Thrilled to share our new paper: SLC33A1 is the long-sought ER GSSG exporter, maintaining redox homeostasis in the ER. Huge congratulations to my co-first author @shanshanliu1218 and my PIs @KivancBirsoy and @HiteLabMSKCC for leading this work. https://t.co/hhsiYw1jXB 🧵 1/9
Thrilled to share our new paper: SLC33A1 is the long-sought ER GSSG exporter, maintaining redox homeostasis in the ER. Huge congratulations to my co-first author @shanshanliu1218 and my PIs @KivancBirsoy and @HiteLabMSKCC for leading this work. https://t.co/hhsiYw1jXB 🧵 1/9
Our new work by @shanshanliu1218 and @gadmark addresses a fundamental question: how does ER maintain its unique oxidizing environment, while rest of the cell is reducing? Here, we identify SLC33A1 as the major ER GSSG exporter in mammalian cells. https://t.co/cmbOm2u3t7
In @NatureCellBio: @KivancBirsoy's lab has discovered that the antioxidant glutathione plays a vital role in maintaining smooth operations of a protein-producing hub in the cell called the endoplasmic reticulum by acting as a protein “proofreader.”
🔗: https://t.co/F2cChfBjJT
Check out this impressive work and #tweetorial from @gadmark and @shanshanliu1218! If you’re interested in organellar metabolism and metabolite transport, this is a landmark paper on ER redox metabolism and transport👇
@AlonMillet@shanshanliu1218 Thank you Alon! Your proteomics and RNA-seq analysis were a key part of this story. Really appreciate everything you brought to this
Was an honor to contribute to this tremendous study co-led by the brilliant duo of @gadmark and @shanshanliu1218. Check out the thread below to learn more about how SLC33A1 works to maintain ER redox balance!
Loss of SLC33A1 shifts PDIs toward oxidized states, triggers ER stress, and creates dependency on ERAD. Disease variants linked to Huppke-Brendel syndrome impair GSSG export. This work connects ER redox biology to neurodegeneration and cancer. 8/9