{"entity":{"id":"abl1","kind":"target","name":"ABL1","aka":["c-ABL","ABL","JTK7","ABL proto-oncogene 1, non-receptor tyrosine kinase"],"tldr":"ABL1 is the kinase half of the BCR::ABL1 fusion that causes chronic myeloid leukaemia. The CML drugs bind the ABL1 kinase domain, most in its ATP pocket and asciminib in a separate pocket that locks it shut.","summary":"ABL1 (chromosome 9q34.12) is a non-receptor tyrosine kinase in cytoskeletal remodelling, cell motility and adhesion, receptor endocytosis, autophagy, the DNA damage response and apoptosis; it phosphorylates regulators of actin dynamics such as WASF3, ANXA1, cortactin and ENAH and of adhesion such as BCAR1, CRK, CRKL, DOK1 and NEDD9 (UniProt P00519). The t(9;22) translocation fuses it to BCR, producing the constitutively active kinase of CML and Ph-positive ALL (bcr-abl1-signalling pathway). In OnCo the ABL1 kinase domain is what dasatinib (binding active and inactive conformations, inactive against T315I), ponatinib (a type II inhibitor whose triple bond accommodates the T315I gatekeeper) and asciminib (allosteric, locking ABL1 inactive through the myristoyl pocket, active against T315I at higher dose) bind; the BCR::ABL1 target page carries the fusion and the older inhibitors.","asOf":"2026-09-22","links":[{"label":"HGNC HGNC:76","url":"https://www.genenames.org/data/gene-symbol-report/#!/hgnc_id/HGNC:76"},{"label":"UniProt P00519","url":"https://www.uniprot.org/uniprotkb/P00519/entry"},{"label":"NCBI Gene 25","url":"https://www.ncbi.nlm.nih.gov/gene/25"}],"tags":["wave5-target"],"related":["bcr-abl"],"cancers":["cml-chronic-phase","cml-advanced-phase","all-leukemia"],"sections":[],"technologies":["kinase-inhibitors"],"targets":[],"drugs":["asciminib","dasatinib","ponatinib"],"companies":[],"institutions":[],"pathways":["bcr-abl1-signalling","cml-signalling"],"terms":[],"trials":[],"people":[],"bottlenecks":[],"keyPapers":[],"journals":[],"dependsOn":[],"notes":["Prevalence not recorded in this wave: HGNC and UniProt carry no positivity rates and no other source was consulted."],"provenance":{"editedBy":"OnCo content wave 5 (HGNC REST, UniProt REST, corpus drug and pathway records)","editedOn":"2026-09-22"},"symbol":"ABL1","role":[],"sources":[],"specificity":"broadly-expressed","distribution":"one-type","specificityNote":"Broadly expressed or essential: HPA finds the RNA at low tissue specificity; the 3 medicines aimed at it (Asciminib, Dasatinib, Ponatinib) act on the wild-type protein, so normal tissue is exposed and the therapeutic window comes from the tumour's faster division or its dependence on the protein. HPA ABL1: RNA low tissue specificity; high antibody staining in 1 normal tissue; highest cancer staining carcinoid (1 of 4 high). Distribution: 1 cancer family in the corpus carries a prevalence row, label threshold or catalogue link for it (Leukaemia); Open Targets associates it with 7 specific cancer types at or above 0.5 (chronic myeloid leukemia, acute lymphoblastic leukemia, gastrointestinal stromal tumor, colorectal cancer, dermatofibrosarcoma protuberans, myelodysplastic/myeloproliferative disease and more); the corpus evidence decides and the Open Targets list is quoted for comparison. (Rule 7 of scripts/fetch-target-specificity.ts.)","specificitySources":[{"label":"Human Protein Atlas ABL1 tissue","url":"https://www.proteinatlas.org/ENSG00000097007-ABL1/tissue","note":"RNA tissue and blood lineage specificity, normal tissue antibody staining (version 25.1, CC BY-SA 3.0)"},{"label":"Open Targets ENSG00000097007 associations","url":"https://platform.opentargets.org/target/ENSG00000097007/associations","note":"cancer associations at or above 0.5 (CC0)"}],"hgnc":"HGNC:76","ensembl":"ENSG00000097007","uniprot":"P00519","entrez":"25","firstDescribed":1983,"firstDescribedBasis":"sequence","firstDescribedNote":"Earliest sequence paper UniProt cites for the protein: Groffen et al, Nature, 1983, \"Homology between phosphotyrosine acceptor site of human c-abl and viral oncogene products\".","firstDescribedSource":"https://pubmed.ncbi.nlm.nih.gov/6191223/","biology":"Asciminib's myristoyl-pocket mechanism is distinct from every ATP-site inhibitor, which is why it was approved for all newly diagnosed chronic-phase CML in 2024 and is being tested in Ph-positive ALL; dasatinib with blinatumomab can bring Ph-positive ALL into deep remission without chemotherapy (corpus drug records).","whereFound":["Chronic myeloid leukaemia (BCR::ABL1)","Philadelphia-positive acute lymphoblastic leukaemia"],"targetClass":"kinase","prevalence":[]},"route":"/targets/abl1/","neighbours":{"target":[{"id":"bcr-abl","kind":"target","name":"BCR::ABL1 (Philadelphia chromosome)","route":"/targets/bcr-abl/"}],"cancer":[{"id":"all-leukemia","kind":"cancer","name":"Acute lymphoblastic leukaemia","route":"/cancers/all-leukemia/"},{"id":"cml-advanced-phase","kind":"cancer","name":"Chronic myeloid leukaemia, accelerated and blast phase","route":"/cancers/cml-advanced-phase/"},{"id":"cml-chronic-phase","kind":"cancer","name":"Chronic myeloid leukaemia, chronic phase","route":"/cancers/cml-chronic-phase/"}],"technology":[{"id":"kinase-inhibitors","kind":"technology","name":"Small-molecule kinase inhibitors","route":"/technologies/kinase-inhibitors/"}],"drug":[{"id":"asciminib","kind":"drug","name":"Asciminib","route":"/drugs/asciminib/"},{"id":"dasatinib","kind":"drug","name":"Dasatinib","route":"/drugs/dasatinib/"},{"id":"ponatinib","kind":"drug","name":"Ponatinib","route":"/drugs/ponatinib/"}],"pathway":[{"id":"bcr-abl1-signalling","kind":"pathway","name":"BCR::ABL1 (Philadelphia chromosome)","route":"/pathways/bcr-abl1-signalling/"},{"id":"cml-signalling","kind":"pathway","name":"Chronic myeloid leukaemia (KEGG map)","route":"/pathways/cml-signalling/"}]}}