36 results on '"Mehra, Surabhi"'
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2. Convergent generation of atypical prions in knockin mouse models of genetic prion disease
3. The G51D SNCA mutation generates a slowly progressive α-synuclein strain in early-onset Parkinson’s disease
4. The molecular determinants of a universal prion acceptor.
5. Anti-prion drugs do not improve survival in novel knock-in models of inherited prion disease
6. The Molecular Determinants of a Universal Prion Acceptor
7. Anti-prion drugs do not improve survival in novel knock-in models of inherited prion disease
8. α-Synuclein aggregation nucleates through liquid–liquid phase separation
9. α-Synuclein misfolding and aggregation: Implications in Parkinson’s disease pathogenesis
10. Anti-prion drugs do not improve survival in knock-in models of inherited prion disease
11. Convergent generation of atypical prions in knock-in mouse models of genetic prion disease
12. Sensitized Emission Imaging Allows Nanoscale Surface Polarity Mapping of α‑Synuclein Amyloid Fibrils.
13. The G51D SNCA mutation generates a slowly progressive alpha-synuclein strain in early-onset Parkinson's disease
14. α-Synuclein Aggregation Intermediates form Fibril Polymorphs with Distinct Prion-like Properties
15. Direct Demonstration of Seed Size-Dependent α-Synuclein Amyloid Amplification
16. Co-aggregation and secondary nucleation in the life cycle of human prolactin/galanin functional amyloids
17. Author response: Co-aggregation and secondary nucleation in the life cycle of human prolactin/galanin functional amyloids
18. Size-dependent secondary nucleation and amplification of α-synuclein amyloid fibrils
19. Structural and Functional Insights into α-Synuclein Fibril Polymorphism
20. Effect of Disease-Associated P123H and V70M Mutations on β-Synuclein Fibrillation
21. α-Synuclein aggregation intermediates form fibril polymorphs with distinct prion-like properties
22. α‐Synuclein Spontaneously Adopts Stable and Reversible α‐Helical Structure in Water‐Less Environment
23. Liquid-liquid phase separation and liquid-to-solid transition mediate α-synuclein amyloid fibril containing hydrogel formation
24. Lipopolysaccharide from Gut Microbiota Modulates α-Synuclein Aggregation and Alters Its Biological Function
25. Glycosaminoglycans have variable effects on α-synuclein aggregation and differentially affect the activities of the resulting amyloid fibrils
26. The Familial α-Synuclein A53E Mutation Enhances Cell Death in Response to Environmental Toxins Due to a Larger Population of Oligomers
27. Parkinson’s Disease Associated α-Synuclein Familial Mutants Promote Dopaminergic Neuronal Death in Drosophila melanogaster
28. Comparison of Kinetics, Toxicity, Oligomer Formation, and Membrane Binding Capacity of α-Synuclein Familial Mutations at the A53 Site, Including the Newly Discovered A53V Mutation
29. Cytotoxic Oligomers and Fibrils Trapped in a Gel-like State of α-Synuclein Assemblies
30. Complexation of NAC-Derived Peptide Ligands with the C-Terminus of α-Synuclein Accelerates Its Aggregation
31. Multitude NMR studies of α-synuclein familial mutants: probing their differential aggregation propensities
32. α-synuclein aggregation and its modulation
33. p53 amyloid formation leading to its loss of function: implications in cancer pathogenesis
34. Iron-based nano-particles for Lipolase immobilization and stabilization
35. Complexation of NAC-Derived Peptide Ligands with the C-Terminus of α-Synuclein Accelerates Its Aggregation
36. Anti-prion drugs do not improve survival in knock-in models of inherited prion disease.
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