PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 30015051-3 2018 The Asp816 residue is located at the activation loop (A-loop) of c-Kit and the mutation can eliminate a negative formal charge from the loop region by substituting the acidic asparagic acid residue with neutral valine, histidine, tyrosine or phenylalanine. Aspartic Acid 175-189 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 65-70 21640708-0 2011 Mechanism of activation of human c-KIT kinase by internal tandem duplications of the juxtamembrane domain and point mutations at aspartic acid 816. Aspartic Acid 129-142 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 33-38 16242000-0 2005 CD117+ small cell lung cancer lacks the asp 816-->val point mutation in exon 17. Aspartic Acid 40-43 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 0-5 19915299-3 2009 Sequencing of the KIT DNA revealed a point mutation at codon 816 including a substitution of valine for aspartic acid (D816V). Aspartic Acid 104-117 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 18-21 17173066-2 2007 When mutated on Asp 816 (corresponding to Asp 814 in the mouse), as preferentially found in human mastocytosis and acute myeloid leukemia, Kit became non-sensitive to imatinib mesylate (Gleevec). Aspartic Acid 16-19 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 139-142 17173066-2 2007 When mutated on Asp 816 (corresponding to Asp 814 in the mouse), as preferentially found in human mastocytosis and acute myeloid leukemia, Kit became non-sensitive to imatinib mesylate (Gleevec). Aspartic Acid 42-45 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 139-142 16352739-2 2005 Mastocytosis is often associated with a somatic point mutation in the Kit protooncogene leading to an Asp/Val substitution at position 816 in the kinase domain of this receptor. Aspartic Acid 102-105 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 70-73 21135090-6 2011 We show that STAT1, -3, and -5 proteins are activated downstream of the KIT-Asp(816) mutant. Aspartic Acid 76-79 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 72-75 19540337-7 2009 Frequently found mutations in c-Kit and Flt3 are point mutations of aspartic acid 816 and 835 respectively, in the activation loop of the kinase domains. Aspartic Acid 68-81 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 30-35 12363464-0 2002 Detection of c-kit point mutation Asp-816 --> Val in microdissected pooled single mast cells and leukemic cells in a patient with systemic mastocytosis and concomitant chronic myelomonocytic leukemia. Aspartic Acid 34-37 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 13-18 15542581-2 2005 Mutation of the aspartic acid residue encoded by codon 816 of human c-kit or codon 814 of the murine gene results in an oncogenic form of Kit. Aspartic Acid 16-29 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 68-73 12363464-1 2002 The c-kit mutation Asp-816-->Val is detectable not only in neoplastic mast cells (MCs) in patients with systemic mastocytosis (SM) but also in most associated hematologic non-MC lineage disease (AHNMD). Aspartic Acid 19-22 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 4-9 11494148-0 2001 STAT3 activation is required for Asp(816) mutant c-Kit induced tumorigenicity. Aspartic Acid 33-36 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 49-54 11494148-7 2001 These results demonstrate that activation of STAT3 by Asp(816) mutant c-Kit is required for the anchorage-independent growth and tumorigenicity induced by Asp(816) mutant c-Kit. Aspartic Acid 54-57 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 70-75 11494148-7 2001 These results demonstrate that activation of STAT3 by Asp(816) mutant c-Kit is required for the anchorage-independent growth and tumorigenicity induced by Asp(816) mutant c-Kit. Aspartic Acid 54-57 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 171-176 11494148-7 2001 These results demonstrate that activation of STAT3 by Asp(816) mutant c-Kit is required for the anchorage-independent growth and tumorigenicity induced by Asp(816) mutant c-Kit. Aspartic Acid 155-158 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 70-75 11494148-7 2001 These results demonstrate that activation of STAT3 by Asp(816) mutant c-Kit is required for the anchorage-independent growth and tumorigenicity induced by Asp(816) mutant c-Kit. Aspartic Acid 155-158 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 171-176 12111653-8 2002 The Asn822(Lys) mutation affects a highly conserved codon within the tyrosine kinase activation loop leading, likewise the Asp(816) mutants, to constitutive ligand-independent activation of the KIT receptor. Aspartic Acid 123-126 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 194-197 11494148-1 2001 Activating mutations of c-kit at codon 816 (Asp(816)) have been identified in variety of malignancies, including acute myeloid leukemia (AML), mastocytosis and germ cell tumors. Aspartic Acid 44-47 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 24-29 7512180-3 1994 Sequencing of c-kit cDNA revealed that c-kit genes of HMC-1 cells were composed of a normal, wild-type allele and a mutant allele with two point mutations in codon 560 and codon 816, resulting in intracellular amino acid substitutions of Gly-560 for Val and Val-816 for Asp, respectively. Aspartic Acid 270-273 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 39-44 11369651-5 2001 The phosphatidylinositol-3-kinase (PI-3K)/Akt pathway, but not the Ras-mediated mitogen-activated protein (MAP) kinase pathway, is also constitutively activated by Asp(816) mutant c-Kit. Aspartic Acid 164-167 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 180-185 11369651-9 2001 The investigation of altered signal transduction pathways and the resulting functional consequences mediated by Asp(816) mutant c-Kit should provide important information for the characterization of subsets of leukemia and potential molecular pathways for therapeutic targeting. Aspartic Acid 112-115 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 128-133 11369651-0 2001 Signal transducer and activator of transcription 3 activation is required for Asp(816) mutant c-Kit-mediated cytokine-independent survival and proliferation in human leukemia cells. Aspartic Acid 78-81 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 94-99 11369651-1 2001 Activating mutations of c-kit at codon 816 (Asp(816)) have been implicated in a variety of malignancies, including acute myeloid leukemia (AML). Aspartic Acid 44-47 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 24-29 11369651-3 2001 Changes in the signal transduction pathways responsible for Asp(816) mutant c-Kit-mediated biologic effects are largely undefined. Aspartic Acid 60-63 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 76-81 11369651-4 2001 The results of this study show that Asp(816) mutant c-Kit induces constitutive activation of signal transducer and activator of transcription 3 (STAT3) and STAT1, and up-regulates STAT3 downstream targets, Bcl-x(L) and c-myc. Aspartic Acid 36-39 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 52-57 11378569-2 2001 We have identified activating mutations of c-kit at codon 816 (Asp(816) ) from a revertant of the cytokine-dependent acute myeloid leukemia (AML) cell line, MO7e (D816H), and de novo childhood AML (D816N). Aspartic Acid 63-66 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 43-48 11378569-5 2001 These results suggest a potentially important role of Asp(816) mutations of c-kit in both malignant cell proliferation and resistance to therapy. Aspartic Acid 54-57 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 76-81 9990072-5 1999 All patients with adult sporadic mastocytosis had somatic c-KIT mutations in codon 816 causing substitution of valine for aspartate and spontaneous activation of mast cell growth factor receptor (P = 0.0001). Aspartic Acid 122-131 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 58-63 8547652-3 1996 Sequencing of the whole coding region of the c-kit showed that the point mutation found in HMC-1, P-815, and RBL-2H3 cells was absent in FMA3 cells and that the c-kit cDNA of FMA3 cells carried an in-frame deletion of 21 base pairs (bp) encoding Thr-Gln-Leu-Pro-Tyr-Asp-His at codons 573 to 579 at the juxtamembrane domain. Aspartic Acid 266-269 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 45-50 7536501-7 1995 Since mutations at the same Asp codon constitutively activated KIT in all the human HMC-1, murine P-815, and rat RBL-2H3 cell lines, and since the incorporation of antisense oligonucleotides of c-kit messenger RNA significantly suppressed the proliferation of RBL-2H3 cells, the activating mutations in the Asp codon of the c-kit gene appeared to be involved in neoplastic growth of mast cells. Aspartic Acid 28-31 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 63-66 7691885-5 1993 Sequencing of whole coding region of c-kit cDNA revealed that c-kit genes of HMC-1 cells were composed of a normal, wild-type allele and a mutant allele with two point mutations resulting in intracellular amino acid substitutions of Gly-560 for Val and Val-816 for Asp. Aspartic Acid 265-268 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 62-67