45 results on '"Dong Xiao"'
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2. Aberrance of GAP43/p-GAP43 Closely Associates with the Pathology of Neuron Loss in Prion-Infected Rodent Models
3. Accumulation of Prion Triggers the Enhanced Glycolysis via Activation of AMKP Pathway in Prion-Infected Rodent and Cell Models
4. Abnormal Changes of IL3/IL3R and Its Downstream Signaling Pathways in the Prion-Infected Cell Line and in the Brains of Scrapie-Infected Rodents
5. Navβ2 Intracellular Fragments Contribute to Aβ1-42-Induced Cognitive Impairment and Synaptic Deficit Through Transcriptional Suppression of BDNF
6. Enhanced M-CSF/CSF1R Signaling Closely Associates with PrPSc Accumulation in the Scrapie-Infected Cell Line and the Brains of Scrapie-Infected Experimental Rodents
7. PrPSc Inhibition and Cellular Protection of DBL on a Prion-Infected Cultured Cell via Multiple Pathways
8. Accumulation of Prion Triggers the Enhanced Glycolysis via Activation of AMKP Pathway in Prion-Infected Rodent and Cell Models
9. Abnormal Changes of IL3/IL3R and Its Downstream Signaling Pathways in the Prion-Infected Cell Line and in the Brains of Scrapie-Infected Rodents
10. Overexpression of PLK3 Mediates the Degradation of Abnormal Prion Proteins Dependent on Chaperone-Mediated Autophagy
11. Protein Misfolding Cyclic Amplification Cross-Species Products of Mouse-Adapted Scrapie Strain 139A and Hamster-Adapted Scrapie Strain 263K with Brain and Muscle Tissues of Opposite Animals Generate Infectious Prions
12. Increases of Galectin-1 and its S-nitrosylated form in the Brain Tissues of Scrapie-Infected Rodent Models and Human Prion Diseases
13. The Brain NO Levels and NOS Activities Ascended in the Early and Middle Stages and Descended in the Terminal Stage in Scrapie-Infected Animal Models
14. Serum Resistin Levels May Contribute to an Increased Risk of Acute Cerebral Infarction
15. Proteomic Analyses for the Global S-Nitrosylated Proteins in the Brain Tissues of Different Human Prion Diseases
16. Treatment of SMB-S15 Cells with Resveratrol Efficiently Removes the PrPSc Accumulation In Vitro and Prion Infectivity In Vivo
17. The Levels of Tau Isoforms Containing Exon-2 and Exon-10 Segments Increased in the Cerebrospinal Fluids of the Patients with Sporadic Creutzfeldt-Jakob Disease
18. Enhancement of Autophagy by Histone Deacetylase Inhibitor Trichostatin A Ameliorates Neuronal Apoptosis After Subarachnoid Hemorrhage in Rats
19. FBXW7-Induced MTOR Degradation Forces Autophagy to Counteract Persistent Prion Infection
20. Remarkable Activation of the Complement System and Aberrant Neuronal Localization of the Membrane Attack Complex in the Brain Tissues of Scrapie-Infected Rodents
21. Apparent Reduction of ADAM10 in Scrapie-Infected Cultured Cells and in the Brains of Scrapie-Infected Rodents
22. Analyses of the Similarity and Difference of Global Gene Expression Profiles in Cortex Regions of Three Neurodegenerative Diseases: Sporadic Creutzfeldt-Jakob Disease (sCJD), Fatal Familial Insomnia (FFI), and Alzheimer’s Disease (AD)
23. Disruption of Glycosylation Enhances Ubiquitin-Mediated Proteasomal Degradation of Shadoo in Scrapie-Infected Rodents and Cultured Cells
24. Significant Reduction of the GLUT3 Level, but not GLUT1 Level, Was Observed in the Brain Tissues of Several Scrapie Experimental Animals and Scrapie-Infected Cell Lines
25. Infection of Prions and Treatment of PrP106–126 Alter the Endogenous Status of Protein 14-3-3 and Trigger the Mitochondrial Apoptosis Possibly via Activating Bax Pathway
26. Global Protein Differential Expression Profiling of Cerebrospinal Fluid Samples Pooled from Chinese Sporadic CJD and non-CJD Patients
27. Flotillin-1 Mediates PrPC Endocytosis in the Cultured Cells During Cu2+ Stimulation Through Molecular Interaction
28. Abortive Cell Cycle Events in the Brains of Scrapie-Infected Hamsters with Remarkable Decreases of PLK3/Cdc25C and Increases of PLK1/Cyclin B1
29. Enhanced M-CSF/CSF1R Signaling Closely Associates with PrPSc Accumulation in the Scrapie-Infected Cell Line and the Brains of Scrapie-Infected Experimental Rodents.
30. Comparative Analysis of Gene Expression Profiles Between Cortex and Thalamus in Chinese Fatal Familial Insomnia Patients
31. PrPSc Inhibition and Cellular Protection of DBL on a Prion-Infected Cultured Cell via Multiple Pathways.
32. Overexpression of PLK3 Mediates the Degradation of Abnormal Prion Proteins Dependent on Chaperone-Mediated Autophagy
33. Protein Misfolding Cyclic Amplification Cross-Species Products of Mouse-Adapted Scrapie Strain 139A and Hamster-Adapted Scrapie Strain 263K with Brain and Muscle Tissues of Opposite Animals Generate Infectious Prions
34. Increases of Galectin-1 and its S-nitrosylated form in the Brain Tissues of Scrapie-Infected Rodent Models and Human Prion Diseases
35. Serum Resistin Levels May Contribute to an Increased Risk of Acute Cerebral Infarction
36. The Brain NO Levels and NOS Activities Ascended in the Early and Middle Stages and Descended in the Terminal Stage in Scrapie-Infected Animal Models
37. Treatment of SMB-S15 Cells with Resveratrol Efficiently Removes the PrPSc Accumulation In Vitro and Prion Infectivity In Vivo
38. Proteomic Analyses for the Global S-Nitrosylated Proteins in the Brain Tissues of Different Human Prion Diseases
39. The Levels of Tau Isoforms Containing Exon-2 and Exon-10 Segments Increased in the Cerebrospinal Fluids of the Patients with Sporadic Creutzfeldt-Jakob Disease
40. FBXW7-Induced MTOR Degradation Forces Autophagy to Counteract Persistent Prion Infection
41. Enhancement of Autophagy by Histone Deacetylase Inhibitor Trichostatin A Ameliorates Neuronal Apoptosis After Subarachnoid Hemorrhage in Rats
42. Remarkable Activation of the Complement System and Aberrant Neuronal Localization of the Membrane Attack Complex in the Brain Tissues of Scrapie-Infected Rodents
43. Significant Reduction of the GLUT3 Level, but not GLUT1 Level, Was Observed in the Brain Tissues of Several Scrapie Experimental Animals and Scrapie-Infected Cell Lines
44. Infection of Prions and Treatment of PrP106–126 Alter the Endogenous Status of Protein 14-3-3 and Trigger the Mitochondrial Apoptosis Possibly via Activating Bax Pathway
45. Global Protein Differential Expression Profiling of Cerebrospinal Fluid Samples Pooled from Chinese Sporadic CJD and non-CJD Patients
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