A new concept: Aβ1-42 generates a hyperfunctional proteolytic NCX3 fragment that delays caspase-12 activation and neuronal death. [electronic resource]
Producer: 20121015Description: 10609-17 p. digitalISSN:- 1529-2401
- Amyloid beta-Peptides -- pharmacology
- Animals
- Calcium -- metabolism
- Calcium Channel Blockers -- pharmacology
- Calpain -- metabolism
- Caspase 3 -- metabolism
- Cell Death -- drug effects
- Cell Differentiation -- drug effects
- Cells, Cultured
- Chelating Agents -- pharmacology
- Cricetinae
- Dogs
- Dose-Response Relationship, Drug
- Egtazic Acid -- pharmacology
- Embryo, Mammalian
- Endoplasmic Reticulum -- drug effects
- Enzyme Activation -- drug effects
- Female
- Hippocampus -- cytology
- Male
- Mice
- Mice, Knockout
- Nerve Growth Factor -- pharmacology
- Neurons -- drug effects
- Patch-Clamp Techniques
- Peptide Fragments -- pharmacology
- Proteolysis -- drug effects
- RNA Interference -- physiology
- Rats
- Sodium -- metabolism
- Sodium-Calcium Exchanger -- genetics
- Time Factors
- Transfection
- Up-Regulation -- drug effects
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Publication Type: Journal Article; Research Support, Non-U.S. Gov't
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