Records 1-18 (of 18 Records) |
Query Trace: IL10RB[original query] |
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Next-generation sequencing of host genetics risk factors associated with COVID-19 severity and long-COVID in Colombian population. Angulo-Aguado Mariana, et al. Scientific reports 2024 0 0. (1) 8497 |
Host genetic polymorphisms involved in long-term symptoms of COVID-19. Udomsinprasert Wanvisa, et al. Emerging microbes & infections 2023 0 0. 2239952 |
Transcriptome-wide Summary Data based Mendelian Randomization analysis reveals 38 novel genes associating with Severe COVID-19. Krishnamoorthy Suhas, et al. Journal of medical virology 2022 0 0. |
A translational genomics approach identifies IL10RB as the top candidate gene target for COVID-19 susceptibility. Voloudakis Georgios, et al. NPJ genomic medicine 2022 0 0. (1) 52 |
A translational genomics approach identifies IL10RB as the top candidate gene target for COVID-19 susceptibility G Voloudakis et al, NPJ Genomic Medicine, September 5, 2022
Using a translational genomics approach that integrates COVID-19 genetic susceptibility variants, multi-tissue genetically regulated gene expression (GReX), and perturbagen signatures, we identified IL10RB as the top candidate gene target for COVID-19 host susceptibility. In a series of validation steps, we show that predicted GReX upregulation of IL10RB and higher IL10RB expression in COVID-19 patient blood is associated with worse COVID-19 outcomes and that in vitro IL10RB overexpression is associated with increased viral load and activation of disease-relevant molecular pathways.
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Whole genome sequencing reveals host factors underlying critical Covid-19. Kousathanas Athanasios, et al. Nature 2022 0 0. |
Whole genome sequencing reveals host factors underlying critical Covid-19 A Kousathanas et al, Nature, March 7, 2022
Here, we use whole genome sequencing in 7,491 critically-ill cases compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical Covid-19. We identify 16 new independent associations, including variants within genes involved in interferon signalling (IL10RB, PLSCR1), leucocyte differentiation (BCL11A), and blood type antigen secretor status (FUT2). Using transcriptome-wide association and colocalisation to infer the effect of gene expression on disease severity, we find evidence implicating multiple genes, including reduced expression of a membrane flippase (ATP11A), and increased mucin expression (MUC1), in critical disease. Mendelian randomisation provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5, CD209) and coagulation factor F8, all of which are potentially druggable targets.
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COVID-19 genetic risk variants are associated with expression of multiple genes in diverse immune cell types. Schmiedel Benjamin J, et al. Nature communications 2021 0 0. (1) 6760 |
Whole genome sequencing identifies multiple loci for critical illness caused by COVID-19 Kousathanas, Athanasios et al. medRxiv September 02 2021 |
Genetic mechanisms of COVID-19 and its association with smoking and alcohol consumption. Rao Shuquan, et al. Briefings in bioinformatics 2021 0 0. |
Integrative Genomics Analysis Reveals a 21q22.11 Locus Contributing Risk to COVID-19. Ma Yunlong, et al. Human molecular genetics 2021 0 0. |
IL10RB as a key regulator of COVID-19 host susceptibility and severity. Voloudakis Georgios, et al. medRxiv : the preprint server for health sciences 2021 0 0. |
Actionable druggable genome-wide Mendelian randomization identifies repurposing opportunities for COVID-19. Gaziano Liam et al. Nature medicine 2021 4
To identify therapeutic targets relevant to COVID-19, we conducted Mendelian randomization analyses, deriving genetic instruments based on transcriptomic and proteomic data for 1,263 actionable proteins that are targeted by approved drugs or in clinical phase of drug development. Using summary statistics from the Host Genetics Initiative and the Million Veteran Program, we studied 7,554 patients hospitalized with COVID-19 and >1 million controls. We found significant Mendelian randomization results for three proteins (ACE2, IFNAR2, and IL-10RB).
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Multi-omics highlights ABO plasma protein as a causal risk factor for COVID-19. Hernández Cordero Ana I, et al. Human genetics 2021 2 0. |
Integrative Genomics Analysis Reveals a Novel 21q22.11 Locus Contributing to Susceptibility of COVID-19 Ma, Yunlong et al. medRxiv September 18 2020 |
Multi-omics highlights ABO plasma protein as a causal risk factor for COVID-19 Cordero, Ana I Hernandez et al. medRxiv October 06 2020 |
Actionable druggable genome-wide Mendelian randomization identifies repurposing opportunities for COVID-19 Gaziano, Liam et al. medRxiv November 21 2020 |
A bioinformatic approach to investigating cytokine genes and their receptor variants in relation to COVID-19 progression. Karakas Celik Sevim, et al. International journal of immunogenetics 2020 11 0. |
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