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Jun Yu

Researcher at University of Massachusetts Medical School

Publications -  27
Citations -  861

Jun Yu is an academic researcher from University of Massachusetts Medical School. The author has contributed to research in topics: Heterochromatin & Chromatin. The author has an hindex of 13, co-authored 27 publications receiving 509 citations.

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ATACseqQC: a Bioconductor package for post-alignment quality assessment of ATAC-seq data.

TL;DR: A Bioconductor package, ATACseqQC, for easily generating various diagnostic plots to help researchers quickly assess the quality of their ATAC-seq data, and has been used successfully for preprocessing and assessing several in-house and public ATac-seq datasets.
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CBFβ-SMMHC Inhibition Triggers Apoptosis by Disrupting MYC Chromatin Dynamics in Acute Myeloid Leukemia.

TL;DR: It is demonstrated that CBFβ-SMMHC maintains cell viability by neutralizing RUNX1-mediated repression of MYC expression, which suggests that inhibitors targeting chromatin activity may prove effective in inv(16) leukemia therapy.
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Two contrasting classes of nucleolus-associated domains in mouse fibroblast heterochromatin.

TL;DR: The first genome-scale map of murine NADs in mouse embryonic fibroblasts (MEFs) is determined via deep sequencing of chromatin associated with purified nucleoli via Bioconductor package called NADfinder and it is demonstrated that it identifies NADs more accurately than other peak-calling tools, owing to its critical feature of chromosome-level local baseline correction.
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Robust Identification of Developmentally Active Endothelial Enhancers in Zebrafish Using FANS-Assisted ATAC-Seq.

TL;DR: FANS-assisted ATAC-seq using transgenic zebrafish embryos provides a robust approach for genome-wide identification of active tissue-specific enhancer elements.
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UPR mt scales mitochondrial network expansion with protein synthesis via mitochondrial import in Caenorhabditis elegans.

TL;DR: In this paper, the authors demonstrate that ATFS-1 mediates an adaptable mitochondrial network expansion program that is active throughout normal development, which is an emergent property of the synthesis of highly expressed mitochondrial proteins that exclude ATFS from mitochondrial import, causing UPRmt activation.