Posttranslational modification of mammalian AP endonuclease (APE1).
A key issue in studying mammalian DNA base excision repair is how its component proteins respond to a plethora of cell-signaling mediators invoked by DNA damage and stress-inducing agents such as reactive oxygen species, and how the actions of individual BER proteins are attributed to cell survival or apoptotic/necrotic death. This article reviews the past and recent progress on posttranslational modification (PTM) of mammalian apurinic/apyrimidinic (AP) endonuclease 1 (APE1).
Busso
Carlos S
CS
Department of Otorhinolaryngology and Stanley S. Scott Cancer Center, Louisiana State University Health Sciences Center, New Orleans, LA 70112, USA.
Lake
Michael W
MW
Izumi
Tadahide
T
D000107:Acetylation; D000818:Animals; D043603:DNA-(Apurinic or Apyrimidinic Site) Lyase / Q000737:chemistry / Q000235:genetics / Q000378:metabolism*; D006801:Humans; D008958:Models, Molecular; D010766:Phosphorylation; D011499:Protein Processing, Post-Translational; D054875:Ubiquitination
D043603:DNA-(Apurinic or Apyrimidinic Site) Lyase