Chromosomal Location of Human Ortholog: 9q34.12
Cellular Component: actin cytoskeleton; cell soma; cytoplasm; cytosol; dendrite; extrinsic to internal side of plasma membrane; nuclear body; nucleolus; nucleoplasm; nucleus; perinuclear region of cytoplasm; protein complex
Molecular Function: actin monomer binding; ATP binding; magnesium ion binding; manganese ion binding; mitogen-activated protein kinase binding; nicotinate-nucleotide adenylyltransferase activity; non-membrane spanning protein tyrosine kinase activity; phosphotyrosine binding; protein binding; protein C-terminus binding; protein kinase activity; protein kinase C binding; protein-tyrosine kinase activity; receptor binding; SH2 domain binding; SH3 domain binding; syntaxin binding
Biological Process: actin cytoskeleton organization and biogenesis; cell cycle arrest; DNA damage induced protein phosphorylation; DNA damage response, signal transduction; DNA damage response, signal transduction resulting in induction of apoptosis; elevation of cytosolic calcium ion concentration; establishment of protein localization; innate immune response; mismatch repair; mitochondrial depolarization; mitotic cell cycle; negative regulation of ubiquitin-protein ligase activity; peptidyl-tyrosine phosphorylation; positive regulation of apoptosis; positive regulation of muscle cell differentiation; positive regulation of oxidoreductase activity; positive regulation of peptidyl-tyrosine phosphorylation; positive regulation of protein amino acid phosphorylation; protein amino acid autophosphorylation; regulation of actin cytoskeleton organization and biogenesis; regulation of autophagy; regulation of axon extension; regulation of cell adhesion; regulation of cell proliferation; regulation of endocytosis; regulation of microtubule polymerization; regulation of transcription, DNA-dependent; response to DNA damage stimulus; response to oxidative stress
Disease: Leukemia, Chronic Myeloid
Reference #:  P00519 (UniProtKB)
Alt. Names/Synonyms: Abelson murine leukemia viral oncogene homolog 1; ABL; ABL1; bcr/abl; bcr/c-abl oncogene protein; c-ABL; c-abl oncogene 1, receptor tyrosine kinase; JTK7; p150; Proto-oncogene c-Abl; proto-oncogene tyrosine-protein kinase ABL1; Tyrosine-protein kinase ABL1; v-abl; v-abl Abelson murine leukemia viral oncogene homolog 1
Gene Symbols: ABL1
Molecular weight: 122,873 Da
Basal Isoelectric point: 8.84  Predict pI for various phosphorylation states
CST Pathways:  ErbB/HER Signaling  |  G1/S Checkpoint  |  G2/M DNA Damage Checkpoint  |  Microtubule Dynamics  |  SAPK/JNK Signaling Cascades  |  TGF-ß Signaling  |  Tyrosine Kinases & Substrates
Protein-Specific Antibodies or siRNAs from Cell Signaling Technology® Total Proteins
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