PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 33479180-6 2021 Notably, we found that Alk inhibits Wnt signaling by phosphorylating the tyrosine of Gsk3beta, while Bclaf3 and Prkra suppress regenerating islet-derived (Reg) genes by regulating the expression of epithelial interleukins. Tyrosine 73-81 anaplastic lymphoma kinase Mus musculus 23-26 15208656-5 2004 All X-ALK variants are tyrosine phosphorylated and their subcellular distribution was in agreement with that observed in tumors. Tyrosine 23-31 anaplastic lymphoma kinase Mus musculus 6-9 14586401-6 2003 The NPM-ALK kinase is active in primary tumour tissue and forms a multimeric complex with tyrosine-phosphorylated proteins, that is, Shc. Tyrosine 90-98 anaplastic lymphoma kinase Mus musculus 8-11 10706887-7 2000 ATIC-ALK was constitutively tyrosine phosphorylated and could convert the IL-3-dependent murine hematopoietic cell line BaF3 to cytokine-independent growth. Tyrosine 28-36 anaplastic lymphoma kinase Mus musculus 5-8 16170336-2 2005 Here we report that two small-molecule, structurally related, quinazoline-type compounds, WHI-131 and WHI-154, directly inhibit enzymatic activity of NPM/ALK as demonstrated by in vitro kinase assays using a synthetic tyrosine-rich oligopeptide and the kinase itself as the substrates. Tyrosine 218-226 anaplastic lymphoma kinase Mus musculus 154-157 16170336-3 2005 The inhibition of NPM/ALK activity resulted in malignant T cells in suppression of their growth, induction of apoptosis and inhibition of tyrosine phosphorylation of STAT3, the key effector of the NPM/ALK-induced oncogenesis. Tyrosine 138-146 anaplastic lymphoma kinase Mus musculus 22-25 16170336-3 2005 The inhibition of NPM/ALK activity resulted in malignant T cells in suppression of their growth, induction of apoptosis and inhibition of tyrosine phosphorylation of STAT3, the key effector of the NPM/ALK-induced oncogenesis. Tyrosine 138-146 anaplastic lymphoma kinase Mus musculus 201-204 16170336-4 2005 We also show that the STAT3 tyrosine phosphorylation is mediated in the malignant T cells by NPM/ALK independently of Jak3 kinase as evidenced by the presence of STAT3 phosphorylation in the NPM/ALK-transfected BaF3 cells that do not express detectable Jak3 and in the NPM/ALK-positive malignant T cells with either Jak3 activity impaired by a pan-Jak or Jak3-selective inhibitor or Jak3 expression abrogated by Jak3 siRNA. Tyrosine 28-36 anaplastic lymphoma kinase Mus musculus 97-100 16170336-4 2005 We also show that the STAT3 tyrosine phosphorylation is mediated in the malignant T cells by NPM/ALK independently of Jak3 kinase as evidenced by the presence of STAT3 phosphorylation in the NPM/ALK-transfected BaF3 cells that do not express detectable Jak3 and in the NPM/ALK-positive malignant T cells with either Jak3 activity impaired by a pan-Jak or Jak3-selective inhibitor or Jak3 expression abrogated by Jak3 siRNA. Tyrosine 28-36 anaplastic lymphoma kinase Mus musculus 195-198 16170336-4 2005 We also show that the STAT3 tyrosine phosphorylation is mediated in the malignant T cells by NPM/ALK independently of Jak3 kinase as evidenced by the presence of STAT3 phosphorylation in the NPM/ALK-transfected BaF3 cells that do not express detectable Jak3 and in the NPM/ALK-positive malignant T cells with either Jak3 activity impaired by a pan-Jak or Jak3-selective inhibitor or Jak3 expression abrogated by Jak3 siRNA. Tyrosine 28-36 anaplastic lymphoma kinase Mus musculus 195-198 12748172-7 2003 NIPA interacts with NPM-ALK and other ALK fusions in a tyrosine kinase-dependent manner and is phosphorylated in NPM-ALK-expressing cells on tyrosine and serine residues with serine 354 as a major phosphorylation site. Tyrosine 55-63 anaplastic lymphoma kinase Mus musculus 38-41 12748172-7 2003 NIPA interacts with NPM-ALK and other ALK fusions in a tyrosine kinase-dependent manner and is phosphorylated in NPM-ALK-expressing cells on tyrosine and serine residues with serine 354 as a major phosphorylation site. Tyrosine 55-63 anaplastic lymphoma kinase Mus musculus 38-41 11751994-8 2002 Transfection of BaF3 cells with NPM/ALK resulted in tyrosine phosphorylation of STAT3. Tyrosine 52-60 anaplastic lymphoma kinase Mus musculus 36-39 11522649-4 2001 NPM/ALK-mediated activation of STAT5 was demonstrated by detection of: (a) constitutive tyrosine phosphorylation and enhanced DNA binding ability of STAT5 in NPM/ALK-transformed cells; and (b) NPM/ALK-dependent stimulation of STAT5-mediated transactivation of the beta-casein promoter. Tyrosine 88-96 anaplastic lymphoma kinase Mus musculus 4-7 11522649-4 2001 NPM/ALK-mediated activation of STAT5 was demonstrated by detection of: (a) constitutive tyrosine phosphorylation and enhanced DNA binding ability of STAT5 in NPM/ALK-transformed cells; and (b) NPM/ALK-dependent stimulation of STAT5-mediated transactivation of the beta-casein promoter. Tyrosine 88-96 anaplastic lymphoma kinase Mus musculus 162-165 11522649-4 2001 NPM/ALK-mediated activation of STAT5 was demonstrated by detection of: (a) constitutive tyrosine phosphorylation and enhanced DNA binding ability of STAT5 in NPM/ALK-transformed cells; and (b) NPM/ALK-dependent stimulation of STAT5-mediated transactivation of the beta-casein promoter. Tyrosine 88-96 anaplastic lymphoma kinase Mus musculus 162-165 10706082-7 2000 Expression of full-length ATIC-ALK cDNA in mouse fibroblasts revealed that the fusion protein (a) possesses constitutive tyrosine kinase activity; (b) forms stable complexes with the signaling proteins Grb2 and Shc; (c) induces tyrosine-phosphorylation of Shc; and (d) provokes oncogenic transformation. Tyrosine 121-129 anaplastic lymphoma kinase Mus musculus 31-34 9819383-7 1998 This complex formation leads to the tyrosine phosphorylation and activation of PLC-gamma, which can be corroborated by enhanced production of inositol phosphates (IPs) in NPM-ALK-expressing cells. Tyrosine 36-44 anaplastic lymphoma kinase Mus musculus 175-178 9819383-8 1998 By phosphopeptide competition experiments, we were able to identify the tyrosine residue on NPM-ALK responsible for interaction with PLC-gamma as Y664. Tyrosine 72-80 anaplastic lymphoma kinase Mus musculus 96-99 9819383-9 1998 Using site-directed mutagenesis, we constructed a comprehensive panel of tyrosine-to-phenylalanine NPM-ALK mutants, including NPM-ALK(Y664F). Tyrosine 73-81 anaplastic lymphoma kinase Mus musculus 103-106 22203728-4 2012 It induced concentration-dependent growth inhibition/cytotoxicity of ALK-positive anaplastic large-cell lymphoma (ALCL), non-small cell lung cancer (NSCLC), and neuroblastoma cells, and displayed dose-dependent inhibition of ALK tyrosine phosphorylation in tumor xenografts in mice, with substantial target inhibition (>90%) for more than 12 hours following single oral dosing at 30 mg/kg. Tyrosine 229-237 anaplastic lymphoma kinase Mus musculus 69-72 31943796-11 2020 KEY POINTS: ALK compound mutation was found in a clinical sample that was resistant to lorlatinib after sequential ALK-tyrosine kinase inhibitor (TKI) treatment. Tyrosine 119-127 anaplastic lymphoma kinase Mus musculus 115-118