HCSGD entry for ABL1
1. General information
| Official gene symbol | ABL1 |
|---|---|
| Entrez ID | 25 |
| Gene full name | c-abl oncogene 1, non-receptor tyrosine kinase |
| Other gene symbols | ABL JTK7 bcr/abl c-ABL p150 v-abl |
| Links to Entrez Gene | Links to Entrez Gene |
2. Neighbors in the network
3. Gene ontology annotation
GO ID | GO term | Evidence | Category |
|---|---|---|---|
| GO:0000287 | Magnesium ion binding | IDA | molecular_function |
| GO:0003677 | DNA binding | NAS | molecular_function |
| GO:0003785 | Actin monomer binding | TAS | molecular_function |
| GO:0004515 | Nicotinate-nucleotide adenylyltransferase activity | TAS | molecular_function |
| GO:0004713 | Protein tyrosine kinase activity | IDA | molecular_function |
| GO:0004715 | Non-membrane spanning protein tyrosine kinase activity | IDA | molecular_function |
| GO:0005515 | Protein binding | IPI | molecular_function |
| GO:0005524 | ATP binding | IDA | molecular_function |
| GO:0005634 | Nucleus | IDA NAS TAS | cellular_component |
| GO:0005730 | Nucleolus | IDA | cellular_component |
| GO:0005737 | Cytoplasm | TAS | cellular_component |
| GO:0005739 | Mitochondrion | IEA | cellular_component |
| GO:0005829 | Cytosol | TAS | cellular_component |
| GO:0006298 | Mismatch repair | TAS | biological_process |
| GO:0006355 | Regulation of transcription, DNA-templated | TAS | biological_process |
| GO:0006464 | Cellular protein modification process | NAS | biological_process |
| GO:0006914 | Autophagy | IEA | biological_process |
| GO:0006974 | Cellular response to DNA damage stimulus | IDA | biological_process |
| GO:0006975 | DNA damage induced protein phosphorylation | IDA | biological_process |
| GO:0007155 | Cell adhesion | IEA | biological_process |
| GO:0007411 | Axon guidance | TAS | biological_process |
| GO:0007596 | Blood coagulation | TAS | biological_process |
| GO:0008022 | Protein C-terminus binding | IPI | molecular_function |
| GO:0008630 | Intrinsic apoptotic signaling pathway in response to DNA damage | TAS | biological_process |
| GO:0010506 | Regulation of autophagy | TAS | biological_process |
| GO:0015629 | Actin cytoskeleton | TAS | cellular_component |
| GO:0017124 | SH3 domain binding | IPI | molecular_function |
| GO:0018108 | Peptidyl-tyrosine phosphorylation | IDA | biological_process |
| GO:0019905 | Syntaxin binding | IPI | molecular_function |
| GO:0030036 | Actin cytoskeleton organization | ISS | biological_process |
| GO:0030100 | Regulation of endocytosis | TAS | biological_process |
| GO:0030145 | Manganese ion binding | IDA | molecular_function |
| GO:0030155 | Regulation of cell adhesion | TAS | biological_process |
| GO:0031252 | Cell leading edge | IEA | cellular_component |
| GO:0031965 | Nuclear membrane | IEA | cellular_component |
| GO:0038096 | Fc-gamma receptor signaling pathway involved in phagocytosis | TAS | biological_process |
| GO:0042692 | Muscle cell differentiation | TAS | biological_process |
| GO:0042770 | Signal transduction in response to DNA damage | IDA | biological_process |
| GO:0043065 | Positive regulation of apoptotic process | IDA | biological_process |
| GO:0045087 | Innate immune response | TAS | biological_process |
| GO:0048008 | Platelet-derived growth factor receptor signaling pathway | IEA | biological_process |
| GO:0048471 | Perinuclear region of cytoplasm | IDA | cellular_component |
| GO:0050731 | Positive regulation of peptidyl-tyrosine phosphorylation | IDA | biological_process |
| GO:0051019 | Mitogen-activated protein kinase binding | IPI | molecular_function |
| GO:0051149 | Positive regulation of muscle cell differentiation | TAS | biological_process |
| GO:0051353 | Positive regulation of oxidoreductase activity | IDA | biological_process |
| GO:0051726 | Regulation of cell cycle | IEA | biological_process |
| GO:0070064 | Proline-rich region binding | IDA IPI | molecular_function |
| GO:0071901 | Negative regulation of protein serine/threonine kinase activity | IDA | biological_process |
| GO:2000145 | Regulation of cell motility | TAS | biological_process |
| GO:2000249 | Regulation of actin cytoskeleton reorganization | TAS | biological_process |
| GO:2001020 | Regulation of response to DNA damage stimulus | IDA | biological_process |
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4. Expression levels in datasets
- Meta-analysis result
| p-value up | p-value down | FDR up | FDR down |
|---|---|---|---|
| 0.2178772729 | 0.2450956233 | 0.8976381437 | 0.9533267179 |
- Individual experiment result
( "-" represent NA in the specific microarray platform )
( "-" represent NA in the specific microarray platform )
| Data source | Up or down | Log fold change |
|---|---|---|
| GSE11954 | Down | -0.4591365144 |
| GSE13712_SHEAR | Up | 0.2282706191 |
| GSE13712_STATIC | Up | 0.1897875317 |
| GSE19018 | Up | 0.0328650243 |
| GSE19899_A1 | Down | -0.1460742331 |
| GSE19899_A2 | Down | -0.3416203763 |
| PubMed_21979375_A1 | Up | 0.6214977370 |
| PubMed_21979375_A2 | Up | 0.8608020318 |
| GSE35957 | Down | -0.5173469201 |
| GSE36640 | Down | -0.3134166179 |
| GSE54402 | Down | -0.0217751997 |
| GSE9593 | Down | -0.2770825642 |
| GSE43922 | Down | -0.0316884320 |
| GSE24585 | Up | 0.0909966517 |
| GSE37065 | Down | -0.0141549779 |
| GSE28863_A1 | Up | 0.9032889780 |
| GSE28863_A2 | Up | 0.6813771624 |
| GSE28863_A3 | Down | -0.0042141376 |
| GSE28863_A4 | Down | -0.1164468565 |
| GSE48662 | Down | -0.0239232242 |
5. Regulation relationships with compounds/drugs/microRNAs
- Compounds
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- Drugs
Name | Drug | Accession number |
|---|---|---|
| Adenosine triphosphate | DB00171 | NUTR00017 | EXPT00007 |
| Imatinib | DB00619 | APRD01028 | EXPT02967 | DB03261 |
| Dasatinib | DB01254 | - |
| N-[4-Methyl-3-[[4-(3-Pyridinyl)-2-Pyrimidinyl]Amino]Phenyl]-3-Pyridinecarboxamide | DB03878 | EXPT02657 |
| Nilotinib | DB04868 | - |
| XL228 | DB05184 | - |
| Bosutinib | DB06616 | - |
| 2-{[(6-OXO-1,6-DIHYDROPYRIDIN-3-YL)METHYL]AMINO}-N-[4-PROPYL-3-(TRIFLUOROMETHYL)PHENYL]BENZAMIDE | DB07831 | - |
| 1-[4-(PYRIDIN-4-YLOXY)PHENYL]-3-[3-(TRIFLUOROMETHYL)PHENYL]UREA | DB08043 | - |
| MYRISTIC ACID | DB08231 | - |
| 6-(2,6-DICHLOROPHENYL)-2-{[3-(HYDROXYMETHYL)PHENYL]AMINO}-8-METHYLPYRIDO[2,3-D]PYRIMIDIN-7(8H)-ONE | DB08339 | - |
| 5-[3-(2-METHOXYPHENYL)-1H-PYRROLO[2,3-B]PYRIDIN-5-YL]-N,N-DIMETHYLPYRIDINE-3-CARBOXAMIDE | DB08350 | - |
| 2-amino-5-[3-(1-ethyl-1H-pyrazol-5-yl)-1H-pyrrolo[2,3-b]pyridin-5-yl]-N,N-dimethylbenzamide | DB08583 | - |
| Regorafenib | DB08896 | - |
| Ponatinib | DB08901 | - |
- MicroRNAs
- mirTarBase
MiRNA_name | mirBase ID | miRTarBase ID | Experiment | Support type | References (Pubmed ID) |
|---|---|---|---|---|---|
| hsa-miR-203a | MIMAT0000264 | MIRT003032 | Luciferase reporter assay | Functional MTI | 18538733 |
| hsa-miR-29a-3p | MIMAT0000086 | MIRT007197 | Luciferase reporter assay | Functional MTI | 23428668 |
| hsa-miR-30a-5p | MIMAT0000087 | MIRT007359 | Luciferase reporter assay//qRT-PCR | Functional MTI | 23287430 |
| hsa-miR-484 | MIMAT0002174 | MIRT042250 | CLASH | Functional MTI (Weak) | 23622248 |
| hsa-miR-342-3p | MIMAT0000753 | MIRT043695 | CLASH | Functional MTI (Weak) | 23622248 |
| hsa-miR-149-5p | MIMAT0000450 | MIRT045402 | CLASH | Functional MTI (Weak) | 23622248 |
| hsa-miR-125b-5p | MIMAT0000423 | MIRT046104 | CLASH | Functional MTI (Weak) | 23622248 |
| hsa-let-7b-5p | MIMAT0000063 | MIRT051948 | CLASH | Functional MTI (Weak) | 23622248 |
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- mirRecord
MicroRNA name | mirBase ID | Target site number | MiRNA mature ID | Test method inter | MiRNA regulation site | Reporter target site | Pubmed ID |
|---|---|---|---|---|---|---|---|
| hsa-miR-203a | MIMAT0000264 | NA | hsa-miR-203 | {immunoblotting} | {overexpression} | 18538733 |
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6. Text-mining results about the gene
Gene occurances in abstracts of cellular senescence-associated articles: 4 abstracts the gene occurs.
PubMed ID of the article | Sentenece the gene occurs |
|---|---|
| 25213664 | The malignancy suppression role of miR-23a by targeting the BCR/ABL oncogene in chromic myeloid leukemia |
| 25213664 | The aim of this study was to investigate the role and mechanism of miR-23a in the regulation of BCR/ABL and to provide a new prognostic biomarker for chronic myeloid leukemia (CML) |
| 25213664 | The expression levels of miR-23a and BCR/ABL were assessed in 42 newly diagnosed CML patients, 37 CML patients in first complete remission and 25 healthy controls |
| 25213664 | Quantitative real-time PCR, western blot analysis and colony formation assay were used to evaluate changes induced by overexpression or inhibition of miR-23a or BCR/ABL |
| 25213664 | The microarray results showed that most of the CML patients expressed high levels of BCR/ABL and low levels of miR-23a |
| 25213664 | Real-time RT-PCR and western blot analysis showed that the BCR/ABL levels in miR-23a-transfected cells were lower than those in the control groups |
| 25213664 | Moreover, when K562 cells were treated with 5-aza-2'-deoxycytidine, a DNA methylation inhibitor, BCR/ABL expression was upregulated, which indicates epigenetic silencing of miR-23a in leukemic cells |
| 25213664 | BCR/ABL and miR-23a expressions were inversely related to CML, and BCR/ABL expression was regulated by miR-23a in leukemic cells |
| 25213664 | The epigenetic silencing of miR-23a led to derepression of BCR/ABL expression, and consequently contributes to CML development and progression |
| 24177958 | The c-ABL non-receptor tyrosine kinase and the p53 tumor suppressor protein are pivotal modulators of cellular responses to DNA damage |
| 24177958 | However, a comprehensive understanding of the role of c-ABL kinase in p53-dependent transcription of p21(CIP1/WAF1) and ensuing cell fate decision is still obscure |
| 24177958 | Here, we demonstrate that c-ABL tyrosine kinase regulates p53-dependent induction of p21 |
| 24177958 | When these cells were simultaneously treated with a c-ABL kinase inhibitor, STI571, or a c-ABL-specific siRNA along with adriamycin, the p53-dependent p21 induction was dramatically diminished, even though p53 is substantially induced |
| 24177958 | 4 mug/ml) cells became apoptotic, and the simultaneous presence of a c-ABL kinase inhibitor STI571 augmented the extent of apoptosis |
| 24177958 | In summary, c-ABL appears to promote senescence or inhibit apoptosis, depending on the extent of DNA damage |
| 22791394 | Misregulation of c-Abl, as seen in the constitutively active BCR-ABL, is the leading cause of human chronic myeloid leukemia |
| 22791394 | Here, we report an important role for c-Abl in replicative senescence and immortalization by regulating the expression of two tumor suppressors that induce cellular senescence, p53 and p16(INK4a) |
| 22791394 | Deleting p53 allows c-Abl (-/-) p53 (-/-) MEFs to bypass senescence to be spontaneously immortalized |
| 22791394 | Cell immortalization, but not senescence, was generally accompanied by mutations in p53 in both wildtype and c-Abl (-/-) MEFs, although the spectrum is different from that of human tumors |
| 22791394 | The role for c-Abl in regulating cell senescence and immortalization might explain some of the developmental defects in c-Abl (-/-) mice and how BCR-ABL transforms cells |
| 8985343 | Furthermore, v-src cooperated with an immortalizing gene, like simian virus 40 large T, polyomavirus large T, E6 and E7 of human papillomavirus, or an activated p53 mutant, to induce anchorage-independent growth of primary cultures but failed to do so with cytoplasmic transforming genes, like v-abl, v-ras, or v-raf, which did not confer indefinite division potential |
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