Down-regulation of PERK enhances resistance to ionizing radiation
Journal Article
·
· Biochemical and Biophysical Research Communications
Highlights: •PERK enhances the sensitivity of cancer cells to ionizing radiation. •Down-regulation of PERK results in enhanced DNA repair. •Ionizing radiation-induced apoptosis is inhibited in PERK-down regulated cancer cells. -- Abstract: Although, ionizing radiation (IR) has been implicated to cause stress in endoplasmic reticulum (ER), how ER stress signaling and major ER stress sensors modulate cellular response to IR is unclear. Protein kinase RNA-like endoplasmic reticulum kinase (PERK) is an ER transmembrane protein which initiates unfolded protein response (UPR) or ER stress signaling when ER homeostasis is disturbed. Here, we report that down-regulation of PERK resulted in increased clonogenic survival, enhanced DNA repair and reduced apoptosis in irradiated cancer cells. Our study demonstrated that PERK has a role in sensitizing cancer cells to IR.
- OSTI ID:
- 22242177
- Journal Information:
- Biochemical and Biophysical Research Communications, Journal Name: Biochemical and Biophysical Research Communications Journal Issue: 1 Vol. 441; ISSN 0006-291X; ISSN BBRCA9
- Country of Publication:
- United States
- Language:
- English
Similar Records
The structure of the PERK kinase domain suggests the mechanism for its activation
The structure of the PERK kinase domain suggests the mechanism for its activation
Multivesicular body formation enhancement and exosome release during endoplasmic reticulum stress
Journal Article
·
Sun May 01 00:00:00 EDT 2011
· Acta Crystallographica. Section D: Biological Crystallography
·
OSTI ID:22351226
The structure of the PERK kinase domain suggests the mechanism for its activation
Journal Article
·
Fri Aug 31 00:00:00 EDT 2012
· Acta Crystallogr. D
·
OSTI ID:1040896
Multivesicular body formation enhancement and exosome release during endoplasmic reticulum stress
Journal Article
·
Thu Nov 10 23:00:00 EST 2016
· Biochemical and Biophysical Research Communications
·
OSTI ID:22696685