//
sign in
Profile
by @danabra.mov
Profile
by @dansshadow.bsky.social
Profile
by @jimpick.com
AviHandle
by @danabra.mov
AviHandle
by @dansshadow.bsky.social
AviHandle
by @katherine.computer
EventsList
by @katherine.computer
ProfileHeader
by @dansshadow.bsky.social
ProfileHeader
by @danabra.mov
ProfileMedia
by @danabra.mov
ProfilePlays
by @danabra.mov
ProfilePosts
by @danabra.mov
ProfilePosts
by @dansshadow.bsky.social
ProfileReplies
by @danabra.mov
Record
by @atsui.org
Skircle
by @danabra.mov
StreamPlacePlaylist
by @katherine.computer
+ new component
Profile
Loading...

Loading...
studying genetic and environmental contributions to cell fitness in cancer and immunity | biology-engineering-biotechnology | #HPLM | current: investigator @Morgridge_Inst, assistant prof @UW-Madison
Jason Cantor
1/12 🛣️ Mapping nitrogen metabolism has lagged carbon due to substrate diversity. In @natmetabolism.nature.com, we introduce a platform to do this mapping at scale and identify mechanisms by which differentiation state dictates pyrimidine synthesis. 🧵👇 🔗 www.nature.com/articles/s42...
1mo
Milan Savani
Pleased to share our recent work out today in @natmetabolism.nature.com. This study addresses a longstanding mystery - NRF2-driven cancers increase cysteine acquisition (via xCT) by ~5x - so where does all that cysteine go?
2mo
Lucas Sullivan
2mo
Nature Metabolism
Nature Metabolism, Published online: 07 April 2026; doi:10.1038/s42255-026-01499-8Previously uncharacterized cysteine-derived conjugates, including with endogenous sugar metabolites, accumulate in cancer cells with constitutive NRF2 activation and account for some of the increased cystine uptake that cannot be explained by conventional cysteine metabolism.
dlvr.it
Excess cysteine drives conjugate formation and impairs proliferation of NRF2-activated cancer cells