A close connection between the PERK and IRE arms of the UPR and the transcriptional regulation of autophagy

•Microarray of HCT116 cells.•Autophagy genes upregulated.•PERK and IRE1 important for regulation. Endoplasmic reticulum (ER) stress is known to lead to activation of both the unfolded protein response (UPR) and autophagy. Although regulatory connections have been identified between the UPR and autop...

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Bibliographic Details
Published in:Biochemical and biophysical research communications 2015-01, Vol.456 (1), p.305-311
Main Authors: Deegan, Shane, Koryga, Izabela, Glynn, Sharon A., Gupta, Sanjeev, Gorman, Adrienne M., Samali, Afshin
Format: Article
Language:English
Subjects:
Adaptor Proteins, Signal Transducing - metabolism
Autophagy
Autophagy - genetics
DNA, Complementary - metabolism
eIF-2 Kinase - metabolism
Endoplasmic Reticulum Stress
Endoribonucleases - metabolism
ER stress
Gene Expression Profiling
Gene Expression Regulation
HCT116 Cells
Humans
IRE1
Membrane Proteins - metabolism
Oligonucleotide Array Sequence Analysis
PERK
Protein-Serine-Threonine Kinases - metabolism
Proteins - metabolism
Proto-Oncogene Proteins - metabolism
Sequestosome-1 Protein
Tumor Suppressor Proteins - metabolism
Unfolded Protein Response
Unfolded protein response (UPR)
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Summary:•Microarray of HCT116 cells.•Autophagy genes upregulated.•PERK and IRE1 important for regulation. Endoplasmic reticulum (ER) stress is known to lead to activation of both the unfolded protein response (UPR) and autophagy. Although regulatory connections have been identified between the UPR and autophagy, it is still unclear to what extent the UPR regulates the genes involved at the different stages of the autophagy pathway. Here, we carried out a microarray analysis of HCT116 cells subjected to ER stress and observed the transcriptional upregulation of a large cohort of autophagy-related genes. Of particular interest, we identified the transcriptional upregulation of the autophagy receptor genes SQSTM1/p62, NBR1 and BNIP3L/NIX in response to ER stress and show that the inhibition of the UPR transmembrane receptors, PERK and IRE1, abrogates this upregulation.
ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2014.11.076