Absence of p53-Dependent Apoptosis Combined With Nonhomologous End-Joining Deficiency Leads to a Severe Diabetic Phenotype in Mice

Documenti analoghi

• Ku70 Functions in Addition to Nonhomologous End Joining in Pancreatic β-Cells: A Connection to β-Catenin Regulation
  di: Tavana, Omid, et al.
  Pubblicazione: (2013)
• Absence of p53-dependent apoptosis leads to UV radiation hypersensitivity, enhanced immunosuppression and cellular senescence
  di: Tavana, Omid, et al.
  Pubblicazione: (2010)
• A novel Ku70 function in colorectal homeostasis separate from nonhomologous end joining
  di: Puebla-Osorio, N, et al.
  Pubblicazione: (2013)
• Repair of double-strand breaks by nonhomologous end joining in the absence of Mre11
  di: Di Virgilio, Michela, et al.
  Pubblicazione: (2005)
• Deficiency of human BRCA2 leads to impaired homologous recombination but maintains normal nonhomologous end joining
  di: Xia, Fen, et al.
  Pubblicazione: (2001)