Characterization of a human 12/15-lipoxygenase promoter variant associated with atherosclerosis identifies vimentin as a promoter binding protein.

doi:10.1371/journal.pone.0042417

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

Community

Back to search

Article

Characterization of a human 12/15-lipoxygenase promoter variant associated with atherosclerosis identifies vimentin as a promoter binding protein.

PloS one - 1 Jan 2012

Samanta Susmita, Anderson Kurtis, Moran Sean, Hawke David, Gorenstein David, Fornage Myriam

Abstract excerpt

BACKGROUND: Sequence variation in the human 12/15 lipoxygenase (ALOX15) has been associated with atherosclerotic disease. We functionally characterized an ALOX15 promoter polymorphism, rs2255888, previously associated with carotid plaque burden. METHODOLOGY/PRINCIPAL FINDINGS: We demonstrate specific in vitro and in vivo binding of the cytoskeletal protein, vimentin, to the ALOX15 promoter. We show that the two...

Read the complete abstract on PubMed

Topics

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

Share to Arachidonate 15-Lipoxygenase

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Atherosclerosis

Share to Luciferases

Share to MCF-7 Cells

Share to NIH 3T3 Cells

Share to Oligonucleotides

Share to Salts

Share to Vimentin

Source

Open in PubMed Open full text

Identifiers

PMID: 22879973
DOI: 10.1371/journal.pone.0042417
PMCID: PMC3413658

Genes

ALOX15

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

Characterization of a human 12/15-lipoxygenase promoter variant associated with atherosclerosis identifies vimentin as a promoter binding protein.PMID 22879973Read ↗

Functional polymorphism in ALOX15 results in increased allele-specific transcription in macrophages through binding of the transcription factor SPI1.Semantic proximity Read ↗

FURIN Expression in Vascular Endothelial Cells Is Modulated by a Coronary Artery Disease-Associated Genetic Variant and Influences Monocyte Transendothelial Migration.Semantic proximity Read ↗

15-Lipoxygenase gene variants are associated with carotid plaque but not carotid intima-media thickness.Semantic proximity Read ↗

Influence of a Coronary Artery Disease-Associated Genetic Variant on FURIN Expression and Effect of Furin on Macrophage Behavior.Semantic proximity Read ↗

No association of two functional polymorphisms in human ALOX15 with myocardial infarction.Semantic proximity Read ↗

A near null variant of 12/15-LOX encoded by a novel SNP in ALOX15 and the risk of coronary artery disease.Semantic proximity Read ↗

Effects of mutant p53 expression on human 15-lipoxygenase-promoter activity and murine 12/15-lipoxygenase gene expression: Evidence that 15-lipoxygenase is a mutator geneSemantic proximity Read ↗

Association of polymorphisms in the ALOX15B gene with coronary artery disease.Semantic proximity Read ↗

Functional characterization of annexin A5 gene promoter allelic variants.Semantic proximity Read ↗

Genomic organization, amplification, fine mapping, and intragenic polymorphisms of the human hemidesmosomal tetraspanin CD151 gene.Semantic proximity Read ↗

Two SNPs in the promoter region of the CTLA-4 gene affect binding of transcription factors and are associated with human myasthenia gravis.Semantic proximity Read ↗

Phenotypic and molecular characterization of the exon 13-15 duplication in LDLR: Implications for familial hypercholesterolemia.Semantic proximity Read ↗

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