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Selective Occupation by E2F and RB of Loci Expressed by RNA Polymerase III.
Sizer, Rebecca E; Butterfield, Sienna P; Hancocks, Lucy A; Gato De Sousa, Leonor; White, Robert J.
Afiliação
  • Sizer RE; Department of Biology, University of York, York YO10 5DD, UK.
  • Butterfield SP; Department of Biology, University of York, York YO10 5DD, UK.
  • Hancocks LA; Department of Biology, University of York, York YO10 5DD, UK.
  • Gato De Sousa L; Department of Biology, University of York, York YO10 5DD, UK.
  • White RJ; Department of Biology, University of York, York YO10 5DD, UK.
Cancers (Basel) ; 16(3)2024 Jan 23.
Article em En | MEDLINE | ID: mdl-38339234
ABSTRACT
In all cases tested, TFIIIB is responsible for recruiting pol III to its genetic templates. In mammalian cells, RB binds TFIIIB and prevents its interactions with both promoter DNA and pol III, thereby suppressing transcription. As TFIIIB is not recruited to its target genes when bound by RB, the mechanism predicts that pol III-dependent templates will not be occupied by RB; this contrasts with the situation at most genes controlled by RB, where it can be tethered by promoter-bound sequence-specific DNA-binding factors such as E2F. Contrary to this prediction, however, ChIP-seq data reveal the presence of RB in multiple cell types and the related protein p130 at many loci that rely on pol III for their expression, including RMRP, RN7SL, and a variety of tRNA genes. The sets of genes targeted varies according to cell type and growth state. In such cases, recruitment of RB and p130 can be explained by binding of E2F1, E2F4 and/or E2F5. Genes transcribed by pol III had not previously been identified as common targets of E2F family members. The data provide evidence that E2F may allow for the selective regulation of specific non-coding RNAs by RB, in addition to its influence on overall pol III output through its interaction with TFIIIB.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Tipo de estudo: Prognostic_studies Idioma: En Ano de publicação: 2024 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Tipo de estudo: Prognostic_studies Idioma: En Ano de publicação: 2024 Tipo de documento: Article