ArticleMolecular and cellular biology1994
Oncogenic activation of the Lck protein accompanies translocation of the LCK gene in the human HSB2 T-cell leukemia.
Article in Molecular and cellular biology, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 64 citations in OpenAlex.
- Simulating neuronal development: exploring potential mechanisms for central nervous system metastasis in acute lymphoblastic leukemia.Frontiers in oncology · 2023Article
- PIM Kinase Inhibitors Block the Growth of Primary T-cell Acute Lymphoblastic Leukemia: Resistance Pathways Identified by Network Modeling Analysis.Molecular cancer therapeutics · 2020Article
- Molecular Classification of Primary Immunodeficiencies of T Lymphocytes.Advances in immunology · 2018Review
- E2A-PBX1 Remodels Oncogenic Signaling Networks in B-cell Precursor Acute Lymphoid Leukemia.Cancer research · 2016Article
- Identifying three-dimensional structures of autophosphorylation complexes in crystals of protein kinases.Science signaling · 2015Article
- Genomics and drug profiling of fatal TCF3-HLF-positive acute lymphoblastic leukemia identifies recurrent mutation patterns and therapeutic options.Nature genetics · 2015Article
- The mutational landscape in pediatric acute lymphoblastic leukemia deciphered by whole genome sequencing.Human mutation · 2015Article
- LCK: a new biomarker candidate for the early diagnosis of acute myocardial infarction.Molecular biology reports · 2014Article
- TYK2-STAT1-BCL2 pathway dependence in T-cell acute lymphoblastic leukemia.Cancer discovery · 2013Article
- A role for Rap2 in recycling the extended conformation of LFA-1 during T cell migration.Biology open · 2012Article
- Nuclear localization of lymphocyte-specific protein tyrosine kinase (Lck) and its role in regulating LIM domain only 2 (Lmo2) gene.Biochemical and biophysical research communications · 2012Article
- The Gαq/11 proteins contribute to T lymphocyte migration by promoting turnover of integrin LFA-1 through recycling.PloS one · 2012Article
- Suppressor of cytokine signaling 1 interacts with oncogenic lymphocyte-specific protein tyrosine kinase.Oncology reports · 2011Article
- A cell-based screen for inhibitors of protein folding and degradation.Cell stress & chaperones · 2010Article
- Deletion of the protein tyrosine phosphatase gene PTPN2 in T-cell acute lymphoblastic leukemia.Nature genetics · 2010Article
- Enforced SOCS1 and SOCS3 expression attenuates Lck-mediated cellular transformation.International journal of oncology · 2010Article
- Intermediate-affinity LFA-1 binds alpha-actinin-1 to control migration at the leading edge of the T cell.The EMBO journal · 2008Article
- Penalized model-based clustering with cluster-specific diagonal covariance matrices and grouped variables.Electronic journal of statistics · 2008Article
- Characterization of human palmitoyl-acyl transferase activity using peptides that mimic distinct palmitoylation motifs.The Biochemical journal · 2003Article
- Development of T-leukaemias in CD45 tyrosine phosphatase-deficient mutant lck mice.The EMBO journal · 2000Article
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3 authors at 1 institution in 1 country.
Funding
Abstract
The tyrosine protein kinase p56lck transduces signals important for antigen-induced T-cell activation. In transgenic mice, p56lck is oncogenic when overexpressed or expressed as a mutant, catalytically activated enzyme. In humans, the LCK gene is located at the breakpoint of the t(1;7)(p34;q34) chromosomal translocation. This translocation positions the beta T-cell receptor constant region enhancer upstream of the LCK gene without interrupting the LCK coding sequences, and a translocation of this sort occurs in both the HSB2 and the SUP-T-12 T-cell lines. We have found that, although the level of the p56lck protein in HSB2 cells is elevated approximately 2-fold in comparison with that in normal T-cell lines, total cellular tyrosine protein phosphorylation is elevated approximately 10-fold. Increased levels of phosphotyrosine in HSB2 cells resulted from mutations in the LCK gene that activated its function as a phosphotransferase and converted it into a dominant transforming oncogene. The oncogenic p56lck in HSB2 cells contained one amino acid substitution within the CD4/CD8-binding domain, two substitutions in the kinase domain, and an insertion of Gln-Lys-Pro (QKP) between the SH2 and kinase domains. In NIH 3T3 fibroblasts, three of these mutations cooperated to produce the fully oncogenic form of this p56lck variant. These results suggest that mutation of LCK may contribute to some human T-cell leukemias.
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