Skip To Main Content
Jason McCoy on Muck Rack

Jason McCoy

As seen in: Nature, ZDNet, Cell Press, Journal Inquirer, The Forum of Fargo-Moorhead, Detroit Lakes Tribune, V13
Is this you? As a journalist, you can create a free Muck Rack account to customize your profile, list your contact preferences, and upload a portfolio of your best work. Claim your profile

Get in touch with Jason

Contact Jason, search articles and posts on X, monitor coverage, and track replies from one place.

Learn more about Muck Rack

Actions

Share this page

Is this you?

As a journalist, you can create a free Muck Rack account to customize your profile, list your contact preferences, and upload a portfolio of your best work.
Claim your profile

Articles

Letter: Fargo needs to put children first

|
By Jason McCoy
| The Forum of Fargo-Moorhead Verified
As a Fargo parent, I want my kids to grow up healthy and free from addiction. That’s why I support efforts to end the sale of flavored nicotine products and strengthen tobacco retail licensing. Flavors like candy and fruit play a central role in youth initiation. The vast majority of young people who vape report starting with flavored products, and nicotine addiction increases lifelong risks for heart disease, cancer and stroke.
Open in Who Shared Issue with article?

Mutations in mitochondrial ferredoxin FDX2 suppress frataxin deficiency - Nature

|
By Joshua D. Meisel, Presli P. Wiesenthal, Maria R Miranda, María Miranda, Jason McCoy, Gary Ruvkun
| Nature Verified
Abstract Frataxin is a key component of an ancient, mitochondrial iron–sulfur cluster biosynthetic machinery, serving as an allosteric activator of the cysteine desulfurase NFS1 (refs. 1,2,3,4,5). Loss of frataxin levels underlies Friedreich’s ataxia6, the most common inherited ataxia. Yeast, Caenorhabditis elegans and human cells can tolerate loss of frataxin when grown in ‘permissive’ low oxygen tensions7. Here we conducted an unbiased, genome-scale forward genetic screen in C.
Open in Who Shared Issue with article?

METTL17 is an Fe-S cluster checkpoint for mitochondrial translation

|
By Tslil Ast, Yuzuru Itoh, Jason McCoy, Shayan Sadre
| Cell Press Verified
Highlights • The Fe-S proteome is destabilized when the synthesis of its cofactor is impaired • METTL17, a mitoribosome assembly factor, is depleted without Fe-S cluster biosynthesis • METTL17 binds a previously unrecognized [4Fe4S]2+ cluster • Overexpression of METTL17 rescues the bioenergetic defects of frataxin null cells Summary Friedreich’s ataxia (FA) is a debilitating, multisystemic disease caused by the depletion of frataxin (FXN), a mitochondrial iron-sulfur (Fe-S) cluster biogenesis...
Open in Who Shared Issue with article?
See all 14 licensed articles (15 Total)