Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Induction of endoplasmic reticulum stress by deletion of Grp78 depletes Apc mutant intestinal epithelial stem cells.

Oncogene - 15 Jun 2017

van Lidth de Jeude J F, Meijer B J, Wielenga M C B, Spaan C N, Baan B, Rosekrans S L, Meisner S, Shen Y H, Lee A S, Paton J C, Paton A W, Muncan V, van den Brink G R, Heijmans J

Abstract excerpt

Intestinal epithelial stem cells are highly sensitive to differentiation induced by endoplasmic reticulum (ER) stress. Colorectal cancer develops from mutated intestinal epithelial stem cells. The most frequent initiating mutation occurs in Apc, which results in hyperactivated Wnt signalling. This causes hyperproliferation and reduced sensitivity to chemotherapy, but whether these mutated stem cells are sensitive...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Adenomatous Polyposis Coli Protein
Share to beta Catenin

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Colonic Neoplasms

Share to Endoplasmic Reticulum Chaperone BiP

Share to Endoplasmic Reticulum Stress

Share to Heat-Shock Proteins

Share to Stem Cells

Share to Wnt Signaling Pathway

Source

Open in PubMed Open full text

Identifiers

PMID: 27819675
DOI: 10.1038/onc.2016.326
PMCID: PMC8272398

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Induction of endoplasmic reticulum stress by deletion of Grp78 depletes Apc mutant intestinal epithelial stem cells.PMID 27819675Read ↗

ER stress and the unfolded protein response in gastrointestinal stem cells and carcinogenesisSemantic proximity Read ↗

ER stress causes rapid loss of intestinal epithelial stemness through activation of the unfolded protein response.Semantic proximity Read ↗

Integration of UPRER and Oxidative Stress Signaling in the Control of Intestinal Stem Cell ProliferationSemantic proximity Read ↗

SELENOP modifies sporadic colorectal carcinogenesis and WNT signaling activity through LRP5/6 interactionsSemantic proximity Read ↗

Mitochondrial function controls intestinal epithelial stemness and proliferationSemantic proximity Read ↗

ER stress transcription factor Xbp1 suppresses intestinal tumorigenesis and directs intestinal stem cellsSemantic proximity Read ↗

GRP78/BiP Is Required for Cell Proliferation and Protecting the Inner Cell Mass from Apoptosis during Early Mouse Embryonic DevelopmentSemantic proximity Read ↗

Adenomatous polyposis coli mutants dominantly activate Hsf1-dependent cell stress pathways through inhibition of microtubule dynamics.Semantic proximity Read ↗

Targeted deletion of ER chaperone GRP94 in the liver results in injury, repopulation of GRP94-positive hepatocytes, and spontaneous hepatocellular carcinoma development in aged mice.Semantic proximity Read ↗

Sequential cancer mutations in cultured human intestinal stem cells.Semantic proximity Read ↗

Orphan Gpr182 suppresses ERK-mediated intestinal proliferation during regeneration and adenoma formationSemantic proximity Read ↗

Diet-induced changes in the colonic microenvironment reduce polyp development in APC <sup>Min/+</sup> Msh2 <sup>-/-</sup> mice by triggering ER stressSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.