Example sentences for: abl

How can you use “abl” in a sentence? Here are some example sentences to help you improve your vocabulary:

  • The cell surface expressed integrins can control this process by physically interacting with the extracellular matrix proteins and other cell surface proteins on endothelial cells lining the blood vessel wall [ 1 ] . These integrins signal adhesion and migration by communicating with several tyrosine kinases inside the cell, including the Focal Adhesion Kinase (FAK) and Src family kinases [ 1 2 ] . Src kinases control the activation of FAK, as well as the tyrosine phosphorylation of critical substrates that regulate adhesion and migration [ 3 ] . Indeed, colon cancer cells with high metastatic potential have elevated levels of Src activity or activating mutations in the Src gene [ 4 5 ] . One Src substrate that is involved in regulating an important signaling node in this process is the adaptor protein p130 cas (Cas) [ 6 7 8 9 10 ] . Cas appears to play a central role in the transformation process by several oncogenes including ras, ornithine decarboxylase (ODC), v-Src, v-crk, and Bcr-Abl, as these tumors all have elevated levels of tyrosine phosphorylated Cas [ 6 11 12 13 ] . Cells from mice that lack Cas have much reduced migration and are resistant to transformation by v-Src, while expression of Cas anti-sense RNA in cells transformed with ras, v-Src or ODC result in reversion of the transformed phenotype [ 11 14 15 ] . Furthermore, increased expression of Cas can rescue cell migration and adhesion in cells expressing the tumor suppressor PTEN, and can enhance cell migration and adhesion in normal cells, with a major role being played by the substrate domain [ 16 17 ] .

  • Ena, a member of the Ena/VASP family proteins that catalyse filament formation, and Abl, a protein kinase that binds CAP in mammalian cells, were found to work with CAP in this process.

  • homologue of adenylyl cyclase-associated proteins), Enabled (Ena) and Abelson (Abl).

  • These target proteins include the c-Abl tyrosine kinase, the p53 tumor suppressor, the Chk1 and Chk2 serine/threoine kinase, the p34 subunit of replication protein A (RPA), Chk1 serine/threoine kinase and NBS1 kinase which is mutated in human autosomal recessive disease Nijmegan breakage syndrome [ 16 17 18 19 20 21 22 23 ] . Clinical characteristics of AT patients include hypersensitivity to irradiation, thymic dysplasia, immune defects and higher tendency to develop malignant tumor, suggesting that ATM function is critical in DNA damage repair and tumor suppression.

  • This approach has been successful in producing conditional forms of the Tec family PTK Bmx [ 22], and also the PTKs v-Src [ 23], Hck [ 24] and Abl [ 25], the serine/threonine kinases Raf [ 26] and Akt [ 27], and the dual specificity protein kinase MEK1 [ 23].


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