Crosstalk Between the Endoplasmic Reticulum and mTOR Signaling

Circ Res. 2019 Jan 4;124(1):9-11. doi: 10.1161/CIRCRESAHA.118.314326.

Authors

Ellen Malovrh^{1

2}, Mirko Völkers^{1

2}

Affiliations

¹ From the Department of Cardiology, Angiology, and Pneumology, University Hospital Heidelberg, University of Heidelberg, Germany (E.M., M.V.).
² DZHK (German Centre for Cardiovascular Research), Partner Site Heidelberg/Mannheim, Germany (E.M., M.V.).

PMID: 30605413
DOI: 10.1161/CIRCRESAHA.118.314326

No abstract available

Keywords: Editorials; cardiac hypertrophy; endoplasmic reticulum; protein biosynthesis; protein folding; proteostasis.

Publication types

Editorial
Research Support, Non-U.S. Gov't
Comment

MeSH terms

Activating Transcription Factor 6
Cardiomegaly
Endoplasmic Reticulum Stress*
Endoplasmic Reticulum*
Humans
Mechanistic Target of Rapamycin Complex 1
Ras Homolog Enriched in Brain Protein
Signal Transduction
TOR Serine-Threonine Kinases

Substances

ATF6 protein, human
Activating Transcription Factor 6
RHEB protein, human
Ras Homolog Enriched in Brain Protein
MTOR protein, human
Mechanistic Target of Rapamycin Complex 1
TOR Serine-Threonine Kinases