Example sentences for: abl

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

  • 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.

  • The Rlk fusion proteins also failed to efficiently bind SH3 domains from other kinases, including Abl, Csk and Btk.

  • 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].

  • 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 ] .

  • The proto-oncogene TEL (Translocation, Ets, Leukemia) is a transcriptional repressor that contains a C-terminal Ets family DNA binding domain; a central domain that together with co-repressors recruit histone deacetylases [ 1 2 3 ] ; and an N-terminal SAM (sterile, alpha, motif) domain [ 4 5 6 ] , which we have recently shown forms a polymer [ 7 ] . Chromosomal translocations in a variety of leukemias result in fusion of the SAM domain of TEL to tyrosine kinase domains such as ABL, PDGFβ and JAK2 [ 8 9 10 11 12 13 14 ] or to the transcriptional activators AML1 and ARNT [ 15 16 17 ] . In the tyrosine kinase fusions, SAM domain polymerization leads to constitutive activation of the tyrosine kinase domains, which leads in turn to cell transformation [ 10 12 18 19 ] . Thus, compounds that block TEL-SAM polymerization could be effective in treating these leukemias.

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