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Wang intends to test this strategy out in a C9orf72 BAC mouse model developed by Laura Ranum, also at the University of Florida (Liu et al., 2016).Meanwhile at the University of California in San Diego, Gene Yeo and colleagues are also aiming to eliminate these disease-linked repeat-heavy RNAs, but are targeting them after they’re transcribed.Vincent Dion simply wanted to understand how unstable, repetitive regions of the genome contract and in some cases expand, inciting disease.
They injected an AAV6 virus encoding d Cas9 and the CTG guide RNA into the tail veins of HSA mice harboring 250 CTG repeats in the 3’UTR of a human skeletal muscle actin gene, at two days old.
“I think the potential is very exciting…but those are the hurdles,” said Tom Cooper of Baylor College of Medicine in Houston.
He’s careful not to be too optimistic about treatments coming out of this kind of research anytime soon, but did note that these editing technologies are improving quickly.
As for C9orf72 ALS, a treatment like Wang’s could, theoretically, be of benefit too.
In He La cells harboring 120 C9orf72 repeats, this approach did minimize production of poly-glycine-proline typically produced by repeat-associated translation of the repeat region, suggesting that it may help reduce the expanded repeat’s potential toxicity.
The roadblocks reduced, somewhat, the tell-tale signs of the disease at five weeks, including myotonia.