PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 2552437-5 1989 In contrast, the KRAS protein, which carries an extremely basic domain (residues 172-182, Lys-Asp-Glu-Lys6-Ser-Arg), is phosphorylated by the receptor kinase without the addition of basic proteins. Aspartic Acid 94-97 KRAS proto-oncogene, GTPase Homo sapiens 17-21 29748115-2 2018 A study published in The New England Journal of Medicine reported that KRAS somatic mutations (p.Gly12Val/Asp) were identified in brain arteriovenous malformations of human subjects and endothelial cell-enriched cultures, which might specifically activate the MAPK (mitogen-activated protein kinase)-ERK (extracellular signal-regulated kinase) signaling pathway in brain endothelial cells. Aspartic Acid 106-109 KRAS proto-oncogene, GTPase Homo sapiens 71-75 2666911-3 1989 We report here that three of 15 colon tumors tested contain K-ras codon 12 aspartic acid mutations and one, along with the HCT 116 colon carcinoma cell line, contains a K-ras codon 13 aspartic acid mutation. Aspartic Acid 184-197 KRAS proto-oncogene, GTPase Homo sapiens 169-174 32986951-2 2021 Two of the most frequent oncogenic KRAS mutations observed in patients result in glycine to aspartic acid substitution at either codon 12 (G12D) or 13 (G13D). Aspartic Acid 92-105 KRAS proto-oncogene, GTPase Homo sapiens 35-39 33230296-0 2020 KRAS-regulated glutamine metabolism requires UCP2-mediated aspartate transport to support pancreatic cancer growth. Aspartic Acid 59-68 KRAS proto-oncogene, GTPase Homo sapiens 0-4 33145412-3 2020 A co-crystal structure of peptide KD2 with K-Ras(G12D) GppNHp reveals that this peptide binds in the Switch II groove region with concomitant opening of the Switch II loop and a 40 rotation of the alpha2 helix, and that a threonine residue (Thr10) on KD2 has direct access to the mutant aspartate (Asp12) on K-Ras. Aspartic Acid 288-297 KRAS proto-oncogene, GTPase Homo sapiens 43-48 32335227-6 2020 The structural changes of NS3 are mediated by conserved residues and reveal a subpocket, which we denote as subpocket B, extending beyond the catalytic aspartate 75 towards an allosteric binding site, providing a unique connection between the orthosteric and allosteric sites in the protease. Aspartic Acid 152-161 KRAS proto-oncogene, GTPase Homo sapiens 26-29 3627975-3 1987 The polymerase chain reaction with Ki-ras specific amplimers revealed a guanosine to adenosine transition at the second position of codon 13, resulting in a substitution of glycine by aspartic acid. Aspartic Acid 184-197 KRAS proto-oncogene, GTPase Homo sapiens 35-41 27764698-6 2016 Using several human CRC cell lines and clinical specimens of primary CRC, we demonstrated that the expression of asparagine synthetase (ASNS), an enzyme that synthesizes asparagine from aspartate, was upregulated by mutated KRAS and that ASNS expression was induced by KRAS-activated signaling pathway, in particular PI3K-AKT-mTOR pathway. Aspartic Acid 186-195 KRAS proto-oncogene, GTPase Homo sapiens 224-228 29254168-0 2017 LC-MS-based metabolomics revealed SLC25A22 as an essential regulator of aspartate-derived amino acids and polyamines in KRAS-mutant colorectal cancer. Aspartic Acid 72-81 KRAS proto-oncogene, GTPase Homo sapiens 120-124 29254168-8 2017 Collectively, SLC25A22 acts as an essential metabolic regulator during CRC progression as it promotes the synthesis of aspartate-derived amino acids and polyamines in KRAS mutant CRC cells. Aspartic Acid 119-128 KRAS proto-oncogene, GTPase Homo sapiens 167-171 27764698-5 2016 KRAS mutation causes a marked decrease in aspartate level and an increase in asparagine level in CRC. Aspartic Acid 42-51 KRAS proto-oncogene, GTPase Homo sapiens 0-4 27451147-11 2016 Incubation of KRAS mutant CRC cells with knockdown of SLC25A22 with aspartate increased proliferation and reduced apoptosis, which required GOT1, indicating that oxaloacetate is required for cell survival. Aspartic Acid 68-77 KRAS proto-oncogene, GTPase Homo sapiens 14-18 27764698-6 2016 Using several human CRC cell lines and clinical specimens of primary CRC, we demonstrated that the expression of asparagine synthetase (ASNS), an enzyme that synthesizes asparagine from aspartate, was upregulated by mutated KRAS and that ASNS expression was induced by KRAS-activated signaling pathway, in particular PI3K-AKT-mTOR pathway. Aspartic Acid 186-195 KRAS proto-oncogene, GTPase Homo sapiens 269-273 24852854-4 2014 KRAS codon 12 Gly Asp, Gly, Val, and codon 13 Gly Cys gene mutations were tested using an in-house real-time ARMS PCR method. Aspartic Acid 18-21 KRAS proto-oncogene, GTPase Homo sapiens 0-4 26921316-0 2016 Aspartate Rescues S-phase Arrest Caused by Suppression of Glutamine Utilization in KRas-driven Cancer Cells. Aspartic Acid 0-9 KRAS proto-oncogene, GTPase Homo sapiens 83-87 24138715-9 2014 Keeping in mind that the glycine present at position 12 can be substituted by valine, aspartic acid or cysteine, it could be well understood that each different substitution plays a different role in K-RAS-dependent processes. Aspartic Acid 86-99 KRAS proto-oncogene, GTPase Homo sapiens 200-205 24372240-7 2013 The protein-protein docking showed that the aminoacid residues of NS3 which were interacting with NRBP were found to be Ala 325, Asp 324, Phe 326, Asp 335, Glu 336, Glu 328, Asp 485, Gln 478, Arg 459, Gly 446 and Leu 480. Aspartic Acid 129-132 KRAS proto-oncogene, GTPase Homo sapiens 66-69 23849768-4 2013 Among the tested patients, 76.09% of patients had wt-KRAS genotype and 23.91% were KRAS mutants and the majority of mutations would result in an amino acid substitution of glycine by aspartic acid (68.2%) The predominant mutations are G>A transitions and G>T transversions. Aspartic Acid 183-196 KRAS proto-oncogene, GTPase Homo sapiens 83-87 24372240-7 2013 The protein-protein docking showed that the aminoacid residues of NS3 which were interacting with NRBP were found to be Ala 325, Asp 324, Phe 326, Asp 335, Glu 336, Glu 328, Asp 485, Gln 478, Arg 459, Gly 446 and Leu 480. Aspartic Acid 147-150 KRAS proto-oncogene, GTPase Homo sapiens 66-69 19797353-8 2009 p,p"-DDT, p,p"-DDE and PCB 138 were significantly associated with the two most prevalent KRAS mutations (Val and Asp). Aspartic Acid 113-116 KRAS proto-oncogene, GTPase Homo sapiens 89-93 22558217-7 2012 A newly observed feature of NS3/4A was a high frequency of either Asp or Glu at both P5 and P6 positions in a subset of the most efficient NS3/4A substrates. Aspartic Acid 66-69 KRAS proto-oncogene, GTPase Homo sapiens 28-31 22558217-7 2012 A newly observed feature of NS3/4A was a high frequency of either Asp or Glu at both P5 and P6 positions in a subset of the most efficient NS3/4A substrates. Aspartic Acid 66-69 KRAS proto-oncogene, GTPase Homo sapiens 139-142 23152013-3 2012 However, pooled analysis of randomized controlled studies in Western countries in patients treated with cetuximab has suggested that patients with tumors showing the KRAS p. G13D mutation[a glycine(G)to aspartate(D)transition mutation] have longer overall survival and progression-free survival when compared to patients with other KRAS mutations. Aspartic Acid 203-212 KRAS proto-oncogene, GTPase Homo sapiens 166-170 23152013-3 2012 However, pooled analysis of randomized controlled studies in Western countries in patients treated with cetuximab has suggested that patients with tumors showing the KRAS p. G13D mutation[a glycine(G)to aspartate(D)transition mutation] have longer overall survival and progression-free survival when compared to patients with other KRAS mutations. Aspartic Acid 203-212 KRAS proto-oncogene, GTPase Homo sapiens 332-336 19061898-3 2009 The inhibitor stabilizes the N-terminal domain of NS3p and the substrate-binding site, and correctly aligns catalytic His-Asp residues. Aspartic Acid 122-125 KRAS proto-oncogene, GTPase Homo sapiens 50-54 18175625-19 2006 A molecular study of the neoplastic tissue evidenced a typical mutation of the K-ras gene codon 12: the normal sequence GGT (glycine) was altered into GAT (aspartic acid). Aspartic Acid 156-169 KRAS proto-oncogene, GTPase Homo sapiens 79-84 18097554-7 2008 LS174T cell line had a point mutation of the K-RAS gene at codon 12 (gly12 --> asp; G12D), and HCT 116 and LoVo cell lines had a point mutation of the K-RAS gene at codon 13 (gly13 --> asp; G13D). Aspartic Acid 82-85 KRAS proto-oncogene, GTPase Homo sapiens 45-50 16060660-1 2005 Mutations in the Kirsten ras (KRAS) gene are present in almost all pancreatic adenocarcinomas, and one common mutation is at codon 12: GGT (Gly) is transformed into GAT (Asp). Aspartic Acid 170-173 KRAS proto-oncogene, GTPase Homo sapiens 17-28 16060660-3 2005 P14 was designed with a 15-base sequence complementary to the antisense strand of KRAS at the GAT (Asp) mutation and conjugated to the nuclear localization signal peptide PKKKRKV. Aspartic Acid 99-102 KRAS proto-oncogene, GTPase Homo sapiens 82-86 16060660-1 2005 Mutations in the Kirsten ras (KRAS) gene are present in almost all pancreatic adenocarcinomas, and one common mutation is at codon 12: GGT (Gly) is transformed into GAT (Asp). Aspartic Acid 170-173 KRAS proto-oncogene, GTPase Homo sapiens 30-34 10344756-2 1999 Using gene targeting, we examined HCT116 cells that contain the Gly-13-->Asp mutation of Ki-ras and activated Ki-ras-disrupted clones derived from HCT116. Aspartic Acid 76-79 KRAS proto-oncogene, GTPase Homo sapiens 92-98 12947056-6 2003 K-ras codon 13 mutations (all with G-A nucleotide transitions resulting in Gly>Asp substitution) and single activating mutations in any of the ras genes were also independent predictors of poor survival in differentiated thyroid carcinomas (P =.027 and P =.007, respectively). Aspartic Acid 82-85 KRAS proto-oncogene, GTPase Homo sapiens 0-5 10915606-3 2000 Our study provides experimental evidence that histidine at position 1658 and aspartic acid at position 1686 constitute together with the previously identified serine at position 1752 (S1752) the catalytic triad of the pestiviral NS3 serine protease. Aspartic Acid 77-90 KRAS proto-oncogene, GTPase Homo sapiens 229-232 10739955-5 2000 Amino acid number 12 of K-Ras (wild type; Gly) was changed to Ser, Arg, Cys, Asp, Ala, or Val, and the mobility shift of the greenish fluorescent bands in the SDS/urea gel was analyzed. Aspartic Acid 77-80 KRAS proto-oncogene, GTPase Homo sapiens 24-29 15734482-12 2005 Of various types of K-ras mutations, 12 Asp often was seen in type 1 and 2 gastric cancers (well-demarcated, elevated tumors), while 12 Val and 12 Ser were often seen in type 3 and 4 cases (infiltrating carcinomas). Aspartic Acid 40-43 KRAS proto-oncogene, GTPase Homo sapiens 20-25 10463479-5 1999 All of the K-ras mutations were G-to-A transition mutations in the second position of codon 13 (glycine --> aspartic acid). Aspartic Acid 111-124 KRAS proto-oncogene, GTPase Homo sapiens 11-16 10022320-2 1998 Two genetic alterations have been identified: the first one is a GGC --> GAT (Gly --> Asp, Asp13p21) mutation at codon 13 in the Ki-ras gene, found in five out of six tumors. Aspartic Acid 92-95 KRAS proto-oncogene, GTPase Homo sapiens 135-141 11624203-11 1999 A molecular study of the neoplastic tissue evidenced a typical mutation of the K-ras gene codon 12:the normal sequence GGT (glycine) was altered into GAT (aspartic acid). Aspartic Acid 155-168 KRAS proto-oncogene, GTPase Homo sapiens 79-84 9669809-16 1998 The types of K-ras mutations in codon 12 were GTT (Val) and GAT (Asp) in each case of hyperplasia; these were identical to those of concomitant carcinomas. Aspartic Acid 65-68 KRAS proto-oncogene, GTPase Homo sapiens 13-18 9399746-5 1997 In two ulcerative colitis patients, a mutation was found in the Ki-ras gene (Gly --> Asp 12 and Gly --> Val 12), and in one patient, a mutation in exon 5 of the p53 gene. Aspartic Acid 88-91 KRAS proto-oncogene, GTPase Homo sapiens 64-70 9645349-6 1998 Analysis of specific KRAS2 mutations showed a strong effect of Asp (GAT) and Val (GTT) mutations, resulting in a very poor survival compared with wild type group, whereas the most common mutation (Cys, TGT) was not associated with prognosis. Aspartic Acid 63-66 KRAS proto-oncogene, GTPase Homo sapiens 21-26 8792713-4 1996 Retrospectively, a K-ras point mutation at codon 12 from GGT (glycine) to GAT (aspartic acid) was detected in the PPJ collected endoscopically 3 yr and 6 months earlier, as well as in the PPJ when PC was diagnosed and in the resected tumor tissue. Aspartic Acid 79-92 KRAS proto-oncogene, GTPase Homo sapiens 19-24 9177684-2 1997 A peptide substrate, Ac-Gly-Glu-Ala-Gly-Asp-Asp-Ile-Val-Pro-Cys-Ser-Met-Ser-Tyr-Thr-Trp-Thr-L ys (biotin) -OH (Sub-1), was hydrolyzed by a recombinant NS3 proteinase fused with maltose binding protein (MBP-NS3) into a product with a free amino moiety at the N-terminus. Aspartic Acid 40-43 KRAS proto-oncogene, GTPase Homo sapiens 151-154 9177684-2 1997 A peptide substrate, Ac-Gly-Glu-Ala-Gly-Asp-Asp-Ile-Val-Pro-Cys-Ser-Met-Ser-Tyr-Thr-Trp-Thr-L ys (biotin) -OH (Sub-1), was hydrolyzed by a recombinant NS3 proteinase fused with maltose binding protein (MBP-NS3) into a product with a free amino moiety at the N-terminus. Aspartic Acid 40-43 KRAS proto-oncogene, GTPase Homo sapiens 206-209 8091650-7 1994 When the P6 aspartic acid was changed to asparagine, lysine, or serine, NS3-mediated cleavage occurred. Aspartic Acid 12-25 KRAS proto-oncogene, GTPase Homo sapiens 72-75 8816895-14 1996 Only one MS case (8%) showed K-ras mutation (codon 13 GGC > GAC; glycine > aspartate), which is in contrast to 2 of the TS cases (15%), showing codon 12 mutations. Aspartic Acid 81-90 KRAS proto-oncogene, GTPase Homo sapiens 29-34 8608574-7 1996 Direct sequence analysis of the K-ras oncogene revealed the mutation at codon 12 substituting the wild-type glycine (GGT) for aspartic acid (GAT) in all cancerous lesions of patients with PBM. Aspartic Acid 126-139 KRAS proto-oncogene, GTPase Homo sapiens 32-37 8641983-6 1996 Mutational types of K-ras at codon 12 in PC were aspartic acid (Asp) in nine cases, both Asp and cysteine in one case, and arginine in one case. Aspartic Acid 49-62 KRAS proto-oncogene, GTPase Homo sapiens 20-25 8641983-6 1996 Mutational types of K-ras at codon 12 in PC were aspartic acid (Asp) in nine cases, both Asp and cysteine in one case, and arginine in one case. Aspartic Acid 64-67 KRAS proto-oncogene, GTPase Homo sapiens 20-25 8616107-9 1995 In stage I disease, the median survival was 46 months in those patients whose tumors had no K-ras mutations and 21 months in those with aspartic acid and serine mutations at K-ras codon 12; in patients with stage IIIA disease, median survival time was 16 months in the K-ras negative group and 7 months in the aspartic acid and serine mutation group. Aspartic Acid 310-323 KRAS proto-oncogene, GTPase Homo sapiens 174-179 8616107-9 1995 In stage I disease, the median survival was 46 months in those patients whose tumors had no K-ras mutations and 21 months in those with aspartic acid and serine mutations at K-ras codon 12; in patients with stage IIIA disease, median survival time was 16 months in the K-ras negative group and 7 months in the aspartic acid and serine mutation group. Aspartic Acid 310-323 KRAS proto-oncogene, GTPase Homo sapiens 174-179 8463133-4 1993 The mutation consisted of a guanine-to-adenine transition in the first base of codon 13 of c-Ki-ras which replaced wild-type glycine with serine, indicating that a putative glycine-to-aspartic acid change is not necessarily the critical event for c-Ki-ras gene activation in codon 13. Aspartic Acid 184-197 KRAS proto-oncogene, GTPase Homo sapiens 91-99 8060313-0 1994 A cell-binding Arg-Gly-Asp sequence is present in close proximity to the major linear antigenic region of HCV NS3. Aspartic Acid 23-26 KRAS proto-oncogene, GTPase Homo sapiens 110-113 7914513-0 1994 A K-ras 13Gly-->Asp mutation is recognized by HLA-DQ7 restricted T cells in a patient with colorectal cancer. Aspartic Acid 19-22 KRAS proto-oncogene, GTPase Homo sapiens 2-7 8385060-4 1993 This method allows detection of aspartic acid mutations of the c-Ki-ras gene at codons 12 and 13. Aspartic Acid 32-45 KRAS proto-oncogene, GTPase Homo sapiens 63-71 8463133-4 1993 The mutation consisted of a guanine-to-adenine transition in the first base of codon 13 of c-Ki-ras which replaced wild-type glycine with serine, indicating that a putative glycine-to-aspartic acid change is not necessarily the critical event for c-Ki-ras gene activation in codon 13. Aspartic Acid 184-197 KRAS proto-oncogene, GTPase Homo sapiens 247-255 1870574-5 1991 The highest mode of point mutation of K-ras oncogene was GGT to GAT coded aspartic acid. Aspartic Acid 74-87 KRAS proto-oncogene, GTPase Homo sapiens 38-43 1327034-8 1992 Colon cancer is mainly associated with mutations leading to substitution of the normal glycine at amino acid position 12 of K-ras by either valine or aspartic acid, and mutations in N-ras are not exceptional. Aspartic Acid 150-163 KRAS proto-oncogene, GTPase Homo sapiens 124-129 2147282-4 1990 Site-directed mutagenesis of the His-53, Asp-77, and Ser-138 residues of NS3 that compose the proposed catalytic triad implicates this domain as a serine protease. Aspartic Acid 41-44 KRAS proto-oncogene, GTPase Homo sapiens 73-76 1793483-5 1991 It leads to the substitution of glycine by aspartic acid in the resulting p21 protein, a consistent amino acid substitution found so far in all types of human cancer exhibiting a codon 13-mutated Ki-ras gene. Aspartic Acid 43-56 KRAS proto-oncogene, GTPase Homo sapiens 196-202 2404571-0 1990 Glycine to aspartic acid mutations at codon 13 of the c-Ki-ras gene in human gastrointestinal cancers. Aspartic Acid 11-24 KRAS proto-oncogene, GTPase Homo sapiens 54-62 2205309-6 1990 Eighty percent of the mutations involved substitution of aspartic acid for glycine (G----A) in the 12th or 13th codons of N-ras or K-ras. Aspartic Acid 57-70 KRAS proto-oncogene, GTPase Homo sapiens 131-136 2404571-6 1990 In all three mutations of c-Ki-ras at codon 13 which had been seldom found in human cancers, glycine to aspartic acid mutations due to identical G to A transition at the second nucleotide were observed. Aspartic Acid 104-117 KRAS proto-oncogene, GTPase Homo sapiens 26-34 34227245-0 2021 Oncogenic KRAS creates an aspartate metabolism signature in colorectal cancer cells. Aspartic Acid 26-35 KRAS proto-oncogene, GTPase Homo sapiens 10-14