33 results on '"Iijima-Ando, Kanae"'
Search Results
2. Drosophila Model of Alzheimer’s Amyloidosis
3. Transgenic Drosophila models of Alzheimer’s disease and tauopathies
4. Tau Ser262 phosphorylation is critical for Aβ42-induced tau toxicity in a transgenic Drosophila model of Alzheimerʼs disease
5. A DNA damage-activated checkpoint kinase phosphorylates tau and enhances tau-induced neurodegeneration
6. Transgenic cAMP Response Element Reporter Flies for Monitoring Circadian Rhythms
7. Interaction of N-Terminal Acetyltransferase with the Cytoplasmic Domain of β-Amyloid Precursor Protein and Its Effect on Aβ Secretion
8. Loss of Axonal Mitochondria Promotes Tau-Mediated Neurodegeneration and Alzheimer's Disease–Related Tau Phosphorylation Via PAR-1
9. Membrane-Microdomain Localization of Amyloid β-Precursor Protein (APP) C-terminal Fragments Is Regulated by Phosphorylation of the Cytoplasmic Thr668 Residue
10. O4-04-04: Disruption of mitochondrial transport promotes tau toxicity through Alzheimer's disease-related tau phosphorylation
11. P2-268: Inhibition of Sin3A/HDAC activity suppresses amyloid β-42 accumulation and toxicity through multiple mechanisms
12. O4-04-03: DNA damage-activated Ser/Thr kinases phosphorylate tau and enhance tau-induced neurodegeneration
13. P1-177: Studying mechanisms underlying Aβ42-induced tau toxicity in transgenic Drosophila models
14. Regulation of Energy Stores and Feeding by Neuronal and Peripheral CREB Activity in Drosophila
15. Mitochondrial Mislocalization Underlies Aβ42-Induced Neuronal Dysfunction in a Drosophila Model of Alzheimer's Disease
16. Transgenic Drosophila models of Alzheimer’s disease and tauopathies
17. JNK/FOXO-mediated Neuronal Expression of Fly Homologue of Peroxiredoxin II Reduces Oxidative Stress and Extends Life Span
18. Drosophila Models of Alzheimer's Amyloidosis: The Challenge of Dissecting the Complex Mechanisms of Toxicity of Amyloid-β 42
19. P1-028: Overexpression of neprilysin reduces Abeta42-induced neuron loss and intraneuronal Abeta42 deposits, but causes age-dependent axon pathology in drosophila
20. Overexpression of Neprilysin Reduces Alzheimer Amyloid-β42 (Aβ42)-induced Neuron Loss and Intraneuronal Aβ42 Deposits but Causes a Reduction in cAMP-responsive Element-binding Protein-mediated Transcription, Age-dependent Axon Pathology, and Premature Death in Drosophila
21. Aβ42 Mutants with Different Aggregation Profiles Induce Distinct Pathologies in Drosophila
22. Physiological Mouse Brain Aβ Levels Are Not Related to the Phosphorylation State of Threonine-668 of Alzheimer's APP
23. P1–398: Characterization of the effect of protein contexts harboring polyglutamine stretch on CREB activity in Drosophila
24. P1-006: Distinct accumulation properties of Aβ42 in the brain are associated with specific pathological phenotypes in Drosophila
25. Drosophila models of Alzheimer's amyloidosis: the challenge of dissecting the complex mechanisms of toxicity of amyloid-beta 42.
26. Inhibition of Sin3A/HDAC activity suppresses amyloid β-42 accumulation and toxicity through multiple mechanisms
27. Studying mechanisms underlying Aβ42-induced tau toxicity in transgenic Drosophila models
28. DNA damage-activated Ser/Thr kinases phosphorylate tau and enhance tau-induced neurodegeneration
29. Disruption of mitochondrial transport promotes tau toxicity through Alzheimer's disease-related tau phosphorylation.
30. Membrane-Microdomain Localization of Amyloid β-Precursor Protein (APP) C-terminal Fragments Is Regulated by Phosphorylation of the Cytoplasmic Thr668 Residue.
31. Overexpression of neprilysin reduces alzheimer amyloid-beta42 (Abeta42)-induced neuron loss and intraneuronal Abeta42 deposits but causes a reduction in cAMP-responsive element-binding protein-mediated transcription, age-dependent axon pathology, and premature death in Drosophila.
32. Interaction of N-terminal acetyltransferase with the cytoplasmic domain of beta-amyloid precursor protein and its effect on A beta secretion.
33. Transgenic cAMP response element reporter flies for monitoring circadian rhythms.
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