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40 results for “fine-mapping”
Database for GWAS SVatalog: a visualization tool to aid fine-mapping of GWAS loci with structural variations.
<p>GWAS SVatalog is a novel visualization tool and database for structural variants (SV) found in a predominantly European population of 101 individuals with Cystic Fibrosis (CF). Aside from the CF-causing variants on chromosome 7 and the LD block in which they lie, the remainder of the genome is comparable to a the 1000 Genomes healthy European population. This data is a collection of SV calls and their linkage disequilibrium (LD) statistics with GWAS-significant SNPs reported in the GWAS Catalog.</p> <p> </p> <p>The goal of this project is to provide a resource to aid fine mapping of GWAS loci using SVs. GWAS loci are generally identified by SNPs which account for an incomplete proportion of genetic variation and phenotypic heritability. Their relevance to the phenotype might be limited, tagging other polymorphisms, such as SVs, that could be the cause of the association signal. To leverage this data to its full potential, visit the <a href="https://svatalog.research.sickkids.ca/" target="_blank" rel="noopener">GWAS SVatalog</a> web tool. Here, interactive visualizations can illustrate SVs identified in high LD with GWAS-significant SNPs, suggesting putative causal variation that could guide additional functional investigation.</p> <p> </p> <p>For more information on how to use GWAS SVatalog, visit the<a href="https://gwas-svatalog-docs.readthedocs.io/en/latest/index.html" target="_blank" rel="noopener noreferrer"> documentation</a>.</p> <p> </p> <p>This project was accomplished in collaboration with the <a href="https://lab.research.sickkids.ca/strug/" target="_blank" rel="noopener">Strug Lab</a> at <a href="https://www.sickkids.ca/en/" target="_blank" rel="noopener">The Hospital for Sick Children (SickKids)</a>, <a href="https://www.tcag.ca/" target="_blank" rel="noopener">The Center for Applied Genomics (TCAG)</a>, and <a href="https://www.utoronto.ca/" target="_blank" rel="noopener">University of Toronto</a>.</p>
Fine-mapped summary statistics for protein coding regions (i.e. cis regions) based on the Olink Explore 1536 and Explore Expansion technologies
<p>This data set contains fine-mapping results performed by SuSie for cis regions ±500kb around the protein coding gene) for protein targets as measured by the Olink Explore 1536 and Explore Expansion technologies in 1,180 individuals from EPIC Norfolk study (https://www.epic-norfolk.org.uk/). Only protein targets where fine-mapping predicted at least one credible set were included in the results. </p>
Data in support of "An exploration of linkage fine-mapping on sequences from case-control studies"
<p>These data were simulated for an exploration of linkage fine-mapping on sequences from case-control studies. The code to generate and analyze the data is available on GitHub in the scripts at <a href="https://github.com/SFUStatgen/PBJ0">https://github.com/SFUStatgen/PBJ0</a>. Queries may be directed to Payman Nickchi at <a href="mailto:pnickchi@sfu.ca">pnickchi@sfu.ca</a> or Charith (Bhagya) Karunarathna at <a href="mailto:ch757276@dal.ca">ch757276@dal.ca</a>.</p>
Data in support of "An exploration of linkage fine-mapping on sequences from case-control studies"
<p>These data were simulated for an exploration of linkage fine-mapping on sequences from case-control studies. The scripts to generate and analyze the data are available at <a href="https://github.com/SFUStatgen/PBJ0">https://github.com/SFUStatgen/PBJ0</a>. Queries may be directed to Payman Nickchi at <a href="mailto:pnickchi@sfu.ca">pnickchi@sfu.ca</a> or Charith (Bhagya) Karunarathna at <a href="mailto:ch757276@dal.ca">ch757276@dal.ca</a>.</p> <p><strong>README file for All_data directory</strong></p> <p><strong>Directory structure</strong></p> <p>The All_data directory consists of this README file and 500 sub-directories named DatasetX, for X=1 to 500. Within each DatasetX sub-directory are further sub-directories named alt and null containing files named pop_data.RData and sample_data.RData.</p> <p><strong>alt <em>versus</em> null directories</strong></p> <p>The files in the alt and null directories contain the same variant data but different phenotype data. In particular, under the null hypothesis, disease status is simulated at random according to a 5% prevalence in the population, whereas under the alternative hypothesis disease status is simulated according to a penetrance model that depends on causal SNVs. The R script to simulate data<br> under the alternative hypothesis is in the file 1_SimulateData.R in the Github repository <a href="https://github.com/SFUStatgen/PBJ0">https://github.com/SFUStatgen/PBJ0</a>.</p> <p><strong>pop_data.RData and sample_data.RData files</strong></p> <p>The data structures contained in the pop_data.RData and sample_data.RData files are described below. The structure is the same under both the null and alternative hypothesis.</p> <p><strong>pop_data.RData</strong></p> <p>From R, load("pop_data.RData") loads a list named pop_data whose elements describe the population’s haplotype and phenotype data. The list elements are as follows.</p> <ul> <li>Variants: a matrix of variants for the population of 6200 haplotypes <ul> <li>rows are SNVs,</li> <li>columns are sequences</li> </ul> </li> <li>Positions: a data frame of SNV positions <ul> <li>rows are SNVs,</li> <li>column 1 is the SNV name and column 2 is the SNV position in base pairs</li> </ul> </li> <li>Population.Mapping: a data frame telling us how the sequences are paired into individuals <ul> <li>rows are individuals</li> <li>First column 1 is an individual ID from 1,…,3100; columns 2 and 3 are the sequence IDs of the first and second sequence for that individual where the sequence IDs are the column names of the Variants matrix.</li> </ul> </li> <li>Genotype.Matrix: a matrix of genotypes (i.e. variant counts) for the 3100 individuals <ul> <li>rows are SNVs</li> <li>columns are the individuals</li> </ul> </li> <li>causal_region: a vector containing the lower- and upper-limit of the causal region in base pairs.</li> <li>cSNV: a vector containing the IDs of the causal SNVs, where the SNV IDs are the row names of the Variants matrix.</li> <li>DISCRETE: a list with the following elements. <ul> <li>CaseIndividuals: vector of IDs of the affected individuals in the population.</li> <li>ControlIndividuals: vector of IDs of the unaffected in the population.</li> <li>BinaryTrait: a vector of trait status (0=unaffected, 1=affected) for each individual.</li> </ul> </li> </ul> <p><strong>Note:</strong> Within the same DatasetX directory, the only difference between the pop_data data structures under the null and alternative hypothesis is the phenotype information contained in their respective DISCRETE list elements. Both the null and alternative pop_data data structure share list elements: Variants, Positions, Population.Mapping, Genotype.Matrix, causal_region and cSNV.</p> <p><strong>sample_data.RData</strong></p> <p>From R, load("sample_data.RData") loads a list whose elements describe the sequences and phenotypes of the sample of 50 affected individuals (cases) and 50 unaffected individuals (controls) from the population.</p> <ul> <li>Haps: a list with two elements. <ul> <li>sample_haps: a matrix of 200 sequences for the 50 cases and 50 controls. Rows are SNVs and columns are sequences, with the sequences of sampled cases appearing first (i.e. first 100 columns), followed by the sequences of sampled controls (i.e. last 100 columns). Sequences include only those SNVs that are polymorphic in the sample.</li> <li>ccStatus: a vector indicating the case/control status of the individual to which the sequence belongs, with case=1 and control=0.</li> </ul> </li> <li>Genos: a list with two elements. <ul> <li>sample_genos: a matrix of 100 genotypes for the 50 cases and 50 controls. Rows are SNVs and columns are genotypes, with genotypes of cases appearing first, followed by genotypes of controls.</li> <li>ccStatus: a vector indicating the case/control status of each individual, with case=1 and control=0.</li> </ul> </li> <li>Posn: a data frame of SNV positions for each SNV that is polymorphic in the sample. The first column is the SNV name and the second is the SNV position in base pairs. Posn is a subset of pop_data$Positions.</li> <li>poly_cSNV: a vector of IDs for causal SNVs that are polymorphic in the sample.</li> <li>CaseIND: a vector of individual IDs for the case individuals (see pop_data$Population.Mapping).</li> <li>ControlIND: a vector of individual IDs for the control individuals (see pop_data$Population.Mapping).</li> <li>CaseHapID: a vector of IDs for the sequences that belong to cases (see the sequence IDs in the column names of the matrix pop_data$Variants).</li> <li>ControlHapID: a vector of IDs for the sequences that belong to controls (see the sequence IDs in the column names of the matrix pop_data$Variants).</li> </ul> <p> </p>
Results from the revision of MultiSuSiE improves multi-ancestry fine-mapping in All of Us whole-genome sequencing data
<p>afr47041.zip, lat36378.zip, and eur115620.zip contain All of Us Summary Statistics used in the revised version of "MultiSuSiE improves multi-ancestry fine-mapping in All of Us whole-genome sequencing data". Summary statistics for three cohorts are included: Afr47k, Lat36k, and Eur116k. These cohorts have not been downsampled to have equal levels of missingness.</p> <p>pips.tsv contains fine-mapped variants with PIP > 0.01 via MultiSuSiE from the revised version of "MultiSuSiE improves multi-ancestry fine-mapping in All of Us whole-genome sequencing data". Subcohorts with the _unmatched suffix have not been downsampled to have equal levels of phenotyped missingness across ancestries. </p> <p>MultiSuSiE-main.zip contains the MultiSuSiE software packages (corresponds to the Github repo on 10/16/2025).</p> <p>Please cite:</p> <p>Rossen, Jordan, et al. "MultiSuSiE improves multi-ancestry fine-mapping in All of Us whole-genome sequencing data." <em>medRxiv</em> (2024): 2024-05.</p> <p> </p>
Improved multi-ancestry fine-mapping identifies cis-regulatory variants underlying molecular traits and disease risk
<p>sushie.molqtl.weights.tar.gz contains ancestry-specific eQTL and pQTL weights trained on mRNA and protein levels measured in American European, American African, and American Hispanic ancestries from TOPMed-MESA and GENOA studies. Column “a1” is the counting allele.</p> <p>mesa.*.fusion.tar.gz contains the weights in FUSION format.</p> <p>sushie_real_data_results.tar.gz contains all the real data analyzed in the sushie project.</p> <p>sushie_sim_data_results.tar.gz contains all the sim data analyzed in the sushie project.</p> <p>sushie_analysis_codes.tar.gz contains all the codes and scripts to generate and analyze these data.</p>
Fine-mapping gene-based associations via knockoff analysis of biobank-scale data with applications to UK Biobank
<p>The results of BIGKnock analyses of manuscript ''Fine-mapping gene-based associations via knockoff analysis of biobank-scale data with applications to UK Biobank''</p>
Genetic fine-mapping results for 56 NMR metabolites measured in 246,683 UK Biobank participants
<p>Fine-mapping credible sets for 56 metabolites measured in 246,683 UK Biobank participants using the Nightingale Health platform. Fine-mapping was performed using the https://github.com/AlasooLab/reGSusie workflow.<br><br>The 56_metabolites_finemapping_credible_sets.tsv file contains the fine-mapped credible sets for all 56 metabolites. The *_coloc5_final.tsv.gz files contain the log Bayes factors for each metabolite in each fine-mapped region. </p>
Supplemental material for: Genome-wide association study and fine-mapping using imputed sequences to prioritize candidate genes for 30 complex traits in 50,309 Holstein bulls
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Regionalpcs ROSMAP Fine-mapped QTLs
<p>This dataset contains DAP-G fine-mapped QTL results for the following study:</p> <p><strong><em>"regionalpcs improve discovery of DNA methylation associations with complex traits"</em></strong></p> <p>Tiffany Eulalio*<sup>1</sup>, Min Woo Sun<sup>1</sup>, Olivier Gevaert<sup>1</sup>, Michael D. Greicius<sup>2</sup>, Thomas J. Montine<sup>3</sup>, Daniel Nachun*‡<sup>3</sup>, Stephen B. Montgomery*‡<sup>1,3</sup></p> <p>‡ These authors contributed equally as senior authors</p> <p>* Corresponding authors: Tiffany Eulalio (<a href="mailto:eulalio@alumn.stanford.edu">eulalio@alumn.stanford.edu</a>), Daniel Nachun (<a href="mailto:dnachun@stanford.edu">dnachun@stanford.edu</a>), Stephen B. Montgomery (<a href="mailto:smontgom@stanford.edu">smontgom@stanford.edu</a>)</p> <p> Author affiliations:</p> <p>1. Department of Biomedical Data Science, Stanford University, Stanford, CA</p> <p>2. Department of Neurology & Neurological Sciences, Stanford University, Stanford, CA</p> <p>3. Department of Pathology, Stanford University, Stanford, CA</p> <p> </p> <p><strong>Dataset description</strong>:</p> <p>The DAP-G results are organized by region type (full gene, gene body, preTSS, and promoters), cell type (astrocytes, endothelial cells, neurons, oligodendrocytes, and bulk), and summary type (averages and regionalpcs).</p>
Data from: A gene for genetic background in Zea mays: fine-mapping enhancer of teosinte branched1.2 to a YABBY class transcription factor
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Data from: Genetic basis of octanoic acid resistance in Drosophila sechellia: functional analysis of a fine-mapped region
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The utility of the Laplace effect size prior distribution in Bayesian fine-mapping studies
<p>Data needed to reproduce the figures and tables in the paper entitled 'The utility of the Laplace effect size prior distribution in Bayesian fine-mapping studies' submitted for publication.</p>
Data from: Identification of X-linked quantitative trait loci affecting cold tolerance in Drosophila melanogaster and fine-mapping by selective sweep analysis
Drosophila melanogaster is a cosmopolitan species that colonizes a great variety of environments. One trait that shows abundant evidence for naturally segregating genetic variance in different populations of D. melanogaster is cold tolerance. Previous work has found quantitative trait loci (QTL) exclusively on the second and the third chromosomes. To gain insight into the genetic architecture of cold tolerance on the X chromosome and to compare the results with our analyses of selective sweeps, a mapping population was derived from a cross between substitution lines that solely differed in the origin of their X chromosome: one originates from a European inbred line, the other one from an African inbred line. We found a total of six QTL for cold tolerance factors on the X chromosome of D. melanogaster. Although the composite interval mapping revealed slightly different QTL profiles between sexes, a coherent model suggests that most QTL overlapped between sexes and each explained around 5-14% of the genetic variance (which may be slightly overestimated). The allelic effects were largely additive, but we also detected two significant interactions. Taken together, this provides evidence for multiple QTL that are spread along the entire X chromosome and whose effects range from low to intermediate. One detected transgressive QTL influences cold tolerance in different ways for the two sexes. While females benefit from the European allele increasing their cold tolerance, males tend to do better with the African allele. Finally, using selective sweep mapping the candidate gene CG16700 for cold tolerance co-localizing with a QTL was identified.
Data from: Identification of X-linked quantitative trait loci affecting cold tolerance in Drosophila melanogaster and fine-mapping by selective sweep analysis
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Data from: Fine-mapping nicotine resistance loci in Drosophila using a multiparent advanced generation inter-cross population
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Genetic identification, replication, and functional fine-mapping of expression quantitative trait loci in primary human liver tissue [Agilent]
GEO Series GSE25935. Homo sapiens. 464 samples. Type: Expression profiling by array.
Endogenous fine-mapping of functional regulatory elements in complex genetic loci in HAP1 [scRNA-seq]
GEO Series GSE285461. Homo sapiens. 18 samples. Type: Expression profiling by high throughput sequencing.
Genetic identification, replication, and functional fine-mapping of expression quantitative trait loci in primary human liver tissue [Illumina Expression Array]
GEO Series GSE28893. Homo sapiens. 60 samples. Type: Expression profiling by array.
Systematic fine-mapping and functional studies of prostate cancer risk variants [RNA-seq]
GEO Series GSE197816. Homo sapiens. 6 samples. Type: Expression profiling by high throughput sequencing.
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Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
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DANDI Archive for NWB datasets
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International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.