Research Topics
Genomes and Genes
| Jian Zhi WangSummaryAffiliation: Tongji Medical College Country: China Publications
| Collaborators
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Detail Information
Publications
Temporal correlation of the memory deficit with Alzheimer-like lesions induced by activation of glycogen synthase kinase-3Yue Wang
Department of Pathophysiology, Key Laboratory of Neurological Disease of National Education Committee, Tongji Medical College, Huazhong University of Science and Technical, Wuhan, China
J Neurochem 106:2364-74. 2008..Our data provide direct evidence demonstrating that activation of GSK-3 by WT/GFX may cause memory deficit through tau hyperphosphorylation and suppression of ACh in hippocampus...
Role of melatonin in Alzheimer-like neurodegenerationJian Zhi Wang
Pathophysiology Department, Key Laboratory of Neurological Diseases of Hubei Province, Tongji Medical School, Huazhong University of Science and Technology, Wuhan, China
Acta Pharmacol Sin 27:41-9. 2006..The capacity of melatonin to prevent or ameliorate tau and Abeta pathology further enhances its potential in the prevention or treatment of AD...- Microtubule-associated protein tau in development, degeneration and protection of neuronsJian Zhi Wang
Pathophysiology Department, Hubei Provincial Key Laboratory of Neurological Diseases, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, PR China
Prog Neurobiol 85:148-75. 2008..The primary aim of this review is to summarize the latest developments and perspectives in our understanding about the roles of tau, especially hyperphosphorylation, in the development, degeneration and protection of neurons... - 17beta-estradiol attenuates glycogen synthase kinase-3beta activation and tau hyperphosphorylation in Akt-independent mannerHai Rong Shi
Department of Pathophysiology, Key Laboratory of Neurological Disease of Ministry of Education and Hubei Province, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, PR China
J Neural Transm 115:879-88. 2008..We found that betaE2 could attenuate Wort/GFX-induced GSK-3beta activation and tau hyperphosphorylation with Akt-independent manner. It suggests that betaE2 may arrest AD-like tau hyperphosphorylation by directly targeting GSK-3beta... - Prolonged Alzheimer-like tau hyperphosphorylation induced by simultaneous inhibition of phosphoinositol-3 kinase and protein kinase C in N2a cellsGuo Gang Xu
Department of Pathophysiology, Institute of Neuroscience, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China
Acta Biochim Biophys Sin (Shanghai) 37:349-54. 2005.... - Dehydroevodiamine attenuates tau hyperphosphorylation and spatial memory deficit induced by activation of glycogen synthase kinase-3 in ratsJun Hua Peng
Pathophysiology Department, Hubei Provincial Key Laboratory of Neurological Disease, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, PR China
Neuropharmacology 52:1521-7. 2007.... - Peroxynitrite induces Alzheimer-like tau modifications and accumulation in rat brain and its underlying mechanismsYong Jie Zhang
Pathophysiology Department, Key Laboratory of Neurological Disease of Hubei Province, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, PR China
FASEB J 20:1431-42. 2006..Our findings reveal a common upstream stimulator and a potential therapeutic target for Alzheimer-like neurodegeneration... - Tau overexpression inhibits cell apoptosis with the mechanisms involving multiple viability-related factorsHai Hong Wang
Department of Pathophysiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
J Alzheimers Dis 21:167-79. 2010.... - Bip enhanced the association of GSK-3β with tau during ER stress both in vivo and in vitroZan Chao Liu
Department of Pathology and Pathophysiology, Key Laboratory of Neurological Disease of National Education Ministry and Hubei Province, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
J Alzheimers Dis 29:727-40. 2012..All these data suggest an essential role of Bip in GSK-3β dependent tau hyperphosphorylation in ER stress by promoting the binding of GSK-3β to tau... - Biphasic effects of forskolin on tau phosphorylation and spatial memory in ratsQing Tian
Department of Pathophysiology, Key Laboratory of Neurological Disease Education Ministry of China, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, Chin a
J Alzheimers Dis 17:631-42. 2009..These data suggest that the upregulation of PKA by forskolin to a certain level may activate PP-2A but that the latter can ameliorate the PKA-induced tau phosphorylation and memory impairment in the rats... - Tau dephosphorylation potentiates apoptosis by mechanisms involving a failed dephosphorylation/activation of Bcl-2Xin an Liu
Department of Pathophysiology, Huazhong University of Science and Technology, Wuhan, China
J Alzheimers Dis 19:953-62. 2010..These data suggest that tau dephosphorylation by PP2Ac facilitates cell apoptosis with the mechanisms involving a failed dephosphorylation/activation of Bcl-2... - Proteasome inhibition increases tau accumulation independent of phosphorylationYing Hua Liu
Department of Pathophysiology, Hubei Provincial Key Laboratory of Neurological Diseases, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, PR China
Neurobiol Aging 30:1949-61. 2009.... - Acetyl-L-carnitine ameliorates spatial memory deficits induced by inhibition of phosphoinositol-3 kinase and protein kinase CXia Jiang
Department of Pathophysiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
J Neurochem 118:864-78. 2011..These results suggest that ALCAR could ameliorate WT/GFX-induced spatial memory deficits through inhibition tau hyperphosphorylation and modulation of memory-associated proteins... - Relationship of adult neurogenesis with tau phosphorylation and GSK-3β activity in subventricular zoneXiao ping Hong
Department of Pathophysiology, Key Laboratory of Neurological Diseases of Education Committee of China, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People s Republic of China
Neurochem Res 36:288-96. 2011..The SVZ neurogenesis was also unaffected in tau knockout and human tau transgenic mice. These results suggest that tau phosphorylation and GSK-3 activation may not be essential for adult SVZ neurogenesis... - Overexpression of tau proteins antagonizes amyloid-beta-potentiated apoptosis through mitochondria-caspase-3 pathway in N2a cellsZe Fen Wang
Department of Pathophysiology, Key Laboratory of Neurological Diseases of Educational Ministry of China, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
J Alzheimers Dis 20:145-57. 2010..These findings provide an explanation of the chronic nature of neurodegeneration of neurons with neurofibrillary pathology of abnormal hyperphosphorylated tau in AD and related tauopathies... - Essential role of tau phosphorylation in adult hippocampal neurogenesisXiao ping Hong
Department of Pathophysiology, Key Laboratory of Neurological Diseases of Education Committee of China, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People s Republic of China
Hippocampus 20:1339-49. 2010..It suggests that spatial/temporal manipulation of tau phosphorylation may be compensatory for the neuron loss in neurological disorders, including AD... - Acetyl-L-carnitine attenuates okadaic acid induced tau hyperphosphorylation and spatial memory impairment in ratsYang Yang Yin
Department of Pathophysiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, PR China
J Alzheimers Dis 19:735-46. 2010..Our study provides the first in vivo evidence that ALCAR can attenuate AD-like PP2A inhibition, tau hyperphosphorylation, and spatial memory deficit of the rats. It suggests that ALCAR may hold potential in AD treatment... - Inhibition of melatonin biosynthesis induces neurofilament hyperphosphorylation with activation of cyclin-dependent kinase 5Shaohui Wang
Department of Pathophysiology, Institute of Neuroscience, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, PR China
Neurochem Res 32:1329-35. 2007..These results suggest that inhibition of melatonin biosynthesis may activate cdk-5 and thus induces Alzheimer-like hyperphosphorylation of neurofilament proteins... - Glycogen synthase kinase-3β regulates leucine-309 demethylation of protein phosphatase-2A via PPMT1 and PME-1Xiu Qing Yao
Department of Pathophysiology, Key Laboratory of Neurological Diseases of Chinese Ministry of Education, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, PR China
FEBS Lett 586:2522-8. 2012..GSK-3 could negatively regulate PP2A regulatory subunit protein level. We conclude that GSK-3β can inhibit PP2A by increasing the inhibitory L309-demethylation involving upregulation of PME-1 and inhibition of PPMT1... - Folate/vitamin-B12 prevents chronic hyperhomocysteinemia-induced tau hyperphosphorylation and memory deficits in aged ratsWei Wei
Department of Pathophysiology, Key Laboratory of Neurological Disease of Education Committee of China, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
J Alzheimers Dis 27:639-50. 2011..These data demonstrate that folate/vit-B12 supplementation is also effective in a chronic hyperhomocysteinemia model in reversing the AD-like tau pathologies and memory deficits... - Melatonin arrests peroxynitrite-induced tau hyperphosphorylation and the overactivation of protein kinases in rat brainJun Yin
Department of Pathophysiology, Hua Zhong University of Science and Technology, Wuhan, China
J Pineal Res 41:124-9. 2006..We conclude that MEL can efficiently arrest peroxynitrite-induced tau hyperphosphorylation, and the underlying mechanism may involve scavenging the reactive species and suppressing the activated GSK-3beta and p38 MAPK family... - Constant illumination induces Alzheimer-like damages with endoplasmic reticulum involvement and the protection of melatoninZhi Qun Ling
Department of Pathology and Pathophysiology, Key Laboratory of Neurological Disease of National Education Ministry and Hubei Province, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
J Alzheimers Dis 16:287-300. 2009..It is suggested that melatonin deficiency may be an upstream effector responsible for the AD-like behavioral and molecular pathologies with ER stress-involved mechanisms... 
Kinases and phosphatases and tau sites involved in Alzheimer neurofibrillary degenerationJian Zhi Wang
Pathophysiology Department, Tongji Medical College, Huazhong University of Science and Technology, Wuhan P R China
Eur J Neurosci 25:59-68. 2007..These findings suggest that activation of PP-2A or inhibition of either both GSK-3beta and cdk5 or one of these two kinases plus PKA or CaMKII might be required to inhibit Alzheimer neurofibrillary degeneration...- Pesticides induce spatial memory deficits with synaptic impairments and an imbalanced tau phosphorylation in ratsNing Ning Chen
Department of Pathophysiology, Key Laboratory of Chinese Ministry of Education for Neurological Diseases, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, PR China
J Alzheimers Dis 30:585-94. 2012..Additionally, neuron loss in the hippocampus and cortex was observed upon administration of the pesticides. These results indicate that the pesticides exposure could induce AD-like pathology and cognitive abnormality in rats... - I(2)(PP2A) regulates p53 and Akt correlatively and leads the neurons to abort apoptosisGong Ping Liu
Pathophysiology Department, Key Laboratory of Neurological Disease of Education Committee of China, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, PR China
Neurobiol Aging 33:254-64. 2012..This finding contributes to the understanding of why most neurons in AD brain do not undergo apoptosis... - Acetyl-L-carnitine attenuates homocysteine-induced Alzheimer-like histopathological and behavioral abnormalitiesPeng Zhou
Department of Pathophysiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, P R China
Rejuvenation Res 14:669-79. 2011..Our data suggest that ALC could be a promising candidate for arresting Hcy-induced AD-like pathological and behavioral impairments... - Neuroglobin attenuates Alzheimer-like tau hyperphosphorylation by activating Akt signalingLi Ming Chen
Pathophysiology Department, Key Laboratory of Neurological Disease of Education Committee of China, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
J Neurochem 120:157-64. 2012..Our data indicate that Ngb may attenuate tau hyperphosphorylation through activating Akt signaling pathway, implying a therapeutic target for AD... - Berberine attenuates calyculin A-induced cytotoxicity and Tau hyperphosphorylation in HEK293 cellsGuang Yu
Department of Pathophysiology, Key Laboratory of Neurological Disease of National Education Ministry, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
J Alzheimers Dis 24:525-35. 2011..Our findings suggest that berberine may be a potential therapeutic drug for AD... - Nitration and oligomerization of tau induced by peroxynitrite inhibit its microtubule-binding activityYong Jie Zhang
Pathophysiology Department, Neuroscience Institute, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
FEBS Lett 579:2421-7. 2005.... - Inhibition of protein phosphatases induces transport deficits and axonopathyYing Yang
Pathophysiology Department, Hubei Provincial Key Laboratory of Neurological Diseases, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
J Neurochem 102:878-86. 2007.... - Upregulation of astrocytes protein phosphatase-2A stimulates astrocytes migration via inhibiting p38 MAPK in tg2576 miceXiu Ping Liu
Pathophysiology Department, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, People s Republic of China
Glia 60:1279-88. 2012.... - Betaine attenuates Alzheimer-like pathological changes and memory deficits induced by homocysteineGao Shang Chai
Department of Pathophysiology, Key Laboratory of Neurological Diseases of Chinese Ministry of Education, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
J Neurochem 124:388-96. 2013..Our data suggest that betaine could be a promising candidate for arresting Hcy-induced AD-like pathological changes and memory deficits... - NGF promotes long-term memory formation by activating poly(ADP-ribose)polymerase-1Shao Hui Wang
Department of Pathophysiology, Key Laboratory of Neurological Disease of Education Ministry of China, Tongji Medical College of Huazhong University of Science and Technology, Wuhan 430030, China
Neuropharmacology 63:1085-92. 2012..Our data provide the first evidence that NGF supplement facilitates synaptic plasticity and the memory ability through PARP-1-mediated protein polyADP-ribosylation and activation of PKA-CREB pathway... - Activation of glycogen synthase kinase-3 inhibits long-term potentiation with synapse-associated impairmentsLing Qiang Zhu
Department of Pathophysiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, People s Republic of China
J Neurosci 27:12211-20. 2007..We conclude that upregulation of GSK-3 impairs the synaptic plasticity both functionally and structurally, which may underlie the GSK-3-involved memory deficits... - Glycogen synthase kinase-3β regulates Tyr307 phosphorylation of protein phosphatase-2A via protein tyrosine phosphatase 1B but not SrcXiu Qing Yao
Department of Pathophysiology, Key Laboratory of Neurological Diseases of Chinese Ministry of Education, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, P R China
Biochem J 437:335-44. 2011..The results of the present study suggest that GSK-3β inhibits PP2A by increasing the inhibitory Tyr307 phosphorylation and decreasing the expression of PP2A, and the mechanism involves inhibition of PTP1B and CREB... - Phosphorylation of tau antagonizes apoptosis by stabilizing beta-catenin, a mechanism involved in Alzheimer's neurodegenerationHong Lian Li
Department of Pathophysiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China
Proc Natl Acad Sci U S A 104:3591-6. 2007..Our findings suggest that tau phosphorylation may lead the neurons to escape from an acute apoptotic death, implying the essence of neurodegeneration seen in the AD brains and related tauopathies... - Estradiol attenuates tau hyperphosphorylation induced by upregulation of protein kinase-AXin an Liu
Pathophysiology Department, Tongji Medical College, Hua Zhong University of Science and Technology, Wuhan, 430030, PR China
Neurochem Res 33:1811-20. 2008..These data provide the first evidence that 17beta-estradiol can inhibit PKA overactivation and the PKA-induced tau hyperphosphorylation, implying a preventive role of 17beta-estradiol in AD-like tau pathology... - Protein phosphatase 2A facilitates axonogenesis by dephosphorylating CRMP2Ling Qiang Zhu
Department of Pathophysiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, People s Republic of China
J Neurosci 30:3839-48. 2010..Our results reveal a mechanistic link between PP2A and axonogenesis/axonopathy, suggesting that upregulation of PP2A may be a promising therapeutic for some neurodegenerative disorders... - Homocysteine induces tau phosphorylation by inactivating protein phosphatase 2A in rat hippocampusChang E Zhang
Department of Pathology and Pathophysiology, Hubei Provincial Key Laboratory of Neurological Disease, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China
Neurobiol Aging 29:1654-65. 2008..These results suggest that homocysteine may be an upstream effector to induce AD-like tau hyperphosphorylation through inactivating PP2A... - Synaptic released zinc promotes tau hyperphosphorylation by inhibition of protein phosphatase 2A (PP2A)Xu Ying Sun
Department of Pathophysiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China
J Biol Chem 287:11174-82. 2012..Together, these results suggest that synaptically released zinc promotes tau hyperphosphorylation through PP2A inhibition... - LiCl attenuates thapsigargin-induced tau hyperphosphorylation by inhibiting GSK-3β in vivo and in vitroZheng Qi Fu
Department of Pathophysiology, Key Laboratory of Neurological Disease of National Education Ministry, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
J Alzheimers Dis 21:1107-17. 2010..Our data provide further evidence supporting the role of ER stress in tau hyperphosphorylation and the protective role of lithium... - EPAC null mutation impairs learning and social interactions via aberrant regulation of miR-124 and Zif268 translationYing Yang
Key Laboratory of Neurological Disease, Ministry of Education, China, and Department of Pathophysiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China
Neuron 73:774-88. 2012..Thus, EPAC proteins control miR-124 transcription in the brain for processing spatial learning and social interactions... - Effects of tau phosphorylation on proteasome activityQing Guo Ren
Department of Pathophysiology, Hubei Provincial Key Laboratory of Neurological Diseases, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, PR China
FEBS Lett 581:1521-8. 2007..Furthermore, tau hyperphosphorylation could partially reverse lactacystin-induced inhibition of proteasome. These results suggest that phosphorylation of tau plays a dual role in modulating the activity of proteasome... - Upregulation of AKT attenuates amyloid-β-induced cell apoptosisGang Yin
Department of Pathophysiology, the Key Laboratory of Neurological Diseases of the Ministry of Education, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
J Alzheimers Dis 25:337-45. 2011..Our data suggest that upregulation of AKT could be a promising therapeutic strategy for arresting Aβ toxicity in AD patients... - Tau becomes a more favorable substrate for GSK-3 when it is prephosphorylated by PKA in rat brainShi Jie Liu
Pathophysiology Department, Neuroscience Institute, Tongji Medical College, Hua-Zhong University of Science and Technology, Wuhan 430030, People's Republic of China
J Biol Chem 279:50078-88. 2004..These data provide a novel mechanism of the hyperphosphorylation of tau and identify both PKA and GSK-3 as promising therapeutic targets for AD and other tauopathies... - Effect of melatonin and melatonylvalpromide on beta-amyloid and neurofilaments in N2a cellsXiao Chuan Wang
Department of Pathophysiology, Hubei Provincial Key Laboratory in Neurological Diseases, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, PR China
Neurochem Res 33:1138-44. 2008..These results suggest that Mtv may be a better candidate in arresting the intracellular accumulation of Abeta and protecting the cells from Abeta-related toxicity... - GSK-3 beta inhibits presynaptic vesicle exocytosis by phosphorylating P/Q-type calcium channel and interrupting SNARE complex formationLing Qiang Zhu
Department of Pathophysiology, Institute of Neuroscience, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, People s Republic of China
J Neurosci 30:3624-33. 2010..These results indicate that GSK-3beta negatively regulates synaptic vesicle fusion events via interfering with Ca(2+)-dependent SNARE complex formation... - Zinc induces protein phosphatase 2A inactivation and tau hyperphosphorylation through Src dependent PP2A (tyrosine 307) phosphorylationYan Xiong
Department of Pathophysiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
Neurobiol Aging 34:745-56. 2013..We concluded that zinc induces PP2A inactivation and tau hyperphosphorylation through Src-dependent pathway, regulation of zinc homeostasis may be a promising therapeutic for AD and the related tauopathies... - Hyperhomocysteinemia increases beta-amyloid by enhancing expression of gamma-secretase and phosphorylation of amyloid precursor protein in rat brainChang E Zhang
Department of Pathophysiology, Key Laboratory of Neurological Disease of Education Committee of China, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China
Am J Pathol 174:1481-91. 2009..It is suggested that hyperhomocysteinemia may serve as an upstream factor for increased Abeta production as seen in patients with Alzheimer disease... - Correlation between choline signal intensity and acetylcholine level in different brain regions of ratXiao Chuan Wang
Department of Pathophysiology, Institute of Neuroscience, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, PR China
Neurochem Res 33:814-9. 2008..127 (S1BF cortex), respectively (y means acetylcholine, and x means Cho). These data suggest that the Cho signal intensity observed by (1)H MRS may be used as an indicator of acetylcholine level in different brain regions of the rats... - Activation of glycogen synthase kinase-3 inhibits protein phosphatase-2A and the underlying mechanismsGong Ping Liu
Pathophysiology Department, Key Laboratory of Neurological Disease of Hubei Province, Tongji Medical College, Hua Zhong University of Science and Technology, Wuhan 430030, PR China
Neurobiol Aging 29:1348-58. 2008..The activation of GSK-3 increased the expression and the activity of proteasome system. It suggests that activation of GSK-3 inhibits PP-2A through up-regulation of I(2)(PP-2A) with hnRNP A18-involved mechanism... - Disease-modified glycogen synthase kinase-3β intervention by melatonin arrests the pathology and memory deficits in an Alzheimer's animal modelCai Xia Peng
Pathophysiology Department, Key Laboratory of Education Ministry for Neurological Disorders, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, P R China
Neurobiol Aging 34:1555-63. 2013..Our finding suggests that melatonin treatment only at proper timing could arrest AD by targeting the activated GSK-3β, which provides primary evidence for the importance and strategy in developing disease-modifying interventions of AD... - Methylglyoxal induces tau hyperphosphorylation via promoting AGEs formationXiao Hong Li
Department of Pathophysiology, Key Laboratory of Neurological Diseases of Education Committee of China, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China
Neuromolecular Med 14:338-48. 2012..Thus, targeting MG may be a promising therapeutic strategy to prevent AD-like tau hyperphosphorylation... - The c-Jun N-terminal kinase inhibitor SP600125 is neuroprotective in amygdala kindled ratsXu Chen
Department of Neurosurgery, Tongji Hospital, Huazhong University of Science and Technology, Jiefang Ave 1095, 430030 Wuhan, China
Brain Res 1357:104-14. 2010..The JNK inhibitor SP600125 can show a protective effect on hippocampal neurons in TLE by inhibiting JNK activation... - Expression of the hyperphosphorylated tau attenuates ER stress-induced apoptosis with upregulation of unfolded protein responseXin an Liu
Pathophysiology Department, Key Laboratory of Neurological Disease of National Education Ministry and Hubei Province, Tongji Medical College, Huazhong University of Science and Technology, 430030, Wuhan, China
Apoptosis 17:1039-49. 2012..Our data suggest that tau hyperphosphorylation could attenuate the ER stress-induced apoptosis with the mechanism involving upregulation of UPR system... - PTPA activates protein phosphatase-2A through reducing its phosphorylation at tyrosine-307 with upregulation of protein tyrosine phosphatase 1BYu Luo
Department of Pathophysiology, Key Laboratory of Neurological Diseases of Chinese Ministry of Education, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030 PR China
Biochim Biophys Acta 1833:1235-43. 2013..Our data indicate that PTPA may activate PP2A through activating PTP1B and thus reducing the level of P-PP2AC, therefore upregulation of PTPA may represent a potential strategy in rescuing PP2A and arresting tau pathology in AD... - Melatonin attenuates scopolamine-induced memory/synaptic disorder by rescuing EPACs/miR-124/Egr1 pathwayXiong Wang
Department of Pathophysiology, Key Laboratory of Neurological Diseases of Education Committee of China, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, People s Republic of China
Mol Neurobiol 47:373-81. 2013..Our studies provide a novel underlying epigenetic mechanism for melatonin to attenuate the synaptic disorder and could benefit drug discovery in neurodegenerative diseases... - Inhibition of autophagy causes tau proteolysis by activating calpain in rat brainJia Yu Zhang
Department of Pathophysiology, Huazhong University of Science and Technology, Wuhan, People s Republic of China
J Alzheimers Dis 16:39-47. 2009..Our data suggest that the lysosomal autophagic system may not degrade tau in the normal adult rat brain and inhibition of autophagy may induce tau proteolysis through activating calpain... - Cytoglobin up-regulated by hydrogen peroxide plays a protective role in oxidative stressDan Li
Department of Pathophysiology and Hubei Provincial Key Laboratory of Neurological Diseases, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
Neurochem Res 32:1375-80. 2007..The Cygb-siRNA could exacerbate cell death upon H(2)O(2)-treatment, as demonstrated by MTT cell viability assay. Thus, Cygb in neuronal cells might be specifically induced under oxidative stress to protect them from death... - Dehydroevodiamine attenuates calyculin A-induced tau hyperphosphorylation in rat brain slicesJiang Fang
Department of Pathophysiology, Hubei Provincial Key Laboratory of Neurological Diseases, Huazhong University of Science and Technology, Wuhan 430030, China
Acta Pharmacol Sin 28:1717-23. 2007.... - Effect of amyloid peptides on serum withdrawal-induced cell differentiation and cell viabilityYi Peng Wang
Department of Pathophysiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China
Cell Res 14:467-72. 2004..These results suggest that the overproduction of A beta could not arrest cell differentiation induced by serum deprivation and that, at least to a certain degree and in a limited time period, is not toxic to cell viability... - Abnormal hyperphosphorylation of tau: sites, regulation, and molecular mechanism of neurofibrillary degenerationJian Zhi Wang
Pathophysiology Department, Key Laboratory of Ministry of Education of China for Neurological Disorders, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, PR China
J Alzheimers Dis 33:S123-39. 2013..In this article we briefly review the progress made in these areas of research... - AGEs induce Alzheimer-like tau pathology and memory deficit via RAGE-mediated GSK-3 activationXiao Hong Li
Department of Pathophysiology, Key Laboratory of Neurological Diseases of Education Committee of China, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
Neurobiol Aging 33:1400-10. 2012.... - Quantitative MR phase-corrected imaging to investigate increased brain iron deposition of patients with Alzheimer diseaseWen zhen Zhu
Department of Radiology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
Radiology 253:497-504. 2009..The aim of this study was to investigate the correlation of brain iron accumulation with the severity of cognitive impairment in patients with Alzheimer disease (AD)... - Overactivation of glycogen synthase kinase-3 by inhibition of phosphoinositol-3 kinase and protein kinase C leads to hyperphosphorylation of tau and impairment of spatial memoryShi Jie Liu
Pathophysiology Department, Neuroscience Institute, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
J Neurochem 87:1333-44. 2003.... - Hyperphosphorylation of microtubule-associated tau protein plays dual role in neurodegeneration and neuroprotectionYao Zhang
Li Yuan Hospital, Key Laboratory of Neurological Disorders of Education Ministry of China, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, PR China
Pathophysiology 16:311-6. 2009..The primary aim of this review is to summarize the latest developments and perspectives in our understanding about the roles of tau hyperphosphorylation in neurodegeneration and neuroprotection... - Protective effect of granulocyte colony-stimulating factor on intracerebral hemorrhage in ratLei Zhang
Hubei Provincial Key Laboratory of Neurological Disease, Pathophysiology Department, Tongji Medical College, Hua Zhong University of Science and Technology, 430030, Wuhan, People s Republic of China
Neurochem Res 34:1317-23. 2009..Our results reveal that G-CSF is also protective for the ICH with the mechanisms involving proliferation of neural stem cells, the migration of HSCs and the activation of astrocytes... - Elevated levels of phosphorylated neurofilament proteins in cerebrospinal fluid of Alzheimer disease patientsYuan-Yuan Hu
Tongji Medical College, HUST, Wuhan 430030, PR China
Neurosci Lett 320:156-60. 2002.... - Alzheimer-like tau phosphorylation induced by wortmannin in vivo and its attenuation by melatoninShi-Jie Liu
Department of Pathophysiology, Tongji Medical College, Huazhong Science and Technical University, Wuhan 430030, China
Acta Pharmacol Sin 23:183-7. 2002..CONCLUSION: Wortmannin induced in vivo Alzheimer-like hyperphosphorylation of tau at Ser396/404, and melatonin inhibited partially the pathological processes... - Melatonin ameliorated okadaic-acid induced Alzheimer-like lesionsYi-peng Wang
Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China
Acta Pharmacol Sin 25:276-80. 2004.... - Alzheimer neurofibrillary degeneration: therapeutic targets and high-throughput assaysKhalid Iqbal
New York State Institute for Basic Research in Developmental Disabilities, Staten Island, New York 10314 6399, USA
J Mol Neurosci 20:425-9. 2003..Development of high-throughput screening assays for potential drugs aimed at these therapeutic targets is currently under way... - Effects of endogenous beta-amyloid overproduction on tau phosphorylation in cell cultureZe-Fen Wang
Pathophysiology Department, Hubei Provincial Key Laboratory of Neurological Diseases, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
J Neurochem 98:1167-75. 2006..These results suggest that endogenously overproduced Abeta induces increased tau phosphorylation through activation of GSK-3, and that inactivation of PKC is at least one of the mechanisms involved in GSK-3 activation... - Significance and mechanism of Alzheimer neurofibrillary degeneration and therapeutic targets to inhibit this lesionKhalid Iqbal
Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, Staten Island 10314 6399, USA
J Mol Neurosci 19:95-9. 2002.... - Melatonin attenuates isoproterenol-induced protein kinase A overactivation and tau hyperphosphorylation in rat brainDan-Ling Wang
Department of Pathophysiology, Institute of Neuroscience, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
J Pineal Res 37:11-6. 2004.... - Alzheimer-like phosphorylation of tau and neurofilament induced by cocaine in vivoShi-Jie Liu
Pathophysiology Department, Neuroscience Institute, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China
Acta Pharmacol Sin 24:512-8. 2003..CONCLUSION: Peritoneal injection of cocaine induces Alzheimer-like hyperphosphorylation of tau and neurofilament in rat brain, and the effect may be not relevant to an increase in overexpression or overactivation of CDK5... - Inhibition of melatonin biosynthesis activates protein kinase a and induces Alzheimer-like tau hyperphosphorylation in ratsLing-Qiang Zhu
Department of Pathophysiology, Institute of Neuroscience, Tongji Medical College, Huazhong University of Science and Technology, Wuhan
Chin Med Sci J 20:83-7. 2005..CONCLUSION: Decreased melatonin may be involved in Alzheimer-like tau hyperphosphorylation, and overactivation of PKA may play a crucial role in this process... - Attenuation of okadaic acid-induced hyperphosphorylation of cytoskeletal proteins by heat preconditioning and its possible underlying mechanismsYa Fei Xu
Pathophysiology Department, Neuroscience Institute, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, People's Republic of China
Cell Stress Chaperones 9:304-12. 2004.... - Correlation of behavior changes and BOLD signal in Alzheimer-like rat modelZheng-Hui Hu
Department of Physics and Bio-X disciplinary Laboratory, Zhejiang University, Hangzhou, China
Acta Biochim Biophys Sin (Shanghai) 36:803-10. 2004..62. These results suggest that resting T2* signal may serve as a noninvasive quantitative marker in predicting AD-like spatial memory deficits and tau hyperphosphorylation... - Effect of inhibiting melatonin biosynthesis on spatial memory retention and tau phosphorylation in ratLing Qiang Zhu
Department of Pathophysiology, Institute of Neuroscience, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
J Pineal Res 37:71-7. 2004..These results strongly support the involvement of decreased melatonin in Alzheimer-like spatial memory impairment and tau hyperphosphorylation, and PP-2A may play a role in mediating aberrant melatonin-induced lesions... - Paired helical filaments (PHFs) are a family of single filament structures with a common helical turn period: negatively stained PHF imaged by TEM and measured before and after sonication, deglycosylation, and dephosphorylationGeorge C Ruben
Department of Biological Sciences, Dartmouth College, Hanover, New Hampshire 03755, USA
Microsc Res Tech 67:175-95. 2005..5-0.6 nm and 0.7-1.0 nm, respectively, and the right-hand helicity of the PHF was lost after deglycosylation. Dephosphorylation with PP-2A reduced the PHF wide regions by 6.0 nm and the thin regions by 2.6 nm... - Overexpression of dishevelled-1 attenuates wortmannin-induced hyperphosphorylation of cytoskeletal proteins in N2a cellHai-Hong Wang
Department of Pathophysiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China
Acta Pharmacol Sin 26:679-84. 2005..CONCLUSION: Overexpression of mouse DVL-1 protein inhibits wortmannin-induced hyperphosphorylation of neurofilament and tau in N2a cells... - Melatonin protects SH-SY5Y neuroblastoma cells from calyculin A-induced neurofilament impairment and neurotoxicityShu Peng Li
Department of Pathophysiology, Institute of Neuroscience, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, P.R. China
J Pineal Res 36:186-91. 2004..It is concluded that inhibition of PP-2A/PP-1 by CA induces abnormalities in NF metabolism and cell survival, and melatonin efficiently arrests the lesions... - Overexpression of amyloid precursor protein inhibits neurite outgrowth and disrupts cytoskeleton in N2a cellsZe-Fen Wang
Department of Pathophysiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China
Chin Med J (Engl) 117:775-8. 2004 - Melatonin attenuates beta-amyloid-induced inhibition of neurofilament expressionYing-chun Zhang
Department of Pathophysiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China
Acta Pharmacol Sin 25:447-51. 2004..CONCLUSION: Overproduction of A beta inhibits neurofilament expression, and melatonin attenuates the A beta-induced lesion in cytoskeletal protein... - Effects of melatonin on wortmannin-induced tau hyperphosphorylationYan-Qiu Deng
Department of Pathophysiology, Institute of Neuroscience, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China
Acta Pharmacol Sin 26:519-26. 2005..CONCLUSION: Wortmannin is an effective tool for reproducing Alzheimer-like tau hyperphosphorylation cell model and melatonin/vitamin E can effectively protect the cells from wortmannin-induced impairments... - Effect of melatonin on calyculin A-induced tau hyperphosphorylationXia-Chun Li
Department of Pathophysiology, Institute of Neuroscience, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, PR China
Eur J Pharmacol 510:25-30. 2005.... - Effects of EGF and bFGF on expression of microtubule-associated protein tau and MAP-2 mRNA in human umbilical cord mononuclear cellsWen Hai Yan
Department of Pathophysiology, Medical College of Zhengzhou University, Zhengzhou 450052, PR China
Cell Biol Int 29:153-7. 2005..The same upregulatory tendency was noted for tau mRNA expression. It is concluded that MNCs derived from human UCB cells may express some neural specific molecules that can be upregulated by cytokines, especially EGF and bFGF together... - [Mechanism of tau hyperphosphorylation in brain cortex of diabetic rats and effect of LiCl]Zhong-sen Qu
Department of Pathophysiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China
Zhongguo Yi Xue Ke Xue Yuan Xue Bao 28:244-8. 2006..05). CONCLUSION: The hyperphosphorylation of tau can be induced by activation of GSK-3 in diabetic rats. Lithium protects tau from hyperphosphorylation and may rescue memory retention in the rats by inhibiting GSK-3 activity... - [Effect of different culture media on viability and tau protein expression in rat hippocampal slices]Ying-chun Zhang
Department of Pathophysiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China
Zhongguo Yi Xue Ke Xue Yuan Xue Bao 27:513-7. 2005..CONCLUSION: The slices from 2 or 4 week-old rat hippocampi and DMEM/F12 medium may be the preferred choice for tau associated researches. An ideal Alzheimer's disease model may be established based on the results of these researches... - Concurrent alterations of O-GlcNAcylation and phosphorylation of tau in mouse brains during fastingXu Li
Department of Pathophysiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, Hubei, P.R. China
Eur J Neurosci 23:2078-86. 2006.... - Inhibition of protein phosphatase 2A induces phosphorylation and accumulation of neurofilaments in metabolically active rat brain slicesCheng-Xin Gong
Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, New York, NY 10314, USA
Neurosci Lett 340:107-10. 2003..These findings suggest that the hyperphosphorylation and accumulation of NF found in AD brain could have been caused by the down-regulation of PP2A... - [Duration of tau hyperphosphorylation and spatial memory deficit induced by single injection of Forskolin into lateral ventricle of rat]Jun-Xia Zhang
Department of Pathophysiology, Tongji Medical College, Huazhong Science and Technical University, Wuhan 430030, China
Zhongguo Yi Xue Ke Xue Yuan Xue Bao 28:355-9. 2006..The level of tau phosphorylation in hippocampus is somehow correlated with the spatial memory deficit in rats... - Acute anoxia induces tau dephosphorylation in rat brain slices and its possible underlying mechanismsRong Liu
Department of Pathophysiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
J Neurochem 94:1225-34. 2005..These data suggest that acute anoxia induces tau dephosphorylation, and that PP-2A may play a key role in tau dephosphorylation induced by acute anoxia... - [Alteration of beta-amyloid and glutamate transporter in the brain of diabetes rats and the underlying mechanism]Zhong-sen Qu
Department of Pathophysiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China
Zhongguo Yi Xue Ke Xue Yuan Xue Bao 27:708-11. 2005..05) in LiCl treated group, accompanied by a decreased activity of GSK-3. CONCLUSION: Overproduction of Abeta and impaired glutamate transporter exist in DM rats, and increase of GSK-3 may play a crucial role in this process... - [Effect of calpain on the degradation of tau protein in rat brain cortex extracts]Zheng-Yu Fang
Neuroscience Institute Pathophysiology Department Tongji Medical College Huazhong University of Science and Technology Wuhan 430030 China
Sheng Wu Hua Xue Yu Sheng Wu Wu Li Xue Bao (Shanghai) 35:629-34. 2003..These data suggest that both mu-calpain and m-calpain in brain cortex extracts are activated by Ca(2+) and both of them degraded tau protein, although, m-calpain plays a more important role in proteolysis of the tau protein... - Nitric oxide induces tau hyperphosphorylation via glycogen synthase kinase-3beta activationYong-Jie Zhang
Pathophysiology Department, Key Laboratory of Neurological Disease of Hubei Province, Tongji Medical College, Hua-Zhong University of Science and Technology, Wuhan 430030, PR China
FEBS Lett 579:6230-6. 2005..It is suggested that nitric oxide may be an upstream element of tau abnormal hyperphosphorylation in AD... - The involvement of glycogen synthase kinase-3 and protein phosphatase-2A in lactacystin-induced tau accumulationQing-Guo Ren
Department of Pathophysiology, Key Laboratory of Neurological Diseases of Hubei Province, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, PR China
FEBS Lett 580:2503-11. 2006..These results suggest that inhibition of proteasome by lactacystin induces tau accumulation and activation of GSK-3 and inhibition of PP-2A are involved...