Transcription Factor CHOP

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  Subject Areas on Research

  • Activation of gadd153 expression through transient cerebral ischemia: evidence that ischemia causes endoplasmic reticulum dysfunction. 
  • Autophagy provides nutrients but can lead to Chop-dependent induction of Bim to sensitize growth factor-deprived cells to apoptosis. 
  • Bortezomib inhibits PKR-like endoplasmic reticulum (ER) kinase and induces apoptosis via ER stress in human pancreatic cancer cells. 
  • Brain trauma induces X-box protein 1 processing indicative of activation of the endoplasmic reticulum unfolded protein response. 
  • Differential effects of unfolded protein response pathways on axon injury-induced death of retinal ganglion cells. 
  • Effect of nitric oxide on endoplasmic reticulum calcium homeostasis, protein synthesis and energy metabolism. 
  • Genes associated with pro-apoptotic and protective mechanisms are affected differently on exposure of neuronal cell cultures to arsenite. No indication for endoplasmic reticulum stress despite activation of grp78 and gadd153 expression. 
  • Modulation of the unfolded protein response in prostate cancer cells by antibody-directed against the carboxyl-terminal domain of GRP78. 
  • Peroxidative stress selectively down-regulates the neuronal stress response activated under conditions of endoplasmic reticulum dysfunction. 
  • Sodium 4-phenylbutyrate protects against liver ischemia reperfusion injury by inhibition of endoplasmic reticulum-stress mediated apoptosis. 
  • The immunity-related GTPase Irgm3 relieves endoplasmic reticulum stress response during coxsackievirus B3 infection via a PI3K/Akt dependent pathway. 
  • The p53-dependent gamma-ray response of GADD45. 
  • Translocations and amplifications of chromosome 12 in liposarcoma demonstrated by the LSI CHOP breakapart rearrangement probe.