Proto-Oncogene Proteins c-abl
"Proto-Oncogene Proteins c-abl" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus,
MeSH (Medical Subject Headings). Descriptors are arranged in a hierarchical structure,
which enables searching at various levels of specificity.
Non-receptor tyrosine kinases encoded by the C-ABL GENES. They are distributed in both the cytoplasm and the nucleus. c-Abl plays a role in normal HEMATOPOIESIS especially of the myeloid lineage. Oncogenic transformation of c-abl arises when specific N-terminal amino acids are deleted, releasing the kinase from negative regulation.
| Descriptor ID |
D016315
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| MeSH Number(s) |
D08.811.913.696.620.682.725.500 D12.776.624.664.700.167
|
| Concept/Terms |
Proto-Oncogene Proteins c-abl- Proto-Oncogene Proteins c-abl
- Proto Oncogene Proteins c abl
- c-abl, Proto-Oncogene Proteins
- Proto-Oncogene Proteins abl
- Proteins abl, Proto-Oncogene
- Proto Oncogene Proteins abl
- abl, Proto-Oncogene Proteins
- c-abl Proteins
- c abl Proteins
- abl Proto-Oncogene Products
- Products, abl Proto-Oncogene
- Proto-Oncogene Products, abl
- abl Proto Oncogene Products
- abl Proto-Oncogene Proteins
- Proto-Oncogene Proteins, abl
- abl Proto Oncogene Proteins
|
Below are MeSH descriptors whose meaning is more general than "Proto-Oncogene Proteins c-abl".
Below are MeSH descriptors whose meaning is more specific than "Proto-Oncogene Proteins c-abl".
This graph shows the total number of publications written about "Proto-Oncogene Proteins c-abl" by people in this website by year, and whether "Proto-Oncogene Proteins c-abl" was a major or minor topic of these publications.
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| Year | Major Topic | Minor Topic | Total |
|---|
| 1995 | 1 | 0 | 1 |
| 1996 | 4 | 0 | 4 |
| 1997 | 4 | 0 | 4 |
| 1998 | 4 | 0 | 4 |
| 1999 | 1 | 0 | 1 |
| 2000 | 3 | 0 | 3 |
| 2001 | 1 | 0 | 1 |
| 2005 | 1 | 1 | 2 |
| 2010 | 1 | 0 | 1 |
| 2014 | 0 | 1 | 1 |
| 2015 | 3 | 0 | 3 |
| 2016 | 1 | 0 | 1 |
| 2019 | 1 | 0 | 1 |
| 2023 | 0 | 1 | 1 |
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Below are the most recent publications written about "Proto-Oncogene Proteins c-abl" by people in Profiles.
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ABL1 kinase as a tumor suppressor in AML1-ETO and NUP98-PMX1 leukemias. Blood Cancer J. 2023 03 23; 13(1):42.
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BCR-ABL1-like B-Lymphoblastic Leukemia/Lymphoma with FOXP1-ABL1 Rearrangement: Comprehensive Laboratory Identification Allowing Tyrosine Kinase Inhibitor Use. Lab Med. 2019 Oct 10; 50(4):401-405.
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Clinical impact of ABL1 kinase domain mutations and IKZF1 deletion in adults under age 60 with Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukemia (ALL): molecular analysis of CALGB (Alliance) 10001 and 9665. Leuk Lymphoma. 2016 10; 57(10):2298-306.
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c-Abl Mediated Tyrosine Phosphorylation of Aha1 Activates Its Co-chaperone Function in Cancer Cells. Cell Rep. 2015 Aug 11; 12(6):1006-18.
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Cytogenetic, fluorescence in situ hybridization, and genomic array characterization of chronic myeloid leukemia with cryptic BCR-ABL1 fusions. Cancer Genet. 2015 Jul-Aug; 208(7-8):396-403.
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Perspective on computational and structural aspects of kinase discovery from IPK2014. Biochim Biophys Acta. 2015 Oct; 1854(10 Pt B):1595-604.
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c-Abl mediated tyrosine phosphorylation of paxillin regulates LPS-induced endothelial dysfunction and lung injury. Am J Physiol Lung Cell Mol Physiol. 2015 May 15; 308(10):L1025-38.
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Computational study of the "DFG-flip" conformational transition in c-Abl and c-Src tyrosine kinases. J Phys Chem B. 2015 Jan 29; 119(4):1443-56.
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Computational study of Gleevec and G6G reveals molecular determinants of kinase inhibitor selectivity. J Am Chem Soc. 2014 Oct 22; 136(42):14753-62.
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Real-time assessment of relapse risk based on the WT1 marker in acute leukemia and myelodysplastic syndrome patients after hematopoietic cell transplantation. Bone Marrow Transplant. 2015 Jan; 50(1):26-33.