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Cell cycle control by the thyroid hormone in neuroblastoma cells

AuthorsGarcía-Silva, Susana; Pérez-Juste, Germán; Aranda, Ana
Issue Date2002
CitationToxicology 181-182: 179-182 (2002)
AbstractThe thyroid hormone (T3) blocks proliferation and induces differentiation of neuroblastoma N2a-β cells that overexpress the β1 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) p27Kip1 are found in T3-treated cells. The increased levels of p27Kip1 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-β cells, and progression through the restriction point in the cell cycle is blocked. © 2002 Elsevier Science Ireland Ltd. All rights reserved.
Identifiersdoi: 10.1016/S0300-483X(02)00277-9
issn: 0300-483X
e-issn: 1879-3185
Appears in Collections:(IIBM) Artículos
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