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Disease relevance of Retinoblastoma


Psychiatry related information on Retinoblastoma


High impact information on Retinoblastoma

  • The retinoblastoma (Rb) protein negatively regulates the G1-S transition by binding to the E2F transcription factors, until cyclin-dependent kinases phosphorylate Rb, causing E2F release [7].
  • The retinoblastoma tumor suppressor protein (pRb) regulates gene transcription by binding E2F transcription factors. pRb can recruit several repressor complexes to E2F bound promoters; however, native pRb repressor complexes have not been isolated [8].
  • SAHF formation coincides with the recruitment of heterochromatin proteins and the retinoblastoma (Rb) tumor suppressor to E2F-responsive promoters and is associated with the stable repression of E2F target genes [9].
  • Phosphorylation of E2F-1 modulates its interaction with the retinoblastoma gene product and the adenoviral E4 19 kDa protein [10].
  • Transforming growth factor beta 1 (TGF beta 1) causes G1 growth arrest and the accumulation of unphosphorylated retinoblastoma protein (Rb) in responsive cells [11].

Chemical compound and disease context of Retinoblastoma


Biological context of Retinoblastoma


Anatomical context of Retinoblastoma


Gene context of Retinoblastoma


Analytical, diagnostic and therapeutic context of Retinoblastoma


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  8. Native E2F/RBF complexes contain Myb-interacting proteins and repress transcription of developmentally controlled E2F target genes. Korenjak, M., Taylor-Harding, B., Binné, U.K., Satterlee, J.S., Stevaux, O., Aasland, R., White-Cooper, H., Dyson, N., Brehm, A. Cell (2004) [Pubmed]
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  10. Phosphorylation of E2F-1 modulates its interaction with the retinoblastoma gene product and the adenoviral E4 19 kDa protein. Fagan, R., Flint, K.J., Jones, N. Cell (1994) [Pubmed]
  11. TGF beta inhibition of Cdk4 synthesis is linked to cell cycle arrest. Ewen, M.E., Sluss, H.K., Whitehouse, L.L., Livingston, D.M. Cell (1993) [Pubmed]
  12. Identification of cellular proteins that can interact specifically with the T/E1A-binding region of the retinoblastoma gene product. Kaelin, W.G., Pallas, D.C., DeCaprio, J.A., Kaye, F.J., Livingston, D.M. Cell (1991) [Pubmed]
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  18. Physical interaction of the retinoblastoma protein with human D cyclins. Dowdy, S.F., Hinds, P.W., Louie, K., Reed, S.I., Arnold, A., Weinberg, R.A. Cell (1993) [Pubmed]
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