PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 3001107-4 1985 In an attempt to find a protein that might link the receptor tyrosine kinase to these serine/threonine phosphorylation reactions, we have studied the interaction of a partially purified preparation of insulin receptor with purified preparations of serine/threonine kinases known to phosphorylate glycogen synthase. Serine 86-92 ret proto-oncogene Homo sapiens 52-76 27717313-3 2016 Gene analysis in this patient disclosed a heterozygous p.S811F mutation was in Ret gene exon 14, resulting in a substitution of phenylalanine for serine. Serine 146-152 ret proto-oncogene Homo sapiens 79-82 17209045-1 2007 The precise role of STAT3 Ser(727) phosphorylation in RET-mediated cell transformation and oncogenesis is not well understood. Serine 26-29 ret proto-oncogene Homo sapiens 54-57 23872421-9 2013 Collectively, these findings demonstrated the hitherto unrecognized and novel role of specific GFRalpha2 and RET isoforms in mediating NRTN activation of STAT3 and the transcription independent mechanism whereby the mitochondria localized P-Ser-STAT3 mediated NRTN induced neurite outgrowth. Serine 241-244 ret proto-oncogene Homo sapiens 109-112 20682772-7 2010 In agreement with this, mutation of Ser(696), a known PKA phosphorylation site in RET, enhances SHP2 binding to the receptor and eliminates the effect of forskolin on ligand-induced outgrowth. Serine 36-39 ret proto-oncogene Homo sapiens 82-85 20119574-5 2010 We report a RET mutation in exon10, codon 618 that causes substitution of a cysteine by a serine in the cysteine-rich domain of the RET receptor in a three-generation FMTC family composed of 30 members with 11 carriers. Serine 90-96 ret proto-oncogene Homo sapiens 12-15 20119574-5 2010 We report a RET mutation in exon10, codon 618 that causes substitution of a cysteine by a serine in the cysteine-rich domain of the RET receptor in a three-generation FMTC family composed of 30 members with 11 carriers. Serine 90-96 ret proto-oncogene Homo sapiens 132-135 18322301-4 2008 PATIENTS: Fifteen individuals from five kindreds were identified as carriers of a RET protooncogene mutation in exon 11 codon 649 (TCG(Ser)-->TTG(Leu)). Serine 135-138 ret proto-oncogene Homo sapiens 82-85 17209045-2 2007 In this study, we have shown that familial medullary thyroid carcinoma (FMTC) mutants RET(Y791F) and RET(S891A) induced, in addition to Tyr(705) phosphorylation, constitutive STAT3 Ser(727) phosphorylation. Serine 181-184 ret proto-oncogene Homo sapiens 86-89 17209045-2 2007 In this study, we have shown that familial medullary thyroid carcinoma (FMTC) mutants RET(Y791F) and RET(S891A) induced, in addition to Tyr(705) phosphorylation, constitutive STAT3 Ser(727) phosphorylation. Serine 181-184 ret proto-oncogene Homo sapiens 101-104 17209045-3 2007 Using inhibitors and dominant negative constructs, we have demonstrated that RET(Y791F) and RET(S891A) induce STAT3 Ser(727) phosphorylation via a canonical Ras/ERK1/2 pathway and that integration of the Ras/ERK1/2/ELK-1 and STAT3 pathways was required for up-regulation of the c-fos promoter by FMTC-RET. Serine 116-119 ret proto-oncogene Homo sapiens 77-80 17209045-3 2007 Using inhibitors and dominant negative constructs, we have demonstrated that RET(Y791F) and RET(S891A) induce STAT3 Ser(727) phosphorylation via a canonical Ras/ERK1/2 pathway and that integration of the Ras/ERK1/2/ELK-1 and STAT3 pathways was required for up-regulation of the c-fos promoter by FMTC-RET. Serine 116-119 ret proto-oncogene Homo sapiens 92-95 17209045-3 2007 Using inhibitors and dominant negative constructs, we have demonstrated that RET(Y791F) and RET(S891A) induce STAT3 Ser(727) phosphorylation via a canonical Ras/ERK1/2 pathway and that integration of the Ras/ERK1/2/ELK-1 and STAT3 pathways was required for up-regulation of the c-fos promoter by FMTC-RET. Serine 116-119 ret proto-oncogene Homo sapiens 92-95 17209045-10 2007 These data show that FMTC-RET mutants activate a Ras/ERK1/2/STAT3 Ser(727) pathway, which plays an important role in cell mitogenicity and transformation. Serine 66-69 ret proto-oncogene Homo sapiens 26-29 16732321-4 2006 Mutagenesis studies indicated the involvement of the evolutionary conserved residues Ser-649 and Ser-653 in RET-TM oligomerization. Serine 85-88 ret proto-oncogene Homo sapiens 108-114 16732321-4 2006 Mutagenesis studies indicated the involvement of the evolutionary conserved residues Ser-649 and Ser-653 in RET-TM oligomerization. Serine 97-100 ret proto-oncogene Homo sapiens 108-114 15592804-3 2005 The second, a novel mutation in codon 641, changes alanine to serine in the transmembrane domain of the RET protein. Serine 62-68 ret proto-oncogene Homo sapiens 104-107 16772843-2 2006 Screening for MEN 2B revealed a polymorphism of the RET proto-oncogene at codon 691 with a glycine to serine conversion. Serine 102-108 ret proto-oncogene Homo sapiens 14-20 16772843-2 2006 Screening for MEN 2B revealed a polymorphism of the RET proto-oncogene at codon 691 with a glycine to serine conversion. Serine 102-108 ret proto-oncogene Homo sapiens 52-55 16427628-2 2006 We showed that all RET-PTC-1 mutants in which the C in this motif (C376) was replaced with glycine, lysine, threonine or serine lost their activity in vitro. Serine 121-127 ret proto-oncogene Homo sapiens 19-22 16343103-1 2005 OBJECTIVE: We have identified a large kindred with multiple endocrine neoplasia 2A (MEN 2A) due to a mutation at RET codon 609 that results in a cysteine to serine substitution, a mutation previously identified in only one case in the literature. Serine 157-163 ret proto-oncogene Homo sapiens 51-82 16343103-1 2005 OBJECTIVE: We have identified a large kindred with multiple endocrine neoplasia 2A (MEN 2A) due to a mutation at RET codon 609 that results in a cysteine to serine substitution, a mutation previously identified in only one case in the literature. Serine 157-163 ret proto-oncogene Homo sapiens 84-90 16343103-1 2005 OBJECTIVE: We have identified a large kindred with multiple endocrine neoplasia 2A (MEN 2A) due to a mutation at RET codon 609 that results in a cysteine to serine substitution, a mutation previously identified in only one case in the literature. Serine 157-163 ret proto-oncogene Homo sapiens 113-116 15379552-2 2004 In addition to RTK-specific tyrosine phosphorylation, these docking proteins also can be phosphorylated on serine/threonine residues affecting signal transduction. Serine 107-113 ret proto-oncogene Homo sapiens 15-18 15292360-3 2004 Genetic analysis of the RET protooncogene in this family revealed an exon 15 missense mutation at codon 891 that resulted in a serine to alanine amino acid substitution. Serine 127-133 ret proto-oncogene Homo sapiens 24-27 9075701-5 1997 However, also when serine and valine, but not leucine or phenylalanine, were inserted in position 918, the RET TK function was activated and induced, especially in the case of the RET(918Ser), immmediate-early response genes. Serine 19-25 ret proto-oncogene Homo sapiens 180-183 11886862-3 2002 Here we show that increased serine phosphorylation on RET receptor tyrosine kinase following cAMP elevation promotes lamellipodia formation of neuronal cells induced by glial cell line-derived neurotrophic factor (GDNF). Serine 28-34 ret proto-oncogene Homo sapiens 54-57 11886862-4 2002 We identified serine 696 in RET as a putative phosphorylation site by protein kinase A and found that mutation of this serine almost completely inhibited lamellipodia formation by GDNF without affecting activation of the PI3K/AKT signaling pathway. Serine 14-20 ret proto-oncogene Homo sapiens 28-31 11886862-4 2002 We identified serine 696 in RET as a putative phosphorylation site by protein kinase A and found that mutation of this serine almost completely inhibited lamellipodia formation by GDNF without affecting activation of the PI3K/AKT signaling pathway. Serine 119-125 ret proto-oncogene Homo sapiens 28-31 11886862-6 2002 Inhibition of lamellipodia formation by mutation of either serine 696 or tyrosine 1062 was associated with decrease of the Rac1-guanine nucleotide exchange factor (GEF) activity, suggesting that this activity is regulated by two different signaling pathways via serine 696 and tyrosine 1062 in RET. Serine 59-65 ret proto-oncogene Homo sapiens 294-297 11886862-6 2002 Inhibition of lamellipodia formation by mutation of either serine 696 or tyrosine 1062 was associated with decrease of the Rac1-guanine nucleotide exchange factor (GEF) activity, suggesting that this activity is regulated by two different signaling pathways via serine 696 and tyrosine 1062 in RET. Serine 262-268 ret proto-oncogene Homo sapiens 294-297 11338505-3 2001 The familial medullary thyroid carcinoma burdened genealogy shows a new point mutation TCG(Ser)-->GCG(Ala) in codon 891, in the exon 15 of the protooncogene RET. Serine 91-94 ret proto-oncogene Homo sapiens 160-163 10549772-4 1999 RESULTS: Direct sequence DNA analysis of the RET proto-oncogene showed a heterozygosity for a G to C transition at the second nucleotide of codon 620 (exon 10) in the patients, resulting in the replacement of cysteine by a serine residue in the affected Ret protein. Serine 223-229 ret proto-oncogene Homo sapiens 45-48 9075701-5 1997 However, also when serine and valine, but not leucine or phenylalanine, were inserted in position 918, the RET TK function was activated and induced, especially in the case of the RET(918Ser), immmediate-early response genes. Serine 19-25 ret proto-oncogene Homo sapiens 107-110 12734540-4 2003 A germline mutation in cysteine 611 of the RET gene was identified in this family, which introduced an amino-acid change from cysteine to serine. Serine 138-144 ret proto-oncogene Homo sapiens 43-46 9777362-1 1998 A new point mutation, TCG(Ser)-->GCG(Ala) in codon 891, exon 15 of the RET protooncogene was revealed in two patients from a pedigree with familial medullary thyroid carcinoma (FMTC), but not in healthy persons. Serine 26-29 ret proto-oncogene Homo sapiens 74-77 8765374-4 1996 Ten different types of mutations were identified in the MEN 2A/FMTC families (620 Cys-->Arg, 618 Cys-->Ser, Gly, 611 Cys-->Tyr; 634 Cys-->Arg, Tyr, Trp, Phe, Ser, Gly) and all 6 MEN 2B families had a 918 Met-->Thr point mutation. Serine 109-112 ret proto-oncogene Homo sapiens 56-62 7716719-10 1995 CONCLUSIONS: The RET codon 618 Ser mutation could predispose patients with MEN 2A to HD. Serine 31-34 ret proto-oncogene Homo sapiens 17-20 8732448-2 1996 We report an MEN 2A family in which serine (AGC) substitutes for cysteine (TGC) at codon 618 in exon 10 of the RET proto-oncogene. Serine 36-42 ret proto-oncogene Homo sapiens 13-19 8732448-2 1996 We report an MEN 2A family in which serine (AGC) substitutes for cysteine (TGC) at codon 618 in exon 10 of the RET proto-oncogene. Serine 36-42 ret proto-oncogene Homo sapiens 111-114 7716719-10 1995 CONCLUSIONS: The RET codon 618 Ser mutation could predispose patients with MEN 2A to HD. Serine 31-34 ret proto-oncogene Homo sapiens 75-81