FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2118600250> ?p ?o ?g. }

• W2118600250 endingPage "1737" @default.
• W2118600250 startingPage "1729" @default.
• W2118600250 abstract "The RET proto-oncogene encodes a receptor tyrosine kinase whose dysfunction plays a crucial role in the development of several neural crest disorders. Distinct activating RET mutations cause multiple endocrine neoplasia type 2A (MEN2A), type 2B (MEN2B), and familial medullary thyroid carcinoma (FMTC). Despite clear correlations between the mutations found in these cancer syndromes and their phenotypes, the molecular mechanisms connecting the mutated receptor to the different disease phenotypes are far from completely understood. Luciferase reporter assays in combination with immunoprecipitations, and Western and immunohistochemistry analyses were done in order to characterize the signaling properties of two FMTC-associated RET mutations, Y791F and S891A, respectively, both affecting the tyrosine kinase domain of the receptor. We show that these RET-FMTC mutants are monomeric receptors which are autophosphorylated and activated independently of glial cell line-derived neurotrophic factor. Moreover, we show that the dysfunctional signaling properties of these mutants, when compared with wild-type RET, involve constitutive activation of signal transducers and activators of transcription 3 (STAT3). Furthermore, we show that STAT3 activation is mediated by a signaling pathway involving Src, JAK1, and JAK2, differing from STAT3 activation promoted by RET(C634R) which was previously found to be independent of Src and JAKs. Three-dimensional modeling of the RET catalytic domain suggested that the structural changes promoted by the respective amino acids substitutions lead to a more accessible substrate and ATP-binding monomeric conformation. Finally, immunohistochemical analysis of FMTC tumor samples support the in vitro data, because nuclear localized, Y705-phosphorylated STAT3, as well as a high degree of RET expression at the plasma membrane was observed." @default.
• W2118600250 created "2016-06-24" @default.
• W2118600250 creator A5006246608 @default.
• W2118600250 creator A5009928901 @default.
• W2118600250 creator A5017845437 @default.
• W2118600250 creator A5021480821 @default.
• W2118600250 creator A5021546293 @default.
• W2118600250 creator A5029380319 @default.
• W2118600250 creator A5039909670 @default.
• W2118600250 creator A5048249385 @default.
• W2118600250 creator A5052709713 @default.
• W2118600250 creator A5068248575 @default.
• W2118600250 creator A5072526412 @default.
• W2118600250 creator A5075445107 @default.
• W2118600250 date "2005-03-01" @default.
• W2118600250 modified "2023-10-15" @default.
• W2118600250 title "RET-Familial Medullary Thyroid Carcinoma Mutants Y791F and S891A Activate a Src/JAK/STAT3 Pathway, Independent of Glial Cell Line–Derived Neurotrophic Factor" @default.
• W2118600250 cites W1510857662 @default.
• W2118600250 cites W1965404723 @default.
• W2118600250 cites W1977933836 @default.
• W2118600250 cites W1978329718 @default.
• W2118600250 cites W1980815930 @default.
• W2118600250 cites W1981810931 @default.
• W2118600250 cites W1985885351 @default.
• W2118600250 cites W1986191025 @default.
• W2118600250 cites W1994105285 @default.
• W2118600250 cites W2014078232 @default.
• W2118600250 cites W2015127215 @default.
• W2118600250 cites W2017145151 @default.
• W2118600250 cites W2022215206 @default.
• W2118600250 cites W2027322371 @default.
• W2118600250 cites W2028093783 @default.
• W2118600250 cites W2030624761 @default.
• W2118600250 cites W2035258850 @default.
• W2118600250 cites W2036834043 @default.
• W2118600250 cites W2038055852 @default.
• W2118600250 cites W2050904439 @default.
• W2118600250 cites W2051998916 @default.
• W2118600250 cites W2055975094 @default.
• W2118600250 cites W2065283382 @default.
• W2118600250 cites W2074306827 @default.
• W2118600250 cites W2078708536 @default.
• W2118600250 cites W2082584428 @default.
• W2118600250 cites W2094083015 @default.
• W2118600250 cites W2103933335 @default.
• W2118600250 cites W2104499716 @default.
• W2118600250 cites W2113242315 @default.
• W2118600250 cites W2122463327 @default.
• W2118600250 cites W2128805986 @default.
• W2118600250 cites W2132717858 @default.
• W2118600250 cites W2134894529 @default.
• W2118600250 cites W2140786721 @default.
• W2118600250 cites W2141743775 @default.
• W2118600250 cites W2152494905 @default.
• W2118600250 cites W2159429807 @default.
• W2118600250 cites W2162166182 @default.
• W2118600250 cites W2173560213 @default.
• W2118600250 cites W2260407561 @default.
• W2118600250 cites W2316331333 @default.
• W2118600250 cites W2317053903 @default.
• W2118600250 cites W2329619823 @default.
• W2118600250 cites W4232812360 @default.
• W2118600250 cites W4248941167 @default.
• W2118600250 cites W4249648965 @default.
• W2118600250 cites W4300411953 @default.
• W2118600250 doi "https://doi.org/10.1158/0008-5472.can-04-2363" @default.
• W2118600250 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/15753368" @default.
• W2118600250 hasPublicationYear "2005" @default.
• W2118600250 type Work @default.
• W2118600250 sameAs 2118600250 @default.
• W2118600250 citedByCount "85" @default.
• W2118600250 countsByYear W21186002502012 @default.
• W2118600250 countsByYear W21186002502013 @default.
• W2118600250 countsByYear W21186002502014 @default.
• W2118600250 countsByYear W21186002502015 @default.
• W2118600250 countsByYear W21186002502016 @default.
• W2118600250 countsByYear W21186002502017 @default.
• W2118600250 countsByYear W21186002502018 @default.
• W2118600250 countsByYear W21186002502019 @default.
• W2118600250 countsByYear W21186002502020 @default.
• W2118600250 countsByYear W21186002502021 @default.
• W2118600250 countsByYear W21186002502022 @default.
• W2118600250 crossrefType "journal-article" @default.
• W2118600250 hasAuthorship W2118600250A5006246608 @default.
• W2118600250 hasAuthorship W2118600250A5009928901 @default.
• W2118600250 hasAuthorship W2118600250A5017845437 @default.
• W2118600250 hasAuthorship W2118600250A5021480821 @default.
• W2118600250 hasAuthorship W2118600250A5021546293 @default.
• W2118600250 hasAuthorship W2118600250A5029380319 @default.
• W2118600250 hasAuthorship W2118600250A5039909670 @default.
• W2118600250 hasAuthorship W2118600250A5048249385 @default.
• W2118600250 hasAuthorship W2118600250A5052709713 @default.
• W2118600250 hasAuthorship W2118600250A5068248575 @default.
• W2118600250 hasAuthorship W2118600250A5072526412 @default.
• W2118600250 hasAuthorship W2118600250A5075445107 @default.
• W2118600250 hasConcept C104317684 @default.
• W2118600250 hasConcept C108636557 @default.
• W2118600250 hasConcept C13514818 @default.

• next