http://www.cnr.it/ontology/cnr/individuo/prodotto/ID21045
RET/papillary thyroid carcinoma oncogenic signaling through the Rap1 small GTPase. (Articolo in rivista)
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- RET/papillary thyroid carcinoma oncogenic signaling through the Rap1 small GTPase. (Articolo in rivista) (literal)
- Anno
- 2007-01-01T00:00:00+01:00 (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
- 10.1158/0005-5472.CAN-06-0981 (literal)
- Alternative label
De Falco V; Castellone MD; De Vita G; Cirafici AM; Hershman JM; Guerrero C; Fusco A; Melillo RM; Santoro M. (2007)
RET/papillary thyroid carcinoma oncogenic signaling through the Rap1 small GTPase.
in Cancer research (Chic. Ill.); American association for cancer research, Philadelphia [Pa.] (Stati Uniti d'America)
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- De Falco V; Castellone MD; De Vita G; Cirafici AM; Hershman JM; Guerrero C; Fusco A; Melillo RM; Santoro M. (literal)
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- Istituto di Endocrinologia ed Oncologia Sperimentale del CNR ''G.Salvatore'', c/o Dipartimento di Biologia e Patologia Cellulare e Molecolare, Universita' Federico II, Naples, Italy;(De Falco V-Castellone M.D.-De Vita G-Cirafici A.M.-Fusco A.-Melillo R.M.-Santoro M.)
Endocrinology and Metabolism Division, University of California at Los Angeles School of Medicine, Los Angeles, California(Hershman JM)
Instituto de Biologia Molecular y Celular del Cancer, Centro de Investigacion del Cancer (Consejo Superior de Investigaciones Científicas-Universidad de Salamanca), University of Salamanca, Salamanca, Spain (Guerrero C.) (literal)
- Titolo
- RET/papillary thyroid carcinoma oncogenic signaling through the Rap1 small GTPase. (literal)
- Abstract
- RET/papillary thyroid carcinoma (PTC) oncoproteins result from the in-frame fusion of the RET receptor tyrosine kinase with protein dimerization motifs encoded by heterologous genes. Here, we show that RET/PTC1 activates the Rap1 small GTPase. The activation of Rap1 was dependent on the phosphorylation of RET Tyr(1062). RET/PTC1 recruited a complex containing growth factor receptor binding protein 2-associated binding protein 1 (Gab1), CrkII (v-crk sarcoma virus CT10 oncogene homologue II), and C3G (Rap guanine nucleotide exchange factor 1). By using dominant-negative and small interfering duplex (small interfering RNA) oligonucleotides, we show that RET/PTC1-mediated Rap1 activation was dependent on CrkII, C3G, and Gab1. Activation of Rap1 was involved in the RET/PTC1-mediated stimulation of the BRAF kinase and the p42/p44 mitogen-activated protein kinases. Proliferation and stress fiber formation of RET/PTC1-expressing PC Cl 3 thyroid follicular cells were inhibited by the dominant-negative Rap1(N17) and by Rap1-specific GTPase-activating protein. Thus, Rap1 is a downstream effector of RET/PTC and may contribute to the transformed phenotype of RET/PTC-expressing thyrocytes. (literal)
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