Literature DB >> 1321348

Retinoblastoma protein switches the E2F site from positive to negative element.

S J Weintraub1, C A Prater, D C Dean.   

Abstract

Originally E2F sites were identified as elements in the promoters of adenovirus early genes that are necessary for activation of these genes by the early protein E1a (ref. 1). E2F promoter elements have been shown to be important for transcriptional activation of several genes critical for progression through the cell cycle. During the G1 phase of the cell cycle, the E2F protein forms a complex with the cell-cycle protein Rb (ref. 5) and it has been suggested that this binding of Rb to E2F inactivates E2F (ref. 5). Here we show that Rb-E2F is an active complex that, when bound to the E2F site, inhibits the activity of other promoter elements and thus silences transcription. We propose that the ability of this complex to inhibit transcription is integral to the function of Rb and provide evidence that E2F is a positive element in the absence of an active form of Rb. It has been shown that binding of Rb to E2F depends on the phosphorylation state of Rb (only the underphosphorylated form binds) and that the phosphorylation state of Rb changes during progression through the cell cycle. We therefore suggest that the E2F site alternates between a positive and negative element with the phosphorylation/dephosphorylation cycle of Rb. This cyclic activity may be responsible for activating and then inhibiting genes during the cell cycle.

Entities:  

Mesh:

Substances:

Year:  1992        PMID: 1321348     DOI: 10.1038/358259a0

Source DB:  PubMed          Journal:  Nature        ISSN: 0028-0836            Impact factor:   49.962


  216 in total

1.  A mechanism for Rb/p130-mediated transcription repression involving recruitment of the CtBP corepressor.

Authors:  A R Meloni; E J Smith; J R Nevins
Journal:  Proc Natl Acad Sci U S A       Date:  1999-08-17       Impact factor: 11.205

2.  Apoptosis induced by the nuclear death domain protein p84N5 is inhibited by association with Rb protein.

Authors:  J Doostzadeh-Cizeron; R Evans; S Yin; D W Goodrich
Journal:  Mol Biol Cell       Date:  1999-10       Impact factor: 4.138

3.  Distinct cellular factors regulate the c-myb promoter through its E2F element.

Authors:  M R Campanero; M Armstrong; E Flemington
Journal:  Mol Cell Biol       Date:  1999-12       Impact factor: 4.272

4.  E2F is required to prevent inappropriate S-phase entry of mammalian cells.

Authors:  S He; B L Cook; B E Deverman; U Weihe; F Zhang; V Prachand; J Zheng; S J Weintraub
Journal:  Mol Cell Biol       Date:  2000-01       Impact factor: 4.272

5.  Mutagenesis of the pRB pocket reveals that cell cycle arrest functions are separable from binding to viral oncoproteins.

Authors:  F A Dick; E Sailhamer; N J Dyson
Journal:  Mol Cell Biol       Date:  2000-05       Impact factor: 4.272

6.  Regulation of endogenous E2F1 stability by the retinoblastoma family proteins.

Authors:  F Martelli; D M Livingston
Journal:  Proc Natl Acad Sci U S A       Date:  1999-03-16       Impact factor: 11.205

7.  Structural basis of DNA recognition by the heterodimeric cell cycle transcription factor E2F-DP.

Authors:  N Zheng; E Fraenkel; C O Pabo; N P Pavletich
Journal:  Genes Dev       Date:  1999-03-15       Impact factor: 11.361

8.  Histone deacetylase-dependent transcriptional repression by pRB in yeast occurs independently of interaction through the LXCXE binding cleft.

Authors:  B K Kennedy; O W Liu; F A Dick; N Dyson; E Harlow; M Vidal
Journal:  Proc Natl Acad Sci U S A       Date:  2001-07-10       Impact factor: 11.205

9.  Transcriptional repression by the retinoblastoma protein through the recruitment of a histone methyltransferase.

Authors:  L Vandel; E Nicolas; O Vaute; R Ferreira; S Ait-Si-Ali; D Trouche
Journal:  Mol Cell Biol       Date:  2001-10       Impact factor: 4.272

Review 10.  Integration of the pRB and p53 cell cycle control pathways.

Authors:  C L Stewart; A M Soria; P A Hamel
Journal:  J Neurooncol       Date:  2001-02       Impact factor: 4.130

View more

北京卡尤迪生物科技股份有限公司 © 2022-2023.