Paradoxical roles of ATF6α and ATF6β in modulating disease severity caused by mutations in collagen X
Open Access
- 1 September 2018
- journal article
- research article
- Published by Elsevier in Matrix Biology
- Vol. 70, 50-71
Abstract
No abstract availableKeywords
Funding Information
- Seventh Framework Programme (602300)
- The University of Manchester
- The Wellcome Trust Centre for Cell-Matrix Research (203128/Z/16/Z)
This publication has 50 references indexed in Scilit:
- Armet/Manf and Creld2 are components of a specialized ER stress response provoked by inappropriate formation of disulphide bonds: implications for genetic skeletal diseasesHuman Molecular Genetics, 2013
- ATF6α/β-mediated adjustment of ER chaperone levels is essential for development of the notochord in medaka fishMolecular Biology of the Cell, 2013
- Activating Transcription Factor 6 Limits Intracellular Accumulation of Mutant α1-Antitrypsin Z and Mitochondrial Damage in Hepatoma CellsJournal of Biological Chemistry, 2011
- The Endoplasmic Reticulum Stress Sensor, ATF6α, Protects against Neurotoxin-induced Dopaminergic Neuronal DeathJournal of Biological Chemistry, 2011
- Induction of Liver Steatosis and Lipid Droplet Formation in ATF6α-Knockout Mice Burdened with Pharmacological Endoplasmic Reticulum StressMolecular Biology of the Cell, 2010
- Roles for Endoplasmic Reticulum–Associated Degradation and the Novel Endoplasmic Reticulum Stress Response Gene Derlin-3 in the Ischemic HeartCirculation Research, 2010
- The unfolded protein response and its relevance to connective tissue diseasesCell and tissue research, 2009
- Ischemia Activates the ATF6 Branch of the Endoplasmic Reticulum Stress ResponseJournal of Biological Chemistry, 2009
- UPR Pathways Combine to Prevent Hepatic Steatosis Caused by ER Stress-Mediated Suppression of Transcriptional Master RegulatorsDevelopmental Cell, 2008
- XBP1 mRNA Is Induced by ATF6 and Spliced by IRE1 in Response to ER Stress to Produce a Highly Active Transcription FactorCell, 2001