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

The NLRP3 inflammasome is dispensable for ER stress-induced pancreatic β-cell damage in Akita mice.

Biochemical and biophysical research communications - 23 Oct 2015

Wang Jie, Song Mi-Young, Lee Joo Young, Kwon Keun Sang, Park Byung-Hyun

Abstract excerpt

Uncontrolled endoplasmic reticulum (ER) stress activates members of the NOD-like receptor family, which are involved in the pyrin domain containing 3 (NLRP3) inflammasome pathway. This pathway has been proposed to contribute to β-cell dysfunction and death. However, the connection between ER stress and NLRP3 inflammasome activation remains controversial. Here we generated Akita/KO (Ins2(+/C96Y); NLRP3(-/-)) mice...

Read the complete abstract on PubMed

Topics

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

Share to Endoplasmic Reticulum Stress
Share to Inflammasomes

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Insulin-Secreting Cells

Share to Insulin Secretion

Share to Islets of Langerhans

Share to NLR Family, Pyrin Domain-Containing 3 Protein

Share to Protein Denaturation

Share to Tunicamycin

Source

Identifiers

PMID: 26361146
DOI: 10.1016/j.bbrc.2015.09.009

Genes

NLRP3

Variants

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

The NLRP3 inflammasome is dispensable for ER stress-induced pancreatic β-cell damage in Akita mice.PMID 26361146Read ↗

Activation of the NLRP3 inflammasome complex is not required for stress-induced death of pancreatic islets.Semantic proximity Read ↗

An accomplice more than a mere victim: The impact of β-cell ER stress on type 1 diabetes pathogenesisSemantic proximity Read ↗

Endoplasmic reticulum stress, pancreatic β-cell degeneration, and diabetes.Semantic proximity Read ↗

RIPK3-mediated inflammation is a conserved β cell response to ER stressSemantic proximity Read ↗

Targeted disruption of the Chop gene delays endoplasmic reticulum stress–mediated diabetesSemantic proximity Read ↗

Targeted disruption of the Chop gene delays endoplasmic reticulum stress–mediated diabetesSemantic proximity Read ↗

Targeted disruption of the Chop gene delays endoplasmic reticulum stress-mediated diabetes.Semantic proximity Read ↗

Pharmacological Inhibition of Inositol-Requiring Enzyme 1α RNase Activity Protects Pancreatic Beta Cell and Improves Diabetic Condition in Insulin Mutation-Induced Diabetes.Semantic proximity Read ↗

The pore-forming subunit Kir6.1 of the K-ATP channel negatively regulates the NLRP3 inflammasome to control insulin resistance by interacting with NLRP3Semantic proximity Read ↗

Improvement of ER stress-induced diabetes by stimulating autophagy.Semantic proximity Read ↗

<i>Chop</i> / <i>Ddit3</i> depletion in β-cells alleviates ER stress and corrects hepatic steatosisSemantic proximity Read ↗

Inhibition of mTORC1 by ER stress impairs neonatal β-cell expansion and predisposes to diabetes in the Akita mouseSemantic proximity Read ↗

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