Our latest work in @CellCellPress is a cell atlas of chromatin accessibility in 30 human tissues, integrated with prior data from 15 fetal tissues:
- 222 cell types, ~1.2 million cCREs
- Cell type & adult/fetal-specific elements
- Interpretation of GWAS
https://t.co/dHrsGQn0Ks
Great to see @bethanyfixsen and @jamesdhocker featured in the @BrighamMedRes Bulletin! We are sad to see you leave California, but so excited for your new journey in Boston!
https://t.co/dwYKxdPuyT
Single cell sequencing, gene expression, imaging and spatial omics deconvolute the heart's development in exquisite detail @Nature
video: https://t.co/7Q6wnVXbh6
What if 1 million scRNA-seq libraries can be prepared within $1k? Here we go 👉 21 million cells from 623 mouse tissues, spanning 5 life stages & 3 genotypes, all in a SINGLE study by ONE remarkable student Zehao @Tommyz626 from our lab @RockefellerUniv! https://t.co/SIA2okg60w
https://t.co/NGBUL61109
I am very excited to share our recent paper on @Nature . It is a great collaboration with Dr. Murre and Dr. Fisch at UCSD. We discovered a molecular mechanism to shape nuclear morphology. @CCLRI
1. This validates the observation/hypothesis that causal genes for a disease are connected in gene regulatory networks — and shows that we can find them with systematic Perturb-seq and V2G2P. Here we linked 41 CAD GWAS loci to a single pathway in endothelial cells.
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Our latest in @Nature:
Convergence of coronary artery disease genes on endothelial cell programs
https://t.co/5B8tB3IeXI
Incredible work led by Gavin Schnitzler and @kanghelenyihua — a long-standing partnership between our lab and @Dr_RajatGupta
My comments below:
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Our study is out @Nature. We identify non-lipid risk pathways for coronary artery disease using pooled CRISPR-interference for 2,285 genes at GWAS loci. With an amazing team we identified the genetic risk pathways for CAD that act in endothelial cells.
https://t.co/2f48S7d7Sx
Our work using single-molecule chromatin configurations to link TF binding to gene expression is now out on bioRxiv! Amazing effort from @bgrdoughty, @MichaelaThinks, and @juliaschaepe, and an immensely rewarding collaboration with the @BintuLab: https://t.co/u9aNQV4Ub9 [1/n]
The prevalence of suboptimal affinity binding sites within enhancers creates a vulnerability in genomes whereby single-nucleotide changes that optimize affinity, even slightly, can be pathogenic. https://t.co/iKjf6O26b7
Pinpointing causal variants that disrupt development. So proud of the amazing team on this epic enhancer genotype-to-phenotype study. Well Done, Fabian Lim, @JoeSolvason, Genevieve Ryan, Sophia Le, @granton_jindal, Paige Steffen and Simran Jandu!!! https://t.co/iKjf6O26b7
SnapATAC2 is a non-linear dimension reduction algorithm tailored for single-cell omics data including scATAC-seq, scRNA-seq, scHi-C, and multiomics datasets. snapATAC is also efficient in runtime and memory usage.
https://t.co/7zp1vyUVQ0
Gene expression involves thousands of proteins that bind DNA, yet comprehensively mapping these is challenging. We developed ChIP-DIP – a method for simultaneous, genome-wide mapping of hundreds of DNA-protein interactions in a single experiment. https://t.co/NEH92mQTGs
Whole genome association testing in 333,100 individuals across three biobanks identifies rare non-coding single variant and genomic aggregate associations with height https://t.co/BdvKfO8f04 #bioRxiv
I'm delighted to announce that I am joining the talented research community at @BIG_CenterWashU @wusm_pathology. The Han Lab, with a focus on brain #macrophages in neuropathologies, will be open shortly. More info and website coming soon!
Excited to share our collaboration with ENCODE to map enhancer-gene regulatory interactions across the human genome!
We developed a new model that beats ABC by incorporating additional information on promoter class and enhancer-enhancer interactions.
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