Both the classical and alternative non-homologous end joining pathways contribute to the fusion of drastically shortened telomeres induced by TRF2 overexpression

Lignende værker

• Elevated levels of TRF2 induce telomeric ultrafine anaphase bridges and rapid telomere deletions
  af: Nera, Bernadette, et al.
  Udgivet: (2015)
• The function of classical and alternative non-homologous end-joining pathways in the fusion of dysfunctional telomeres
  af: Rai, Rekha, et al.
  Udgivet: (2010)
• TRF2-RAP1 is required to protect telomeres from engaging in homologous recombination-mediated deletions and fusions
  af: Rai, Rekha, et al.
  Udgivet: (2016)
• Up-Regulation of Telomere-Binding Proteins, TRF1, TRF2, and TIN2 Is Related to Telomere Shortening during Human Multistep Hepatocarcinogenesis
  af: Oh, Bong-Kyeong, et al.
  Udgivet: (2005)
• Nucleostemin inhibits TRF1 dimerization and shortens its dynamic association with the telomere
  af: Meng, Lingjun, et al.
  Udgivet: (2011)