scispace - formally typeset
S

Stefan J. Marciniak

Researcher at University of Cambridge

Publications -  136
Citations -  14384

Stefan J. Marciniak is an academic researcher from University of Cambridge. The author has contributed to research in topics: Unfolded protein response & Endoplasmic reticulum. The author has an hindex of 39, co-authored 124 publications receiving 11975 citations. Previous affiliations of Stefan J. Marciniak include Papworth Hospital & Cambridge University Hospitals NHS Foundation Trust.

Papers
More filters
Journal ArticleDOI

Guidelines for the use and interpretation of assays for monitoring autophagy

Daniel J. Klionsky, +1287 more
- 01 Apr 2012 - 
TL;DR: These guidelines are presented for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
Journal ArticleDOI

CHOP induces death by promoting protein synthesis and oxidation in the stressed endoplasmic reticulum

Stefan J. Marciniak, +8 more
- 15 Dec 2004 - 
TL;DR: This work finds that CHOP directly activates GADD34, which promotes ER client protein biosynthesis by dephosphorylating phospho-Ser 51 of the alpha-subunit of translation initiation factor 2 (eIF2alpha) in stressed cells, and protects cells from ER stress by decreasing client protein load and changing redox conditions within the organelle.
Journal ArticleDOI

Endoplasmic Reticulum Stress Signaling in Disease

Stefan J. Marciniak, +1 more
- 01 Oct 2006 - 
TL;DR: This review addresses aspects of the UPR currently understood to be involved in human disease, including their role in diabetes mellitus, atherosclerosis, and neoplasia.
Journal ArticleDOI

Targeted gene correction of α1-antitrypsin deficiency in induced pluripotent stem cells

Kosuke Yusa, +24 more
- 20 Oct 2011 - 
TL;DR: This work shows that a combination of zinc finger nucleases (ZFNs) and piggyBac technology in human iPSCs can achieve biallelic correction of a point mutation in the α1-antitrypsin (A1AT, also known as SERPINA1) gene that is responsible for α1
Journal ArticleDOI

Paneth cells as a site of origin for intestinal inflammation

Timon E. Adolph, +27 more
- 14 Nov 2013 - 
TL;DR: Genetically and environmentally controlled UPR function within Paneth cells may set the threshold for the development of intestinal inflammation upon hypomorphic ATG16L1 function and implicate ileal Crohn’s disease as a specific disorder ofPaneth cells.