Shanshan Liu, PhD
Associate Research Scientist in Cell BiologyCards
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Associate Research Scientist in Cell Biology
Biography
Shanshan Liu, PhD, is an Associate Research Scientist in the Department of Cell Biology at Yale School of Medicine. Her research focuses on organelle metabolism: how organelles establish and adapt distinct biochemical environments, and how disruption of these environments contributes to disease.
She earned her BS in Biology from Shaanxi Normal University in 2015 and her PhD in Molecular Biology and Biochemistry from the National Institute of Biological Sciences, Beijing, in 2021. She completed postdoctoral training in Cell Biology and Metabolism at The Rockefeller University from 2022 to 2026.
Her doctoral research identified adaptive mechanisms that regenerate cytosolic NAD+ and preserve mitochondrial membrane potential during respiratory stress. During her postdoctoral work, she developed endoplasmic reticulum immunopurification (ER-IP) to study ER metabolism and identified SLC33A1 as a major exporter of oxidized glutathione, linking metabolite transport to ER redox balance and protein homeostasis.
At Yale, her independent research program investigates how ER metabolic environments are organized and specialized across cell types. Her laboratory integrates organelle immunopurification, metabolomics, functional genetics, biochemistry, structural biology, and mouse physiology to connect compartment-specific metabolism with physiology and disease.
Appointments
Cell Biology
Associate Research ScientistPrimary
Other Departments & Organizations
Education & Training
- Postdoctoral Fellow
- Rockefeller University (2026)
- PhD
- National Institute of Biological Sciences, Molecular Biology and Biochemistry
- BS
- Shaanxi Normal University, Biology (2015)
Research
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Overview
Our laboratory studies how organelles establish and maintain distinct metabolic environments, and how these environments adapt to physiological demands and disease. We focus on the endoplasmic reticulum (ER), an interconnected organelle essential for protein folding, lipid synthesis, redox balance, and cellular homeostasis.
We investigate how metabolite transport and compartment-specific metabolism support ER function, and how ER metabolic environments are organized and specialized across cell types. Building on the discovery that SLC33A1 exports oxidized glutathione from the ER, we examine the links between metabolite movement, redox regulation, and protein homeostasis.
Our approach combines organelle immunopurification, metabolomics, functional genetics, biochemistry, structural biology, and mouse physiology to connect molecular mechanisms with cellular and organismal function.
Medical Research Interests
ORCID
0000-0001-8293-1025- View Lab Website
Liu Lab | Metabolic Homeostasis in the Secretory Pathway
Research at a Glance
Publications Timeline
Research Interests
Mitochondria
Oxidation-Reduction
Glutathione
Endoplasmic Reticulum
Publications
2026
SLC33A1 exports oxidized glutathione to maintain endoplasmic reticulum redox homeostasis
Liu S, Gad M, Li C, Cho K, Liu Y, Wangdu K, Belay V, Millet A, Kojima H, Sanford H, Wölk M, Urnavicius L, Fedorova M, Patti G, Vinogradova E, Hite R, Birsoy K. SLC33A1 exports oxidized glutathione to maintain endoplasmic reticulum redox homeostasis. Nature Cell Biology 2026, 28: 903-914. PMID: 41998286, DOI: 10.1038/s41556-026-01922-y.Peer-Reviewed Original ResearchThis study identifies SLC33A1 as the transporter that removes oxidized glutathione from the endoplasmic reticulum, maintaining proper protein folding.
2023
Autoregulatory control of mitochondrial glutathione homeostasis
Liu Y, Liu S, Tomar A, Yen F, Unlu G, Ropek N, Weber R, Wang Y, Khan A, Gad M, Peng J, Terzi E, Alwaseem H, Pagano A, Heissel S, Molina H, Allwein B, Kenny T, Possemato R, Zhao L, Hite R, Vinogradova E, Mansy S, Birsoy K. Autoregulatory control of mitochondrial glutathione homeostasis. Science 2023, 382: 820-828. PMID: 37917749, PMCID: PMC11170550, DOI: 10.1126/science.adf4154.Peer-Reviewed Original ResearchThis study shows how mitochondria sense and regulate glutathione, a key antioxidant, through an iron-sulfur cluster feedback mechanism controlling its transporter.A mitochondrial SCF‐FBXL4 ubiquitin E3 ligase complex degrades BNIP3 and NIX to restrain mitophagy and prevent mitochondrial disease
Cao Y, Zheng J, Wan H, Sun Y, Fu S, Liu S, He B, Cai G, Cao Y, Huang H, Li Q, Ma Y, Chen S, Wang F, Jiang H. A mitochondrial SCF‐FBXL4 ubiquitin E3 ligase complex degrades BNIP3 and NIX to restrain mitophagy and prevent mitochondrial disease. The EMBO Journal 2023, 42: embj2022113033. PMID: 36896912, PMCID: PMC10308365, DOI: 10.15252/embj.2022113033.Peer-Reviewed Original ResearchCitationsAltmetricChemical inhibition of mitochondrial fission via targeting the DRP1-receptor interaction
Yang J, Chen P, Cao Y, Liu S, Wang W, Li L, Li J, Jiang Z, Ma Y, Chen S, Zheng S, Qi X, Jiang H. Chemical inhibition of mitochondrial fission via targeting the DRP1-receptor interaction. Cell Chemical Biology 2023, 30: 278-294.e11. PMID: 36827981, DOI: 10.1016/j.chembiol.2023.02.002.Peer-Reviewed Original ResearchCitationsAltmetric
2022
Mitochondrial cristae architecture protects against mtDNA release and inflammation
He B, Yu H, Liu S, Wan H, Fu S, Liu S, Yang J, Zhang Z, Huang H, Li Q, Wang F, Jiang Z, Liu Q, Jiang H. Mitochondrial cristae architecture protects against mtDNA release and inflammation. Cell Reports 2022, 41: 111774. PMID: 36476853, DOI: 10.1016/j.celrep.2022.111774.Peer-Reviewed Original ResearchCitationsAltmetricMeSH KeywordsProtocols for analyzing metabolic derangements caused by increased NADH/NAD+ ratio in cell lines and in mice
Liu S, Ma Y, Jiang H. Protocols for analyzing metabolic derangements caused by increased NADH/NAD+ ratio in cell lines and in mice. STAR Protocols 2022, 3: 101120. PMID: 35106502, PMCID: PMC8784396, DOI: 10.1016/j.xpro.2021.101120.Peer-Reviewed Original ResearchAltmetricIdentification and characterization of novel MPC1 gene variants causing mitochondrial pyruvate carrier deficiency
Jiang H, Alahmad A, Fu S, Fu X, Liu Z, Han X, Li L, Song T, Xu M, Liu S, Wang J, Albash B, Alaqeel A, Catalina V, Prokisch H, Taylor R, McFarland R, Fang F. Identification and characterization of novel MPC1 gene variants causing mitochondrial pyruvate carrier deficiency. Journal Of Inherited Metabolic Disease 2022, 45: 264-277. PMID: 34873722, DOI: 10.1002/jimd.12462.Peer-Reviewed Original ResearchCitationsAltmetric
2021
Multifaceted roles of mitochondrial stress responses under ETC dysfunction – repair, destruction and pathogenesis
Liu S, Liu S, Jiang H. Multifaceted roles of mitochondrial stress responses under ETC dysfunction – repair, destruction and pathogenesis. The FEBS Journal 2021, 289: 6994-7013. PMID: 34918460, DOI: 10.1111/febs.16323.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsCitationsAltmetricGlycerol-3-phosphate biosynthesis regenerates cytosolic NAD+ to alleviate mitochondrial disease
Liu S, Fu S, Wang G, Cao Y, Li L, Li X, Yang J, Li N, Shan Y, Cao Y, Ma Y, Dong M, Liu Q, Jiang H. Glycerol-3-phosphate biosynthesis regenerates cytosolic NAD+ to alleviate mitochondrial disease. Cell Metabolism 2021, 33: 1974-1987.e9. PMID: 34270929, DOI: 10.1016/j.cmet.2021.06.013.Peer-Reviewed Original ResearchThis study shows that boosting glycerol-3-phosphate synthesis restores cellular energy balance and extends lifespan in a mouse model of mitochondrial complex I disease.OXPHOS deficiency activates global adaptation pathways to maintain mitochondrial membrane potential
Liu S, Liu S, He B, Li L, Li L, Wang J, Cai T, Chen S, Jiang H. OXPHOS deficiency activates global adaptation pathways to maintain mitochondrial membrane potential. EMBO Reports 2021, 22: embr202051606. PMID: 33655635, PMCID: PMC8025004, DOI: 10.15252/embr.202051606.Peer-Reviewed Original ResearchCitationsAltmetric
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