Bing Su, PhD, MPH
About
Biography
Dr. Su is the KC Wong Endowed Professor and Director, Shanghai Institute of Immunology, SJTU and Director, SJTUSM - Yale University Institute of Immune Metabolism. He received his B.S. in Cell Biology from Peking University and completed his MPH and PhD graduate studies at Yale University. He continued his postdoctoral research at the University of California. Prof. Su joined SJTU and the Shanghai Institute of Immunology in 2012. The research in his laboratory focuses on the biology of signal transduction mediated by the intracellular protein kinase network such as the mitogen-activated protein kinase (MAPK) cascades and the mammalian target of rapamycine (mTOR) pathway in gut immune responses and in blood vessel function/development. They study the genes that encode either the serine/threonine kinases or their regulators in the kinase pathways. Prof. Su has been recognized as a Distinguished Professor of SJTU School of Medicine. Dr. Su currently holds an adjunct appointment at Yale School of Medicine in the Department of Immunobiology.
Appointments
Immunobiology
Professor AdjunctPrimary
Other Departments & Organizations
Education & Training
- Postdoc training
- UCSD (1995)
- PhD
- Yale University (1991)
- MPH
- Yale University (1987)
- BS
- Peking University (1984)
Research
Overview
The research in my laboratory focuses on the biology of signal transduction mediated by the intracellular protein kinase networks. We study the mitogen-activated protein kinase (MAPK) pathway and the mammalian target of rapamycine (mTOR) pathway. We wish to understand how these intracellular kinase pathways are utilized and regulated by immune system and cardiovascular system. Specifically, we want to reveal their specificity and physiological function in immune responses and in cardiovascular development and function.
We are also working to elucidate the underlying molecular mechanisms by which the kinase pathway-mediated receptor signaling regulates immune cell development, differentiation and effector function, as well as angiogenic signaling for cardiovascular development. Furthermore, we want to study the immune and inflammatory responses in the cardiovascular system and to determine how the MAPK pathway and the mTOR pathway are involved in these processes in physiological and pathological conditions.
To address the questions describe above, we have studied two Ser/Thr protein kinase molecules called MEKK2 and MEKK3 belonging to the MAP3K family in the MAPK pathway, and an adaptor molecule called Sin1, in the mTOR pathway. Thus far, my laboratory has generated knockout mice (both germline and conditional knockout) for these molecules to study their roles in the immune and cardiovascular systems. We have found that both MEKK2 and MEKK3 are key signaling molecules in the immune cells and endothelial cells, are required for multiple receptor-generated signals, and are also required for cellular stress responses.
We also demonstrated that Sin1 is a key regulator of the mTOR complex 2 (mTORC2) and is essential for Akt HM and TM site phosphorylation. Sin1-mTORC2 may also modify many other members of the AGC kinase family such as PKCs and SGK. We will continue to utilize a combination of biochemical and genetic approaches to study the regulation and physiological roles of MEKK2, MEKK3, and Sin1-mTOR signaling in immune and cardiovascular system.
Research at a Glance
Yale Co-Authors
Publications Timeline
Lei Shen
David G. Schatz, PhD
Lichong Yan
Publications
2024
TMED4 facilitates Treg suppressive function via ROS homeostasis in tumor and autoimmune mouse models
Jiang Z, Wang H, Wang X, Duo H, Tao Y, Li J, Li X, Liu J, Ni J, Wu E, Xiang H, Guan C, Wang X, Zhang K, Zhang P, Hou Z, Liu Y, Wang Z, Su B, Li B, Hao Y, Li B, Wu X. TMED4 facilitates Treg suppressive function via ROS homeostasis in tumor and autoimmune mouse models. Journal Of Clinical Investigation 2024 PMID: 39480507, DOI: 10.1172/jci179874.Peer-Reviewed Original ResearchAltmetricConceptsEndoplasmic reticulum stressER-associated degradationSuppressive functionTreg cellsFoxp3 stabilityReactive oxygen speciesSuppressive function of Treg cellsFunction of Treg cellsExacerbated inflammatory phenotypeAnti-tumor immunityTreg suppressive functionRegulatory T cellsTreg cell stabilityT cell hyperactivationAutoimmune mouse modelReactive oxygen species homeostasisTreg signatureT cellsTregsInflammatory phenotypeReactive oxygen species scavengingMouse modelTMED4Excessive reactive oxygen speciesProtein 4Comparative single-cell multiome identifies evolutionary changes in neural progenitor cells during primate brain development
Liu Y, Luo X, Sun Y, Chen K, Hu T, You B, Xu J, Zhang F, Cheng Q, Meng X, Yan T, Li X, Qi X, He X, Guo X, Li C, Su B. Comparative single-cell multiome identifies evolutionary changes in neural progenitor cells during primate brain development. Developmental Cell 2024 PMID: 39481377, DOI: 10.1016/j.devcel.2024.10.005.Peer-Reviewed Original ResearchConceptsEvolutionary changesDistal regulatory elementsGene regulatory mechanismsExtracellular matrixSingle-cell multiomicsProgenitor cellsTranscriptional divergenceEvolutionary divergenceChromatin regionsChromatin accessibilityNeural progenitorsRegulatory elementsSequence changesTranscriptional rewiringGenetic mechanismsMouse prefrontal cortexRegulatory mechanismsPrefrontal cortexHuman neural progenitorsHuman-specific featuresUpper-layer neuronsNeural progenitor cellsChromatinCellular propertiesProgenitor proliferationDisulfiram/copper complex improves the effectiveness of the WEE1 inhibitor Adavosertib in p53 deficient non-small cell lung cancer via ferroptosis
Liu D, Cao J, Ding X, Xu W, Yao X, Dai M, Tai Q, Shi M, Fei K, Xu Y, Su B. Disulfiram/copper complex improves the effectiveness of the WEE1 inhibitor Adavosertib in p53 deficient non-small cell lung cancer via ferroptosis. Biochimica Et Biophysica Acta (BBA) - Molecular Basis Of Disease 2024, 1870: 167455. PMID: 39111630, DOI: 10.1016/j.bbadis.2024.167455.Peer-Reviewed Original ResearchAltmetricConceptsWEE1 inhibitorNon-small cell lung cancerNSCLC cellsCell lung cancerSynergistic therapeutic approachesProtein levelsEffective treatment strategiesPro-oxidant drugsKinase activity of Wee1P53-deficient cellsActivity of Wee1Tumor volumeCombination therapyDSF-CuRepurposing disulfiramTumor weightSolute carrier family 7 memberWee1 protein levelsP53 deficiencyPoor prognosisReduced cell viabilityFunctional p53Lung cancerTreatment strategiesXenograft modelTWIST1+FAP+ fibroblasts in the pathogenesis of intestinal fibrosis in Crohn’s disease
Zhang Y, Wang J, Sun H, Xun Z, He Z, Zhao Y, Qi J, Sun S, Yang Q, Gu Y, Zhang L, Zhou C, Ye Y, Wu N, Zou D, Su B. TWIST1+FAP+ fibroblasts in the pathogenesis of intestinal fibrosis in Crohn’s disease. Journal Of Clinical Investigation 2024, 134: e179472. PMID: 39024569, PMCID: PMC11405050, DOI: 10.1172/jci179472.Peer-Reviewed Original ResearchAltmetricConceptsExcessive extracellular matrixComplication of Crohn's diseaseDextran sulfate sodium saltSingle-cell RNA sequencingMesenchymal stromal cellsTGF-b signalingScRNA-seqCrohn's diseaseIntestinal fibrosisCell transcriptomic profilingRNA sequencingTranscriptome profilingSingle cell transcriptomic profilingInhibition of Twist1Murine colitis modelPathogenesis of intestinal fibrosisAnti-fibrosis drugsExtracellular matrixPharmacological inhibitionFibrotic intestineFibrotic sitesTwist1 expressionECM productionCD patientsIntestinal obstructionSex-biased regulatory changes in the placenta of native highlanders contribute to adaptive fetal development
Yue T, Guo Y, Qi X, Zheng W, Zhang H, Wang B, Liu K, Zhou B, Zeng X, Ouzhuluobu, He Y, Su B. Sex-biased regulatory changes in the placenta of native highlanders contribute to adaptive fetal development. ELife 2024, 12: rp89004. PMID: 38869160, PMCID: PMC11175615, DOI: 10.7554/elife.89004.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsExpression divergenceHigh birth weightFull-term placentaDecreased immune responseSyncytial knotsMale newbornsEndoplasmic reticulum stressPlacental trophoblastsFetal developmentUmbilical cordBirth weightHan migrantsNative TibetansUmbilical artery wallImmune responseStudy of human reproductionPlacentaAdaptation of human populationsHistological changesBetween-population differencesReticulum stressMigrantsHuman reproductionBetween-populationReproductive successSex-biased regulatory changes in the placenta of native highlanders contribute to adaptive fetal development
Yue T, Guo Y, Qi X, Zheng W, Zhang H, Wang B, Liu K, Zhou B, Zeng X, Ouzhuluobu, He Y, Su B. Sex-biased regulatory changes in the placenta of native highlanders contribute to adaptive fetal development. ELife 2024, 12 DOI: 10.7554/elife.89004.5.Peer-Reviewed Original ResearchConceptsExpression divergenceHigh birth weightFull-term placentaDecreased immune responseSyncytial knotsMale newbornsEndoplasmic reticulum stressPlacental trophoblastsFetal developmentUmbilical cordBirth weightHan migrantsNative TibetansUmbilical artery wallImmune responseStudy of human reproductionPlacentaAdaptation of human populationsHistological changesBetween-population differencesReticulum stressMigrantsHuman reproductionBetween-populationReproductive successSUMO-specific protease 1 regulates germinal center B cell response through deSUMOylation of PAX5
Qi J, Yan L, Sun J, Huang C, Su B, Cheng J, Shen L. SUMO-specific protease 1 regulates germinal center B cell response through deSUMOylation of PAX5. Proceedings Of The National Academy Of Sciences Of The United States Of America 2024, 121: e2314619121. PMID: 38776375, PMCID: PMC11145296, DOI: 10.1073/pnas.2314619121.Peer-Reviewed Original ResearchMeSH Keywords and ConceptsConceptsPaired box protein 5GC B cellsSUMO-specific protease 1Activation-induced cytidine deaminaseProtein SUMOylationClass switch recombinationProtein stabilityB cellsProtease 1B cell responsesProtein 5Cytidine deaminaseSENP1Up-regulatedGC B cell responsesSomatic hypermutationSUMOylationDeSUMOylationGerminal centersHigher affinityProduction of class-switched antibodiesGerminal center B cell responsesGC reactionMemory B cellsClass-switched antibodiesDEPDC5 protects CD8+ T cells from ferroptosis by limiting mTORC1-mediated purine catabolism
Li S, Ouyang X, Sun H, Jin J, Chen Y, Li L, Wang Q, He Y, Wang J, Chen T, Zhong Q, Liang Y, Pierre P, Zou Q, Ye Y, Su B. DEPDC5 protects CD8+ T cells from ferroptosis by limiting mTORC1-mediated purine catabolism. Cell Discovery 2024, 10: 53. PMID: 38763950, PMCID: PMC11102918, DOI: 10.1038/s41421-024-00682-z.Peer-Reviewed Original ResearchCitationsAltmetricConceptsCD8+ T cellsPeripheral CD8+ T cellsAnti-tumor immunityT cellsTumor-infiltrating CD8+ T cellsCD8+ T cell homeostasisCD8+ T cell numbersImpaired anti-tumor immunityT cell numbersT-cell protectionT cell homeostasisCancer patient survivalLevels of xanthine oxidasePatient survivalCD8Epilepsy patientsDEPDC5Suppression of ferroptosisMTORC1 signalingFerroptosisMolecular mechanismsImmunityXanthine oxidasePurine catabolismExpressionATP6AP1 was Phast-ID’ed as a long-sought GEF for Rheb
Li S, Ouyang X, Su B. ATP6AP1 was Phast-ID’ed as a long-sought GEF for Rheb. Cell Research 2024, 34: 397-398. PMID: 38744982, PMCID: PMC11143262, DOI: 10.1038/s41422-024-00967-8.Peer-Reviewed Original ResearchCrosstalk between CD8+ T cells and mesenchymal stromal cells in intestine homeostasis and immunity
Chen Y, Sun H, Luo Z, Mei Y, Xu Z, Tan J, Xie Y, Li M, Xia J, Yang B, Su B. Crosstalk between CD8+ T cells and mesenchymal stromal cells in intestine homeostasis and immunity. Advances In Immunology 2024, 162: 23-58. PMID: 38866438, DOI: 10.1016/bs.ai.2024.02.001.Peer-Reviewed Original ResearchConceptsCD8+ T cellsMesenchymal stromal cell populationT cellsStromal cell populationsMHC II moleculesMesenchymal stromal cellsStromal cellsFunction of CD8+ T cellsCD103+ dendritic cellsMHC-IIIntestinal homeostasisCell populationsPotential pathophysiological impactGut-associated lymphoid tissueIgA+ plasma cellsDiseases of inflammationDead cell debrisTissue residencyDendritic cellsFood antigensIL-33Plasma cellsIntestinal toleranceLymphoid tissueImmunostimulatory agents
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