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

Inhibitor kappaB-alpha haplotype GTC is associated with susceptibility to acute respiratory distress syndrome in Caucasians.

Critical care medicine - 1 Mar 2007

Zhai Rihong, Zhou Wei, Gong Michelle N, Thompson B Taylor, Su Li, Yu Chuling, Kraft Peter, Christiani David C

Abstract excerpt

OBJECTIVE: The nuclear factor (NF)-kappaB regulates inflammatory responses and plays important roles in the pathogenesis of acute respiratory distress syndrome (ARDS). Inhibitor kappaB-alpha (NFKBIA) inhibits NF-kappaB and controls its activities. The objective was to determine whether polymorphisms in NFKBIA gene would be associated with ARDS development. DESIGN: Prospective cohort of adults with clinical risk...

Read the complete abstract on PubMed

Topics

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

Share to Analysis of Variance
Share to Critical Care

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to I-kappa B Proteins

Share to Intracellular Signaling Peptides and Proteins

Share to NF-kappa B

Share to Repressor Proteins

Share to Respiratory Distress Syndrome

Share to Transcription Factor RelA

Source

Identifiers

PMID: 17235259
DOI: 10.1097/01.CCM.0000256845.92640.38

Genes

NFKBIA

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Inhibitor kappaB-alpha haplotype GTC is associated with susceptibility to acute respiratory distress syndrome in Caucasians.PMID 17235259Read ↗

An NFKB1 promoter insertion/deletion polymorphism influences risk and outcome in acute respiratory distress syndrome among Caucasians.Semantic proximity Read ↗

Correlations of IL-17 and NF-κB gene polymorphisms with susceptibility and prognosis in acute respiratory distress syndrome in a chinese populationSemantic proximity Read ↗

Insertion/deletion polymorphism in the promoter of NFKB1 influences severity but not mortality of acute respiratory distress syndromeSemantic proximity Read ↗

TLR4/NF-κB signaling pathway gene single nucleotide polymorphisms alter gene expression levels and affect ARDS occurrence and prognosis outcomesSemantic proximity Read ↗

Tumor Necrosis Factor Alpha Gene Polymorphisms Increase Susceptibility to Adenovirus Infection in Children and Are Correlated with Severity of Adenovirus-Associated Pneumonia.Semantic proximity Read ↗

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

The association of IL-10-1082G/A gene polymorphism with the risk of acute lung injury/respiratory distress syndrome (ALI/RDS): A meta-analysis.Semantic proximity Read ↗

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

Genetic heterogeneity and risk of acute respiratory distress syndrome.Semantic proximity Read ↗

Heme oxygenase-1 microsatellite polymorphism and haplotypes are associated with the development of acute respiratory distress syndrome.Semantic proximity Read ↗

Identification of haplotype tag single nucleotide polymorphisms within the nuclear factor-κB family genes and their clinical relevance in patients with major trauma.Semantic proximity Read ↗

Polymorphism in interferon alpha/beta receptor contributes to glucocorticoid response and outcome of ARDS and COVID-19Semantic proximity Read ↗

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