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MeSH Review

Retinoblastoma

 
 
 
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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

References

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