An Investigation into 53BP1 Complex Formation

作者: Kevin C. Roche , Noel F. Lowndes

DOI: 10.1007/978-0-387-69116-9_3

关键词:

摘要: Loss of the control over cellular proliferation can lead to cell death or result in abnormal characteristic cancerous state. Among controls used achieve normal is DNA damage checkpoint pathway that monitors genome integrity (Hartwell and Kastan 1994). 53BP1 was identified as a protein interacts with DNA-binding core domain tumor suppressor p53. The p53-binding region maps C-terminal BRCT domains which are homologous those found breast cancer BRCA1 other proteins involved response, notably budding yeast Rad9. In addition its recently reported role sensing double strand breaks, believed have roles, currently ill understood, many aspects metabolism ranging from transcription class switch recombination 'mediating' response (Chai et al. 1999; Huyen 2004; Sengupta Ward 2004). Here, we investigate complex formation. We oligomerization show this not dependent on presence disulfide bridges.

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