ArticleGenes and immunity2008
Prep1/Pbx2 complexes regulate CCL2 expression through the -2578 guanine polymorphism.
Article in Genes and immunity, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 31 citations in OpenAlex.
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- Host gene-encoded severe lung TB: from genes to the potential pathways.Genes and immunity · 2012Article
- The rs1024611 regulatory region polymorphism is associated with CCL2 allelic expression imbalance.PloS one · 2012Article
- Single nucleotide polymorphism in gene encoding transcription factor Prep1 is associated with HIV-1-associated dementia.PloS one · 2012Article
- Early emergence and selection of a SIV-LTR C/EBP site variant in SIV-infected macaques that increases virus infectivity.PloS one · 2012Article
- Inherited variants in the chemokine CCL2 gene and prostate cancer aggressiveness in a Caucasian cohort.Clinical cancer research : an official journal of the American Association for Cancer Research · 2011Article
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- Regulation of SIV mac 239 basal long terminal repeat activity and viral replication in macrophages: functional roles of two CCAAT/enhancer-binding protein beta sites in activation and interferon beta-mediated suppression.The Journal of biological chemistry · 2010Article
- Heme oxygenase-1 microsatellite polymorphism and haplotypes are associated with the development of acute respiratory distress syndrome.Intensive care medicine · 2009Article
- Confirmation of differential binding of Interferon Regulatory Factor-1 (IRF-1) to the functional and HIV disease-influencing -2578 A/G polymorphism in CCL2.Genes and immunity · 2009Article
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4 authors at 3 institutions in 1 country.
Funding
Abstract
CC-chemokine ligand 2 (CCL2) is the major chemoattractant protein that recruits monocytes to sites of inflammation and increased expression of CCL2 is associated with numerous inflammatory diseases including human immunodeficiency virus-associated dementia (HIV-D). The -2578 guanine polymorphism in the CCL2 promoter has been associated with increased expression of CCL2 as well as pathogenesis of HIV-D; however, the molecular mechanism of regulation is unknown. We propose a molecular model for -2578 G-regulated CCL2 expression in astrocytes, which are major producers of CCL2 in the brain. The -2578 G polymorphism creates a consensus-binding site for the transcriptional regulator Prep1, which along with binding partner Pbx2, preferentially binds the -2578 G allele. CCL2 promoters harboring the G allele under unstimulated conditions exhibit a lower basal activity compared to the ancestral A allele. Upon interleukin-1 beta stimulation, Prep1/Pbx2 complexes maintain the ability to bind -2578 G alleles, yet transcription levels from promoters that harbor the A or G allele are equally activated, suggesting that the -2578 region does not influence CCL2 transcription under proinflammatory conditions. Therefore, promoters that harbor the -2578 G allele undergo a higher fold induction and by extension, individuals homozygous for -2578 G would be expected to exhibit hyper-responsive CCL2 phenotypes during periods of inflammation.
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