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

Leukocyte adhesion deficiency-III is caused by mutations in KINDLIN3 affecting integrin activation.

Nature medicine - 1 Mar 2009

Svensson Lena, Howarth Kimberley, McDowall Alison, Patzak Irene, Evans Rachel, Ussar Siegfried, Moser Markus, Metin Ayse, Fried Mike, Tomlinson Ian, Hogg Nancy

Abstract excerpt

Integrins are the major adhesion receptors of leukocytes and platelets. Beta1 and beta2 integrin function on leukocytes is crucial for a successful immune response and the platelet integrin alpha(IIb)beta3 initiates the process of blood clotting through binding fibrinogen. Integrins on circulating cells bind poorly to their ligands but become active after 'inside-out' signaling through other membrane receptors....

Read the complete abstract on PubMed

Topics

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

Share to Base Sequence
Share to CD18 Antigens

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Leukocyte-Adhesion Deficiency Syndrome

Share to Membrane Proteins

Share to Mutation

Share to Neoplasm Proteins

Share to Reverse Transcriptase Polymerase Chain Reaction

Share to RNA, Messenger

Source

Open in PubMed Open full text

Identifiers

PMID: 19234463
DOI: 10.1038/nm.1931
PMCID: PMC2680140

Genes

FERMT3
RASGRP2

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. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Leukocyte adhesion deficiency-III is caused by mutations in KINDLIN3 affecting integrin activation.PMID 19234463Read ↗

Two mutations in the KINDLIN3 gene of a new leukocyte adhesion deficiency III patient reveal distinct effects on leukocyte function in vitroSemantic proximity Read ↗

Leukocyte adhesion deficiency-I variant syndrome (LAD-Iv, LAD-III): molecular characterization of the defect in an index family.Semantic proximity Read ↗

Loss of Kindlin-3 in LAD-III eliminates LFA-1 but not VLA-4 adhesiveness developed under shear flow conditions.Semantic proximity Read ↗

Novel integrin-dependent platelet malfunction in siblings with leukocyte adhesion deficiency-III (LAD-III) caused by a point mutation in FERMT3.Semantic proximity Read ↗

A new mutation in the KINDLIN‐3 gene ablates integrin‐dependent leukocyte, platelet, and osteoclast function in a patient with leukocyte adhesion deficiency‐IIISemantic proximity Read ↗

The kindlin family: functions, signaling properties and implications for human diseaseSemantic proximity Read ↗

A novel leukocyte adhesion deficiency type III mutation manifests functional importance of the compact FERM domain in kindlin-3.Semantic proximity Read ↗

The Integrin Co-activator Kindlin-3 Is Expressed and Functional in a Non-hematopoietic Cell, the Endothelial CellSemantic proximity Read ↗

A point mutation in KINDLIN3 ablates activation of three integrin subfamilies in humansSemantic proximity Read ↗

Kindlin-3: a new gene involved in the pathogenesis of LAD-III.Semantic proximity Read ↗

LAD-1/variant syndrome is caused by mutations in FERMT3.Semantic proximity Read ↗

Kindlins in FERM adhesionSemantic proximity Read ↗

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