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Deepak Reyon

Researcher at Harvard University

Publications -  53
Citations -  17227

Deepak Reyon is an academic researcher from Harvard University. The author has contributed to research in topics: Genome editing & Transcription activator-like effector nuclease. The author has an hindex of 33, co-authored 51 publications receiving 15306 citations. Previous affiliations of Deepak Reyon include Iowa State University & University of Minnesota.

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Disruption of asxl1 results in myeloproliferative neoplasms in zebrafish.

TL;DR: It is shown that homozygous loss of asxl1 in zebrafish leads to apoptosis of newly formed HSCs by upregulation of bim and bid, which supports the use of as xl1+/− zebra fish as a strategy to identify small-molecule drugs to suppress the growth of asXl1 mutant but not wild-type HSCS in individuals with somatically acquired inactivating mutations of ASXL1.
Posted ContentDOI

The experimental design and data interpretation in “Unexpected mutations after CRISPR–Cas9 editing in vivo” by Schaefer et al. are insufficient to support the conclusions drawn by the authors

TL;DR: It is believed that the conclusions drawn from this study are unsubstantiated by the disclosed experiments as they were designed and carried out and it is impossible to ascribe the observed differences in the subject mice to the effects of CRISPR per se.
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Disruption of the kringle 1 domain of prothrombin leads to late onset mortality in zebrafish.

TL;DR: The conserved function of thrombin in zebrafish is demonstrated and insight into the role of kringle 1 in prothrombin maturation and activity is provided to provide important insight into its pleiotropic functions as well as the management of patients with bleeding disorders.
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Identification of promoter targets of enhancers by epigenetic knockdown using TAL DNA binding proteins

TL;DR: A fundamental question in biology is how an organism’s genome controls cellular differentiation and identity to produce numerous distinct cell types, and this work designed TALs to target over 50 putative distal enhancers to relatively quantitate the contribution on transcriptional activation of the target enhancer.