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

Platelet count mediates the contribution of a genetic variant in LRRC16A to ARDS risk.

Chest - 1 Mar 2015

Wei Yongyue, Wang Zhaoxi, Su Li, Chen Feng, Tejera Paula, Bajwa Ednan K, Wurfel Mark M, Lin Xihong, Christiani David C

Abstract excerpt

BACKGROUND: Platelets are believed to be critical in pulmonary-origin ARDS as mediators of endothelial damage through their interactions with fibrinogen and multiple signal transduction pathways. A prior meta-analysis identified five loci for platelet count (PLT): BAD, LRRC16A, CD36, JMJD1C, and SLMO2. This study aims to validate the quantitative trait loci (QTLs) of PLT within BAD, LRRC16A, CD36, JMJD1C, and...

Read the complete abstract on PubMed

Topics

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

Share to Aged, 80 and over
Share to Critical Illness

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Endothelium, Vascular

Share to Microfilament Proteins

Share to Platelet Count

Share to Respiratory Distress Syndrome

Share to Signal Transduction

Share to Young Adult

Source

Open in PubMed Open full text

Identifiers

PMID: 25254322
DOI: 10.1378/chest.14-1246
PMCID: PMC4347530

Genes

BAD

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 4 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Platelet count mediates the contribution of a genetic variant in LRRC16A to ARDS risk.PMID 25254322Read ↗

A Missense Genetic Variant in LRRC16A/CARMIL1 Improves Acute Respiratory Distress Syndrome Survival by Attenuating Platelet Count Decline.Semantic proximity Read ↗

Inflammation and immune-related candidate gene associations with acute lung injury susceptibility and severity: a validation study.Semantic proximity Read ↗

Genome-wide association study of susceptibility to acute respiratory distress syndrome.Semantic proximity Read ↗

Genome-wide association study of susceptibility to acute respiratory distress syndromeSemantic proximity Read ↗

The genomic landscape of Acute Respiratory Distress Syndrome: a meta-analysis by information content of genome-wide studies of the host responseSemantic proximity Read ↗

A genome- and phenome-wide association study to identify genetic variants influencing platelet count and volume and their pleiotropic effects.Semantic proximity Read ↗

Integrative Genomic Analysis and Functional Studies Reveal GP5, GRN, MPO and MCAM as Causal Protein Biomarkers for Platelet TraitsSemantic proximity Read ↗

Rare coding variants pinpoint genes that control human hematological traits.Semantic proximity Read ↗

A functional genomics approach reveals novel quantitative trait loci associated with platelet signaling pathways.Semantic proximity Read ↗

The Genetic Landscape of Plasma P-Selectin Glycoprotein Ligand levels and Bidirectional Mendelian Randomization to Assess Role in Proinflammatory Cytokine levelsSemantic proximity Read ↗

NETWORK ANALYSIS OF SINGLE-NUCLEOTIDE POLYMORPHISMS ASSOCIATED WITH ABERRANT INFLAMMATION IN TRAUMA PATIENTS SUGGESTS A ROLE FOR VESICLE-ASSOCIATED INFLAMMATORY PROGRAMS INVOLVING CD55.Semantic proximity Read ↗

Genomic Evidence Links Inflammation to Residual Pulmonary Vascular Obstruction and Risk of Pulmonary Embolism RecurrenceSemantic proximity Read ↗

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