ER stress and distinct outputs of the IRE1α RNase control proliferation and senescence in response to oncogenic Ras.
Publication/Presentation Date
9-12-2017
Abstract
Oncogenic Ras causes proliferation followed by premature senescence in primary cells, an initial barrier to tumor development. The role of endoplasmic reticulum (ER) stress and the unfolded protein response (UPR) in regulating these two cellular outcomes is poorly understood. During ER stress, the inositol requiring enzyme 1α (IRE1α) endoribonuclease (RNase), a key mediator of the UPR, cleaves
Volume
114
Issue
37
First Page
9900
Last Page
9905
ISSN
1091-6490
Published In/Presented At
Blazanin, N., Son, J., Craig-Lucas, A. B., John, C. L., Breech, K. J., Podolsky, M. A., & Glick, A. B. (2017). ER stress and distinct outputs of the IRE1α RNase control proliferation and senescence in response to oncogenic Ras. Proceedings of the National Academy of Sciences of the United States of America, 114(37), 9900–9905. https://doi.org/10.1073/pnas.1701757114
Disciplines
Medicine and Health Sciences
PubMedID
28847931
Department(s)
Department of Surgery, Fellows and Residents
Document Type
Article