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Nelson B. Barrientos on Muck Rack

Nelson B. Barrientos

As seen in: BMC Genomics, BioRxiv, Cell Reports
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Articles

Recurrent ZC3H18 mutations stabilize oncogenic endogenous retroviral RNA

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By Tanzina Tanu, Anna Cox, Jennifer Karlow, Priyanka Sharma, Kaiwen Sun, Xueyang He, Madeline K. Roelofs, Ethan Jeon, JiaJia Chen, Constance Wu, Jared Brown, Nelson B. Barrientos, Andrew S. McCallion, Kevin Brown, Stephen J. Chanock, David R. Liu, Tongwu Zhang, Kathleen Burns, Paul L. Boutz, Megan L Insco
| Cell Reports Verified
Keywords endogenous retroviral RNA ERV RNA melanoma nuclear exosome targeting complex NEXT complex nuclear RNA surveillance zebrafish Research topic(s) CP: cancer CP: molecular biology Introduction As healthy cells require appropriate levels of high-quality RNA, dysregulation of RNA homeostasis contributes to diverse human diseases, including cancer. RNA homeostasis requires balanced production and degradation.
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Proof of concept study deploying CRISPR inhibition and activation opens key avenues for systematic biological exploration in zebrafish.

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By Nelson B. Barrientos, Elyse A Shoppell, Rachel J. Boyd, Valeria C. Culotta
| BioRxiv
Abstract The application of CRISPR interference (CRISPRi) and CRISPR activation (CRISPRa) technologies in zebrafish has the potential to expand its capacity for the study of gene function significantly. We report proof-of-principle data evaluating transient expression of a codon optimized CRISPRi/a system for zebrafish across established pigmentary and growth phenotypes.
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Optimized CRISPR inhibition and activation opens key avenues for systematic biological exploration in zebrafish.

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By Nelson B. Barrientos, Rachel J. Boyd, Valeria C. Culotta, Elyse A Shoppell
| BioRxiv
Abstract The application of CRISPR interference (CRISPRi) and CRISPR activation (CRISPRa) technologies in zebrafish has the potential to expand its capacity for the study of gene function significantly. We have developed a codon optimized CRISPRi/a for zebrafish; here we provide proof-of-principle data across established pigmentary and growth phenotypes. We established a zebrafish codon-optimized cas9 gene, harboring mutations D10A and D839A to render the protein catalytically inactive (dCas9).
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