Silencing of the Mutant Huntingtin Gene through CRISPR-Cas9 Improves the Mitochondrial Biomarkers in an In Vitro Model of Huntington’s Disease.

Silencing of the Mutant Huntingtin Gene through CRISPR-Cas9 Improves the Mitochondrial Biomarkers in an In Vitro Model of Huntington’s Disease.

Publication date: Apr 04, 2019

During the 25-year history of the American Society for Neural Therapy and Repair (ASNTR) there have been several breakthroughs in the area of neurotherapeutics, which was the case during the 2014-2105 year when one of us (GLD) had the privilege of serving as its president. During that year, the use of a newly developed gene-editing tool, the CRISPR-Cas9 system, started to skyrocket. Although scientists unraveled the use of “clustered regularly interspaced short palindromic repeats” (CRISPR) and its associated genes from the Cas family as an evolved mechanism of some bacterial and archaeal genomes to protect themselves from being hijacked by invasive viral genes, its use as a therapeutic tool was not fully appreciated until further research revealed how this system operated and how it might be developed technologically to manipulate genes of any species. By 2015, this technology had exploded to the point that close to 2,000 papers that used this technology were published during that year alone.

Dunbar, G.L., Koneru, S., Kolli, N., Sandstrom, M., Maiti, P., and Rossignol, J. Silencing of the Mutant Huntingtin Gene through CRISPR-Cas9 Improves the Mitochondrial Biomarkers in an In Vitro Model of Huntington’s Disease. 06436. 2019 Cell Transplant.

Concepts Keywords
Cas9 Cas9
CRISPR CRISPR
Gene Non-coding RNA
Hijacked Biotechnology
Huntingtin Genetic engineering
Huntington Immune system
Palindromic Genome editing
Species Genetics
Viral Branches of biology
Disease

Semantics

Type Source Name
gene UNIPROT BCAR1
gene UNIPROT CTNND1
gene UNIPROT CSE1L

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