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

Mice Lacking beta2-Integrin Function Remain Glucose Tolerant in Spite of Insulin Resistance, Neutrophil Infiltration and Inflammation.

PloS one - 1 Jan 2015

Meakin Paul J, Morrison Vicky L, Sneddon Claire C, Savinko Terhi, Uotila Liisa, Jalicy Susan M, Gabriel Jennie L, Kang Li, Ashford Michael L J, Fagerholm Susanna C

Abstract excerpt

Beta2-integrins are important in leukocyte trafficking and function, and are regulated through the binding of cytoplasmic proteins, such as kindlin-3, to their intracellular domain. Here, we investigate the involvement of beta2-integrins in the regulation of metabolic disease using mice where the kindlin-3 binding site in the beta2-integrin cytoplasmic tail has been mutated (TTT/AAA-beta2-integrin knock-in (KI)...

Read the complete abstract on PubMed

Topics

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

Share to Adipose Tissue, White
Share to CD18 Antigens

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Diet, High-Fat

Share to Insulin Resistance

Share to Macrophages

Share to Neutrophil Infiltration

Share to T-Lymphocytes

Source

Open in PubMed Open full text

Identifiers

PMID: 26405763
DOI: 10.1371/journal.pone.0138872
PMCID: PMC4583187

Genes

IRS1

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

Mice Lacking beta2-Integrin Function Remain Glucose Tolerant in Spite of Insulin Resistance, Neutrophil Infiltration and Inflammation.PMID 26405763Read ↗

Beta2-Integrins and Interacting Proteins in Leukocyte Trafficking, Immune Suppression, and Immunodeficiency DiseaseSemantic proximity Read ↗

Metabolic phenotypes in a Lyz2Cre recombinase mouse modelSemantic proximity Read ↗

Mechanisms and consequences of myeloid adhesome dysfunction in atherogenesisSemantic proximity Read ↗

Gain-of-function mutation in <i>SKAP2</i> leads to type 1 diabetes and broader autoimmunity through hyperactive integrin signaling in myeloid cellsSemantic proximity Read ↗

A New Mouse Model That Spontaneously Develops Chronic Liver Inflammation and Fibrosis.Semantic proximity Read ↗

The C3a anaphylatoxin receptor is a key mediator of insulin resistance and functions by modulating adipose tissue macrophage infiltration and activation.Semantic proximity Read ↗

Genetic deficiency of Itgb2 or ItgaL prevents autoimmune diabetes through distinctly different mechanisms in NOD/LtJ mice.Semantic proximity Read ↗

Platelet-derived β2m regulates age related monocyte/macrophage functions.Semantic proximity Read ↗

Microvascular insulin resistance associates with enhanced muscle glucose disposal in CD36 deficiency.Semantic proximity Read ↗

Integrins in Health and Disease—Suitable Targets for Treatment?Semantic proximity Read ↗

RIPK2 dictates insulin responses to tyrosine kinase inhibitors in obese miceSemantic proximity Read ↗

From the Cover: Lung-Specific Overexpression of Constitutively Active IKK2 Induces Pulmonary and Systemic Inflammations but Not Hypothalamic Inflammation and Glucose Intolerance.Semantic proximity Read ↗

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