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12篇 您的检索式:作者名="Tse HM"
    题名 作者 年代 出处 被引量
1Mitochondrial neuronal uncoupling proteins:a target for potential disease-modification in Parkinson’s disease Philip显示文摘This review gives a brief insight into the role of mitochondrial dysfunction and oxidative stress in the converging pathogenic processes involved in Parkinson’s disease(PD).Mitochondria provide cellular energy in the form of ATP via oxidative phosphorylation,but as an integral part of this process,superoxides and other reactive oxygen species are also produced.Excessive free radical production contributes to oxidative stress.Cells have evolved to handle such stress via various endogenous anti-oxidant proteins.One such family of proteins is the mitochondrial uncoupling proteins(UCPs),which are anion carriers located in the mitochondrial inner membrane.There are five known homologues(UCP1 to 5),of which UCP4 and 5 are predominantly expressed in neural cells.In a series of previous publications,we have shown how these neuronal UCPs respond to 1-methyl-4-phenylpyridinium(MPP+;toxic metabolite of MPTP)and dopamine-induced toxicity to alleviate neuronal cell death by preserving ATP levels and mitochondrial membrane potential,and reducing oxidative stress.We also showed how their expression can be influenced by nuclear factor kappa-B(NF-B)signaling pathway specifically in UCP4.Furthermore,we previously reported an interesting link between PD and metabolic processes through the protective effects of leptin(hormone produced by adipocytes)acting via UCP2 against MPP+-induced toxicity.There is increasing evidence that these endogenous neuronal UCPs can play a vital role to protect neurons against various pathogenic stresses including those associated with PD.Their expression,which can be induced,may well be a potential therapeutic target for various drugs to alleviate the harmful effects of pathogenic processes in PD and hence modify the progression of this disease.WL Ho Jessica WM Ho Hui-Fang Liu Danny HF So Zero HM Tse Koon-Ho Chan David B Ramsden Shu-Leong Ho 2012Translational Neurodegeneration2012,1,1:3
2Aberrant expression of costimulatory molecules in splenocytes of the mevalonate kinase- deficient mouse model of human hyper-IgD syndrome (HIDS) 显示文摘Hager EJ Piganelli JD Tse HM 2012J Inherit Metab Dis2012,35,1:1
3A multivalent vaccine for type 1 diabetes skews T cell subsets to Th2 phenotype in NOD mice显示文摘Lin MS Tse HM Delmastro MM 2011Immunol Res2011,50,2:1
4A muhivalent vaccine for type 1 diabetes skews T cell subsets to Th2 phenotype in NOD mice 显示文摘Lin MS Tse HM Delmastro MM 2011Immunol Res2011,50,23:1
5Hu- man proinsulin C - peptide reduces high glu- cose - included proliferation and NF - kappaB activation in vascular smooth muscle cells 显示文摘Cifarelli V Luppi P Tse HM 2008Atherosclerosis2008,201,2:1
6Disruption of innate-mediated proinflammatory cytokine and reactive oxygen species third signal leads to antigen-specific hyporesponsiveness 显示文摘Tse HM Milton MJ Schreiner S 2007J Immunol2007,178,2:1
7Human proinsulin C- peptide reduces high glucose-induced proliferation and NF- kappaB activationin vascular smooth muscle cells 显示文摘Cifarelli V Luppi P Tse HM 2008Atherosclerosis2008,201,2:1
8Human proinsulin C-peptide reduces high glucose-induced proliferation and NF-KB activation in vascular smooth muscle cells 显示文摘Cifare Luppi P Tse HM 2008Atherosclerosis2008,201,2:1
9Human proinsulin C- peptide reduces high glucose-induced proliferation and NF-kap- paB activation in vascular smooth muscle cells显示文摘Cifarelli V Luppi P Tse HM 2008Atheroscle- rosis2008,201,2:1
10Human proinsulin C-peptide reduces high glucose-induced proliferation and NF-kappaB activation in vascular smooth muscle cells 显示文摘CifareUi V Luppi P Tse HM 2008Atherosclerosis2008,199,2:1
11Modulatory role of DR4- to DQS-restricted CD4 T-cell responses and type 1 diabetes susceptibility 显示文摘Ge X Piganelli JD Tse HM 2006Diabetes2006,55,12:1
12Human proinsulin C-peptide reduces high glucose-included proliferation and NF-kappa B activation n vascular smooth muscle cells显示文摘Cifarelli V Luppi P Tse HM 2008Atherosclerosis2008,201,2:1
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