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Ashis Saha

Researcher at Johns Hopkins University

Publications -  32
Citations -  5955

Ashis Saha is an academic researcher from Johns Hopkins University. The author has contributed to research in topics: Expression quantitative trait loci & Gene. The author has an hindex of 15, co-authored 30 publications receiving 2882 citations. Previous affiliations of Ashis Saha include Princeton University & Bidhan Chandra Krishi Viswavidyalaya.

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Journal ArticleDOI

The GTEx Consortium atlas of genetic regulatory effects across human tissues

François Aguet, +167 more
- 01 Jan 2020 - 
Posted ContentDOI

The GTEx Consortium atlas of genetic regulatory effects across human tissues

TL;DR: Analysis of the v8 data provides insights into the tissue-specificity of genetic effects, and shows that cell type composition is a key factor in understanding gene regulatory mechanisms in human tissues.
Journal ArticleDOI

Exploring the phenotypic consequences of tissue specific gene expression variation inferred from GWAS summary statistics.

Alvaro N. Barbeira, +263 more
TL;DR: A mathematical expression is derived to compute PrediXcan results using summary data, and the effects of gene expression variation on human phenotypes in 44 GTEx tissues and >100 phenotypes are investigated.
Journal ArticleDOI

Description and performance of track and primary-vertex reconstruction with the CMS tracker

S. Chatrchyan, +2387 more
TL;DR: In this paper, a description of the software algorithms developed for the CMS tracker both for reconstructing charged-particle trajectories in proton-proton interactions and for using the resulting tracks to estimate the positions of the LHC luminous region and individual primary-interaction vertices is provided.
Posted ContentDOI

Unraveling the polygenic architecture of complex traits using blood eQTL metaanalysis

Urmo Võsa, +100 more
- 19 Oct 2018 - 
TL;DR: It is observed that cis-eQTLs can be detected for 88% of the studied genes, but that they have a different genetic architecture compared to disease-associated variants, limiting the ability to use cis- eZTLs to pinpoint causal genes within susceptibility loci.