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• W57595890 abstract "Research Article3 June 1996free access Molecular heterogeneity of RET loss of function in Hirschsprung's disease. F. Carlomagno F. Carlomagno Centro di Endocrinologia ed Oncologia Sperimentale del CNR, Dipartimento di Biologia e Patologia Cellulare e Molecolare, Università di Napoli, Italy. Search for more papers by this author G. De Vita G. De Vita Centro di Endocrinologia ed Oncologia Sperimentale del CNR, Dipartimento di Biologia e Patologia Cellulare e Molecolare, Università di Napoli, Italy. Search for more papers by this author M. T. Berlingieri M. T. Berlingieri Centro di Endocrinologia ed Oncologia Sperimentale del CNR, Dipartimento di Biologia e Patologia Cellulare e Molecolare, Università di Napoli, Italy. Search for more papers by this author V. de Franciscis V. de Franciscis Centro di Endocrinologia ed Oncologia Sperimentale del CNR, Dipartimento di Biologia e Patologia Cellulare e Molecolare, Università di Napoli, Italy. Search for more papers by this author R. M. Melillo R. M. Melillo Centro di Endocrinologia ed Oncologia Sperimentale del CNR, Dipartimento di Biologia e Patologia Cellulare e Molecolare, Università di Napoli, Italy. Search for more papers by this author V. Colantuoni V. Colantuoni Centro di Endocrinologia ed Oncologia Sperimentale del CNR, Dipartimento di Biologia e Patologia Cellulare e Molecolare, Università di Napoli, Italy. Search for more papers by this author M. H. Kraus M. H. Kraus Centro di Endocrinologia ed Oncologia Sperimentale del CNR, Dipartimento di Biologia e Patologia Cellulare e Molecolare, Università di Napoli, Italy. Search for more papers by this author P. P. Di Fiore P. P. Di Fiore Centro di Endocrinologia ed Oncologia Sperimentale del CNR, Dipartimento di Biologia e Patologia Cellulare e Molecolare, Università di Napoli, Italy. Search for more papers by this author A. Fusco A. Fusco Centro di Endocrinologia ed Oncologia Sperimentale del CNR, Dipartimento di Biologia e Patologia Cellulare e Molecolare, Università di Napoli, Italy. Search for more papers by this author M. Santoro M. Santoro Centro di Endocrinologia ed Oncologia Sperimentale del CNR, Dipartimento di Biologia e Patologia Cellulare e Molecolare, Università di Napoli, Italy. Search for more papers by this author F. Carlomagno F. Carlomagno Centro di Endocrinologia ed Oncologia Sperimentale del CNR, Dipartimento di Biologia e Patologia Cellulare e Molecolare, Università di Napoli, Italy. Search for more papers by this author G. De Vita G. De Vita Centro di Endocrinologia ed Oncologia Sperimentale del CNR, Dipartimento di Biologia e Patologia Cellulare e Molecolare, Università di Napoli, Italy. Search for more papers by this author M. T. Berlingieri M. T. Berlingieri Centro di Endocrinologia ed Oncologia Sperimentale del CNR, Dipartimento di Biologia e Patologia Cellulare e Molecolare, Università di Napoli, Italy. Search for more papers by this author V. de Franciscis V. de Franciscis Centro di Endocrinologia ed Oncologia Sperimentale del CNR, Dipartimento di Biologia e Patologia Cellulare e Molecolare, Università di Napoli, Italy. Search for more papers by this author R. M. Melillo R. M. Melillo Centro di Endocrinologia ed Oncologia Sperimentale del CNR, Dipartimento di Biologia e Patologia Cellulare e Molecolare, Università di Napoli, Italy. Search for more papers by this author V. Colantuoni V. Colantuoni Centro di Endocrinologia ed Oncologia Sperimentale del CNR, Dipartimento di Biologia e Patologia Cellulare e Molecolare, Università di Napoli, Italy. Search for more papers by this author M. H. Kraus M. H. Kraus Centro di Endocrinologia ed Oncologia Sperimentale del CNR, Dipartimento di Biologia e Patologia Cellulare e Molecolare, Università di Napoli, Italy. Search for more papers by this author P. P. Di Fiore P. P. Di Fiore Centro di Endocrinologia ed Oncologia Sperimentale del CNR, Dipartimento di Biologia e Patologia Cellulare e Molecolare, Università di Napoli, Italy. Search for more papers by this author A. Fusco A. Fusco Centro di Endocrinologia ed Oncologia Sperimentale del CNR, Dipartimento di Biologia e Patologia Cellulare e Molecolare, Università di Napoli, Italy. Search for more papers by this author M. Santoro M. Santoro Centro di Endocrinologia ed Oncologia Sperimentale del CNR, Dipartimento di Biologia e Patologia Cellulare e Molecolare, Università di Napoli, Italy. Search for more papers by this author Author Information F. Carlomagno1, G. De Vita1, M. T. Berlingieri1, V. Franciscis1, R. M. Melillo1, V. Colantuoni1, M. H. Kraus1, P. P. Di Fiore1, A. Fusco1 and M. Santoro1 1Centro di Endocrinologia ed Oncologia Sperimentale del CNR, Dipartimento di Biologia e Patologia Cellulare e Molecolare, Università di Napoli, Italy. The EMBO Journal (1996)15:2717-2725https://doi.org/10.1002/j.1460-2075.1996.tb00632.x PDFDownload PDF of article text and main figures. ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinked InMendeleyWechatReddit Figures & Info The RET proto-oncogene encodes a receptor with tyrosine kinase activity (RET) that is involved in several neoplastic and non-neoplastic diseases. Oncogenic activation of RET, achieved by different mechanisms, is detected in a sizeable fraction of human thyroid tumors, as well as in multiple endocrine neoplasia types 2A and 2B (MEN2A and MEN2B) and familial medullary thyroid carcinoma tumoral syndromes. Germline mutations of RET have also been associated with a non-neoplastic disease, the congenital colonic aganglionosis, i.e. Hirschsprung's disease (HSCR). To analyse the impact of HSCR mutations on RET function, we have introduced into wild-type RET and activated RET(MEN2A) and RET(MEN2B) alleles three missense mutations associated with HSCR. Here we show that the three mutations caused a loss of function of RET when assayed in two model cell systems, NIH 3T3 and PC12 cells. The effect of different HSCR mutations was due to different molecular mechanisms. The HSCR972 (Arg972–>Gly) mutation, mapping in the intracytoplasmic region of RET, impaired its tyrosine kinase activity, while two extracellular mutations, HSCR32 (Ser32–>Leu) and HSCR393 (Phe393–>Leu), inhibited the biological activity of RET by impairing the correct maturation of the RET protein and its transport to the cell surface. Previous ArticleNext Article Volume 15Issue 111 June 1996In this issue RelatedDetailsLoading ..." @default.
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• W57595890 title "Molecular heterogeneity of RET loss of function in Hirschsprung's disease." @default.
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