Related Experiment Video
Updated: Nov 25, 2025
07:55
Imaging the Intracellular Trafficking of APP with Photoactivatable GFP
Published on: October 17, 2015
12.1K
Corrigendum: Activated PPARγ Abrogates Misprocessing of Amyloid Precursor Protein, Tau Missorting and Synaptotoxicity
Susanne Moosecker1,2, Patrícia Gomes3,4, Chrysoula Dioli3,4
1Department Stress Neurobiology and Neurogenetics, Max Planck Institute of Psychiatry, Munich, Germany.
Frontiers in Cellular Neuroscience
|December 16, 2020
Summary
This study focuses on the correction of a previously published article's Digital Object Identifier (DOI). The corrected DOI ensures proper citation and access to the scientific research within the field of neuroscience.
Area of Science:
- Neuroscience
- Cellular Biology
Context:
- Correction of a previously published article's Digital Object Identifier (DOI).
- Ensuring accurate citation and accessibility of scientific literature.
Purpose:
- To provide the correct DOI for the article 10.3389/fncel.2019.00239.
- Facilitating seamless retrieval of the research paper for the scientific community.
Summary:
- The article DOI: 10.3389/fncel.2019.00239 has been corrected.
- This ensures the integrity and discoverability of the published research.
Impact:
- Improved accessibility to the scientific article.
- Enhanced reliability of citation tracking and academic referencing.
Related Concept Videos
01:37The Unfolded Protein Response
5.9K
The ER is the hub of protein synthesis in a cell. It has robust systems to quality control protein folding and also for degradation of terminally misfolded proteins. Under normal conditions, a small proportion of misfolded proteins that cannot be salvaged need to be transported to the cytoplasm by the ER-associated degradation or ERAD pathways. However, if the ERAD cannot handle the misfolded proteins, the cell activates the unfolded protein response or UPR to adjust the protein folding...
5.9K
01:22Alzheimer's Disease: Treatment
592
Alzheimer's Disease (AD), a neurodegenerative disorder, is pathologically identified by amyloid plaques and neurofibrillary tangles composed of tau protein. AD pharmacotherapy aims to manage cognitive symptoms, delay disease progression, and treat behavioral symptoms. The treatment is primarily symptomatic and palliative, with no definitive disease-modifying therapy available. Cholinesterase inhibitors, including donepezil (Aricept), rivastigmine (Exelon), and galantamine (Razadyne), are...
592
01:12GPCR Desensitization
7.3K
G protein-coupled receptor (GPCR) signaling plays a crucial role in cell functioning. GPCR desensitization is an equally essential process. It allows cells to respond to changing environments and regain sensitivity to new stimuli while preventing unnecessary stimulation when no longer needed. Prolonged exposure to stimuli leads to GPCR desensitization. It involves blocking the receptors from binding and activating additional G proteins. This inhibits activation of downstream effectors, thereby...
7.3K
03:03Amyloid Fibrils
11.2K
Amyloid fibrils are aggregates of misfolded proteins. Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils.
Amyloid deposits were observed as early as 1639 in the liver and the spleen. In 1854, Rudolph Virchow performed iodine staining,...
Amyloid deposits were observed as early as 1639 in the liver and the spleen. In 1854, Rudolph Virchow performed iodine staining,...
11.2K