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David Sims

Researcher at University of Oxford

Publications -  76
Citations -  6290

David Sims is an academic researcher from University of Oxford. The author has contributed to research in topics: Gene & Cancer. The author has an hindex of 33, co-authored 68 publications receiving 4919 citations. Previous affiliations of David Sims include John Radcliffe Hospital & Queen Mary University of London.

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Sequencing depth and coverage: key considerations in genomic analyses

TL;DR: The issue of sequencing depth in the design of next-generation sequencing experiments is discussed and current guidelines and precedents on the issue of coverage are reviewed for four major study designs, including de novo genome sequencing, genome resequencing, transcriptome sequencing and genomic location analyses.
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KDM2B links the Polycomb Repressive Complex 1 (PRC1) to recognition of CpG islands

TL;DR: It is discovered that KDM2B (FBXL10) specifically recognizes non-methylated DNA in CGIs and recruits the polycomb repressive complex 1 (PRC1), which contributes to histone H2A lysine 119 ubiquitylation (H2AK119ub1) and gene repression.
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Correction: Corrigendum: Long non-coding RNAs and enhancer RNAs regulate the lipopolysaccharide-induced inflammatory response in human monocytes

TL;DR: This paper presents a new probabilistic method for estimating the planktonic resolution of the response of the immune system to EMTs, which has shown promise in both the low and high-resolution models.
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The Sorghum bicolor reference genome: improved assembly, gene annotations, a transcriptome atlas, and signatures of genome organization.

TL;DR: Deep sequencing, genetic linkage analysis, and transcriptome data were used to produce and annotate a high-quality reference genome sequence and indicated that tissue type and protein kinase expression had large influences on transcriptional profile clustering.
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Genome-wide profiling of genetic synthetic lethality identifies CDK12 as a novel determinant of PARP1/2 inhibitor sensitivity.

TL;DR: In models of high-grade serous ovarian cancer (HGS-OVCa), CDK12 attenuation was sufficient to confer sensitivity to PARP1/2 inhibition, suppression of DNA repair via homologous recombination, and reduced expression of BRCA1.