Confirmation of differential binding of Interferon Regulatory Factor-1 (IRF-1) to the functional and HIV disease-influencing −2578 A/G polymorphism in CCL2

Mummidi, Srinivas; Bonello, G.; Ahuja, Sunil K.

doi:10.1038/gene.2008.75

Cited by 10 publications

(6 citation statements)

References 5 publications

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“…5b, c, e. and are implicated in regulation of CCL2 expression 80,81 . Therefore, a cumulative effect of multiple TFs at this enhancer is likely to contribute to the regulation of CCL2 expression 77 .…”

Section: Resultsmentioning

confidence: 99%

Conserved regulatory logic at accessible and inaccessible chromatin during the acute inflammatory response in mammals

et al. 2021

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The regulatory elements controlling gene expression during acute inflammation are not fully elucidated. Here we report the identification of a set of NF-κB-bound elements and common chromatin landscapes underlying the acute inflammatory response across cell-types and mammalian species. Using primary vascular endothelial cells (human/mouse/bovine) treated with the pro−inflammatory cytokine, Tumor Necrosis Factor-α, we identify extensive (~30%) conserved orthologous binding of NF-κB to accessible, as well as nucleosome-occluded chromatin. Regions with the highest NF-κB occupancy pre-stimulation show dramatic increases in NF-κB binding and chromatin accessibility post-stimulation. These ‘pre-bound’ regions are typically conserved (~56%), contain multiple NF-κB motifs, are utilized by diverse cell types, and overlap rare non-coding mutations and common genetic variation associated with both inflammatory and cardiovascular phenotypes. Genetic ablation of conserved, ‘pre-bound’ NF-κB regions within the super-enhancer associated with the chemokine-encoding CCL2 gene and elsewhere supports the functional relevance of these elements.

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Section: Resultsmentioning

confidence: 99%

Conserved regulatory logic at accessible and inaccessible chromatin during the acute inflammatory response in mammals

et al. 2021

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“…The -2518G allele increases the binding of several transcription factors to MCP-1, resulting in increased transcriptional activation of its distal promoter (Rovin et al, 1999;Mummidi et al, 2009;Page et al, 2011;Pham et al, 2012). The association between polymorphism in the MCP-1 promoter and increased risk of an individual suffering from CAD was first demonstrated by Szalai et al in 2001(Szalai et al, 2001.…”

Section: Discussionmentioning

confidence: 99%

Association of Monocyte Chemoattractant Protein‐1 (MCP‐1)‐2518A>G Polymorphism with Susceptibility to Coronary Artery Disease: A Meta‐Analysis

Bai

Wang

et al. 2015

Annals of Human Genetics

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SummaryWe attempted to systematically elucidate the association between monocyte chemoattractant protein-1 (MCP-1) -2518A>G polymorphism and risk of coronary artery disease (CAD). Eligible studies were identified through PubMed, EBSCO, and Web of Science Databases. The magnitude of MCP-1 polymorphism effect and its possible mode of action on CAD were estimated. The odds ratio (OR) with 95% confidence intervals (CI) were pooled in a specific genetic model to assess the association. A total of 21 studies were involved. There was significant gene effect on CAD risk in the overall population (likelihood ratio test: p < 0.0001). Patients with GG and AG genotypes had 1.435 (95% CI: 1.183-1.740) and 1.087 (95% CI: 1.008-1.172) times higher risk of CAD than those with AA genotype. These gene effects suggested a recessive model to be appropriate. The pooled OR was 1.362 (95% CI: 1.137-1.631; p uncorrected = 0.001, p FDR = 0.005) in the recessive model. In the ethnicity-stratified analysis, significant association was observed in the Caucasian population (OR = 1.492; 95% CI: 1.106-2.014; p uncorrected = 0.009, p FDR = 0.015), whereas no statistical significant association was detected in the Asian population (adjusted p = 0.124). The results suggested that MCP-1 -2518A>G polymorphism may be associated with susceptibility to CAD, especially in Caucasians.

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“…В частности, показана ассоциация полиморфизма -2578G, расположенного в промоторной области гена CCL2, со снижением риска заражения ВИЧ-1. Наличие мутантного аллеля приводило к изменению связывания транскрипционного фактора IRF-1 и, как следствие, к увеличению ýкспрессии CCL2 [59].…”

Section: ген Ccl2 (Mcp-1 Ccl2)unclassified

Genetic factors influencing HIV entry into target cells

Хаитов¹,

Алексеев²,

Кофиади³

et al. 2019

Bûll. sib. med.

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Succeptibility to HIV and the dynamics of HIV infection progression to AIDS are dependent on unique individual factors. Revealing genetic features of natural resistance to HIV infection is of great importance for the development of effective strategies for disease control. This review presents an analysis of host gene alleles coding receptors and their ligands participating in viral entrance to target cell. These allelic variants and their combinations can have a significant influence on the individual resistance/sensitivity to HIV infection and may be associated with the HIV infection progression to AIDS.

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Confirmation of differential binding of Interferon Regulatory Factor-1 (IRF-1) to the functional and HIV disease-influencing −2578 A/G polymorphism in CCL2

Cited by 10 publications

References 5 publications

Conserved regulatory logic at accessible and inaccessible chromatin during the acute inflammatory response in mammals

Conserved regulatory logic at accessible and inaccessible chromatin during the acute inflammatory response in mammals

Association of Monocyte Chemoattractant Protein‐1 (MCP‐1)‐2518A>G Polymorphism with Susceptibility to Coronary Artery Disease: A Meta‐Analysis

Genetic factors influencing HIV entry into target cells

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