The Non-Cellular Autonomic Mechanism of Neuronal Degeneration: Protein Synthesis and Secretion
A special issue of Life (ISSN 2075-1729). This special issue belongs to the section "Proteins and Proteomics".
Deadline for manuscript submissions: closed (31 July 2021) | Viewed by 486
Special Issue Editors
Interests: non cell autonomus degeneration and proteostasis
Interests: prion diseases and pathological mechanisms related to neurodegeneration
Interests: transcription and translation regulation in aging and neurodegenerative diseases
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
Unfolded protein response (UPR) is a physiological pathway that helps cells to survive in stress conditions. UPR involves three branches in the endoplasmic reticulum: the PERK, IRE1, and ATF6 pathways, leading to protein synthesis reduction, and the activation of protein degradation and chaperone gene transcription. Over activation of URP is associated with many neurodegenerative diseases, such as prion, Parkinson’s, and Alzheimer’s diseases. By blocking this mechanism, you can have a delay in the onset of the pathology, an improvement in behavioral test performance, and neuronal survival in animal models. UPR can spread from one cell to another, leading to a non-cell-autonomous mechanism of neuronal degeneration, which is reasonably ascribed to secreted factors.
In this Special Issue of Life, we want to invite researchers to share their new results and ideas related to UPR in non-neuronal cells involved in neuronal degeneration in the central nervous system (CNS), the alteration of secretion capacity, such as proteins or metabolites, and the transmission and impact of these on other cells.
Dr. Laura Tapella
Dr. Elena Restelli
Dr. Erica Buoso
Guest Editors
Manuscript Submission Information
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Keywords
- unfolded protein response
- protein synthesis
- protein degradation
- secretion
- inflammasome
- non cell autonomous
- neurodegeneration
- aging
