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

Deficiency of Group VIA Phospholipase A2 (iPLA2β) Renders Susceptibility for Chemical-Induced Colitis.

Digestive diseases and sciences - 1 Dec 2015

Jiao Li, Inhoffen Johannes, Gan-Schreier Hongying, Tuma-Kellner Sabine, Stremmel Wolfgang, Sun Zhiwei, Chamulitrat Walee

Abstract excerpt

BACKGROUND: Inflammatory bowel disease results from a combination of dysfunction of intestinal epithelial barrier and dysregulation of mucosal immune system. iPLA2β has multiple homeostatic functions and shown to play a role in membrane remodeling, cell proliferation, monocyte chemotaxis, and apoptosis. The latter may render chronic inflammation and susceptibility for acute injury. AIMS: We aim to evaluate...

Read the complete abstract on PubMed

Topics

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

Share to Apoptosis
Share to Colitis

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Dextran Sulfate

Share to Group VI Phospholipases A2

Share to Immunohistochemistry

Share to Mice, Knockout

Source

Identifiers

PMID: 26182903
DOI: 10.1007/s10620-015-3807-5

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

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

Deficiency of Group VIA Phospholipase A2 (iPLA2β) Renders Susceptibility for Chemical-Induced Colitis.PMID 26182903Read ↗

Sensitization to autoimmune hepatitis in group VIA calcium-independent phospholipase A2-null mice led to duodenal villous atrophy with apoptosis, goblet cell hyperplasia and leaked bile acids.Semantic proximity Read ↗

IQ Motif-Containing GTPase-Activating Protein 2 (IQGAP2) Is a Novel Regulator of Colonic Inflammation in MiceSemantic proximity Read ↗

Akkermansia deficiency and mucin depletion are implicated in intestinal barrier dysfunction as earlier event in the development of inflammation in interleukin-10-deficient miceSemantic proximity Read ↗

Analysis of candidate colitis genes in the Gdac1 locus of mice deficient in glutathione peroxidase-1 and -2.Semantic proximity Read ↗

Zebrafish modeling of intestinal injury, bacterial exposures and medications defines epithelial in vivo responses relevant to human inflammatory bowel diseaseSemantic proximity Read ↗

Neuroaxonal Dystrophy Caused by Group VIA Phospholipase A<sub>2</sub>Deficiency in Mice: A Model of Human Neurodegenerative DiseaseSemantic proximity Read ↗

The roles of sPLA2-IIA (Pla2g2a) in cancer of the small and large intestine.Semantic proximity Read ↗

Ace Deficiency Induces Intestinal Inflammation in ZebrafishSemantic proximity Read ↗

Differential susceptibility to colonic ulceration in mice with genetic deletion of Prostaglandin E synthaseSemantic proximity Read ↗

Aberrant mucin assembly in mice causes endoplasmic reticulum stress and spontaneous inflammation resembling ulcerative colitis.Semantic proximity Read ↗

Eosinophil-derived COX-2 protects against experimental colitis through the PGE <sub>2</sub> -IL-22 axisSemantic proximity Read ↗

Genotype-specific immune responses at the intestinal barrier predispose to colitis in mouse models of chronic granulomatous disease.Semantic proximity Read ↗

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