學歷
美國哈佛大學 分子細胞生物學 博士(2003)
美國加州大學 柏克萊分校 學士(1999)
經歷
上海科技大學生命科學與技術學院常任副教授,PI (2023)
上海同濟大學醫學院教授/特聘研究員,PI (2017)
台灣中央研究院分子生物所博士後研究員(2010)
榮譽
國科會112年度2030跨世代國際年輕傑出學者
論文與著作
Original Research Articles
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- Zhang S, Wang L, Yi S, Li S, Wang H, Wang R, Liu Y, Yan W, Liu C, He K, Ho MS#, 2023, A phosphorylation-dependent switch of the lysosomal V-ATPase assembly regulates α-synuclein clearance in glia, bioRxiv, Dec 8, 2023.12.07.570521
- Wang L, Zhang S, Yi S, Ho MS#, 2023, A new regulator of autophagy initiation in glia, Autophagy, Aug 29;1-3, invited commentary.
- Wang M and Ho MS#, 2023, Profiling neurotransmitter-evoked glial responses by RNA-sequencing analysis, Neural Circuits 17:1252759.
- Zhang S, Yi S, Wang L, Li S, Wang H, Song L, Ou J, Zhang M, Wang M, Zheng Y, Wang R, Yang K, Liu T, Ho MS#, 2023, Cyclin-G-associated kinase GAK/dAux regulates autophagy initiation via ULK1/Atg1 in glia, Proc Natl Acad Sci U S A, Jul 18;120(29):e2301002120 (featured in Logical Thinking Neuroscience and BioArtMED Wechat public forums).
- Li T, Shi W, Ho MS#, Zhang YQ#, 2023, A Pvr–AP-1–Mmp1 signaling pathway is activated in astrocytes upon traumatic brain injury, eLife, 12:RP87258 (featured in Brainnews Wechat public forum).
- Wang L, Wang H, Yi S, Zhang S, Ho MS#, 2022, A LRRK2/dLRRK-mediated lysosomal pathway that contributes to glial cell death and DA neuron survival, Traffic, Oct;23(10):506-520 (featured on the Cover).
- Yang M, Wang H, Chen C, Zhang S, Wang M, Senapati B, Li S, Yi S, Wang L, Zhang M, Yin S, He Y, Xue L, Lin S, Ho MS#, 2021, Glia-derived temporal signals orchestrate neurogenesis in the Drosophila mushroom body, Proc Natl Acad Sci U S A, 118(23):e2020098118 (featured in Logical Thinking Neuroscience Wechat public forum).
- Liu YJ#, Zhang T, Chen S, Cheng D, Wu C, Wang X, Duan D, Zhu L, Lou H, Gong Z, Wang XD#, Ho MS#, Duan S, 2021, The noncanonical role of the protease cathepsin D as a cofilin phosphatase, Cell Res, 31(7):801-813 (last corresponding author).
- Liu YJ, Zhang T, Cheng D, Yang J, Chen S, Wang X, Li X, Duan D, Lou H, Zhu L, Luo J, Ho MS#, Wang XD#, Duan S#, 2020, Late endosomes promote microglia migration via cytosolic translocation of immature protease cathD, Sci Adv, 6(50):eaba5783.
- Cao W, Song L, Cheng J, Yi N, Cai L, Huang FD, Ho MS#, 2017, An automated rapid iterative negative geotaxis assay for analyzing adult climbing behavior in a Drosophila model of neurodegeneration, J Vis Exp, (127):56507.
- Xiao X, Chen C, Yu TM, Ou J, Rui M, Zhai Y, He Y, Xue L, Ho MS#, 2017, Molecular chaperone Calnexin regulates the function of Drosophila sodium channel Paralytic, Front Mol Neurosci, 10:57.
- Song L, He Y, Ou J, Zhao Y, Li R, Cheng J, Lin CH, Ho MS#, 2017, Auxilin underlies progressive locomotor deficits and dopaminergic neuron loss in a Drosophila model of Parkinson’s disease, Cell Rep, 18(5):1132-1143.
Editorials, Reviews, Chapters, and Books
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- Ho MS#, Verkhratsky A#, Duan S#, Parpura V#, 2019, Editorial: Glia in health and disease, Front Mol Neurosci, 12:63.
- Ho MS#, 2014, Neurodevelopment and degeneration, Neurosci Bull, 30(4):539-41.
- Ho MS#, 2017, Neuroglial crosstalk by mitochondria, Neurosci Bull, 33(1):111-112.
- Ho MS#, 2019, Microglia in Parkinson’s disease-Neuroglia in neurodegenerative diseases, Adv Exp Med Biol, 1175:335-353.
- Wang L, Wang H, Ho MS#, 2019, Drosophila glia, Colloquium series on neuroglia in biology and medicine: from physiology to disease, Morgan & Claypool Publishers.
- Ho MS# and Duan, S#, 2013, Purinergic mechanisms in glial cells, invited book chapter, Neuroglia, Oxford University Press, 306-319.
- Yi S, Wang L, Wang H, Ho MS#, Zhang S#, 2022, Pathogenesis of α-synuclein in Parkinson’s Disease: From a Neuron-Glia Crosstalk Perspective, J. Mol. Sci. 23, 14753 (IJMS Top View papers in 2022).
- Cheng J, Lu Q, Song L, Ho MS#, 2018, α-Synuclein Trafficking in Parkinson’s Disease: Insights From Fly and Mouse Models, ASN Neuro, 10:1759091418812587.
Research Interest
分子細胞神經生物學,神經退化性疾病,膠質細胞在行為神經迴路中的功能
本實驗室的長期研究目標是結合果蠅及小鼠等動物模型,用分子細胞生物、顯微成像、行為模式建立等方法,研究腦中主要一類細胞“神經膠質細胞”的發育及功能。神經膠質細胞是腦中活躍的一群細胞,參與調控不同神經迴路與行為模式。我們主要探討膠質細胞與神經元之間互相作用的機制,期能最終解開膠質細胞調控腦迴路、行為及神經退化的生物學機制。
目前實驗室的研究主軸有:
(1)探究膠質細胞調控神經退化疾病的致病機轉。帕金森病是一類好發於老年人的神經退化疾病,其病程長,早期影響生活品質,晚期患者多數無法自理,為家庭和社會帶來嚴重的精神與經濟負擔。已知膠質細胞參與帕金森病的病理過程,但其相關分子機轉及基因調控仍待釐清。過去我們已成功地利用多種實驗技術證明膠質細胞的蛋白質穩態在帕金森病進程中的重要性。接下來,我們將透過不同神經生物學方法,聯結基因功能與多種神經生理指標,探討膠質細胞對神經退化的影響;我們將全面深入探討膠質細胞在保護組織及抗發炎時所使用的相關基因調控和訊息傳導機制,為臨床上的應用提供重要的分子基礎,開發可能的治療靶點,減緩疾病進展;
(2)探究神經膠質細胞調控行為迴路的神經機轉。許多前期研究發現,膠質細胞在控制許本能行為的腦迴路中執行重要的功能,我們實驗室則發現了膠質細胞在果蠅與小鼠的攝食與厭惡性行為中扮演著不可忽視的角色,而這些功能在兩種物種間具保守性。為了進一步了解膠質細胞調控攝食與厭惡性行為迴路中的機制,我們將運用光遺傳及化學遺傳方法選擇性激活膠質細胞,研究對行為的影響;另一方面,我們也將即時記錄動物進行這些行為的時候腦中膠質細胞的變化,包括其功能與細胞形態。歡迎對神經退化疾病及本能行為相關研究感興趣的你加入!
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從分子到認知的整合型神經科學研究
教學及研究本著希望啟發及培育下一代神經科學人才,
將來對了解人類心理狀態、行為的根源及治療神經系統
的疾病有所貢獻。