Sara Sepic

May 23, 2024 | cell.com | Sara Sepic |Brenda A. Schulman

Highlights•Nutrient stress or mTORC1 inhibition induces proteasomal degradation of HMGCS1•HMGCS1 turnover is mediated by CTLH E3 ligase and the Pro/N-degron pathway•Muskelin adaptor facilitates HMGCS1 degradation in cells•HMGCS1 control by mTORC1-CTLH E3 impacts mevalonate metabolites and cell proliferationSummaryMammalian target of rapamycin (mTOR) senses changes in nutrient status and stimulates the autophagic process to recycle amino acids.

May 16, 2024 | cell.com | Sara Sepic |Annette Gross |Helmholtz Zentrum München |Research Unit-Signaling |Kamyar Hadian |Peter Murray | +5 more

Highlights • Supramolecular WDR26-CTLH E3 complex ubiquitylates oligomeric metabolic enzyme NMNAT1 • WDR26-CTLH E3 recognizes internal basic degron of NMNAT1 through WDR26 β-propellers • Degron mimicry of YPEL5’s N terminus inhibits NMNAT1 targeting by WDR26-CTLH E3 • YPEL5-WDR26-CTLH E3 modulates cellular NMNAT1 amounts affecting its metabolic function Summary The yeast glucose-induced degradation-deficient (GID) E3 ubiquitin ligase forms a suite of complexes with interchangeable receptors...