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oai:repisalud.isciii.es:20.500.12105/272422026-02-21T01:16:14Zcom_20.500.12105_2173com_20.500.12105_2051col_20.500.12105_19597

00925njm 22002777a 4500 dc Garcia-Silva, Susana author Perez-Juste, German author Aranda, Ana author 2002-12-27 The thyroid hormone (T3) blocks proliferation and induces differentiation of neuroblastoma N2a-beta cells that overexpress the beta 1 isoform of the T3 receptor. An element in the region responsible for premature termination of transcription mediates a rapid repression of c-myc gene expression by T3. The hormone also causes a decrease of cyclin D1 gene transcription, and is able to antagonize the activation of the cyclin D1 promoter by Ras. In addition, a strong and sustained increase of the levels of the cyclin kinase inhibitor (CKI) p27(Kip1) are found in T3-treated cells. The increased levels of p27(Kip1) lead to a marked inhibition of the kinase activity of the cyclin-CDK2 complexes. As a consequence of these changes, retinoblastoma proteins are hypophosphorylated in T3-treated N2a-beta cells, and progression through the restriction point in the cell cycle is blocked. Toxicology . 2002 Dec 27:181-182:179-82. TOXICOLOGY 12505306 https://hdl.handle.net/20.500.12105/27242 thyroid hormone cell cycle c-myc cyclin D1 p27Kip1 cyclin-dependent kinase-2 Cell cycle control by the thyroid hormone in neuroblastoma cells.