Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8085521 | PMC |
| http://dx.doi.org/10.3389/fphar.2021.653549 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Transmission of unfolded protein response-a regulator of disease progression, severity, and spread in virus infections.
mBio
January 2025
Department of Infectious Diseases, Molecular Virology, Center for Integrative Infectious Disease Research, Medical Faculty Heidelberg, Heidelberg University, Heidelberg, Germany.
The unfolded protein response (UPR) is a cell-autonomous stress response aimed at restoring homeostasis due to the accumulation of misfolded proteins in the endoplasmic reticulum (ER). Viruses often hijack the host cell machinery, leading to an accumulation of misfolded proteins in the ER. The cell-autonomous UPR is the immediate response of an infected cell to this stress, aiming to restore normal function by halting protein translation, degrading misfolded proteins, and activating signaling pathways that increase the production of molecular chaperones.
View Article and Find Full Text PDFUBL5 and Its Role in Viral Infections.
Viruses
December 2024
Key Laboratory of Biosafety Defense (Naval Medical University), Ministry of Education, Naval Medical University (Second Military Medical University), Shanghai 200433, China.
Unlike other ubiquitin-like family members, UBL5 is structurally and functionally atypical, and a novel role in various biological processes and diseases has been discovered. UBL5 can stabilize the structure of the spliceosome, can promote post-transcriptional processing, and has been implicated in both DNA damage repair and protein unfolding reactions, as well as cellular mechanisms that are frequently exploited by viruses for their own proliferation during viral infections. In addition, UBL5 can inhibit viral infection by binding to the non-structural protein 3 of rice stripe virus and mediating its degradation.
View Article and Find Full Text PDFModulating Endoplasmic Reticulum Stress in Gastrointestinal Cancers: Insights from Traditional Chinese Medicine.
Pharmaceuticals (Basel)
November 2024
School of Pharmacy, Hangzhou Normal University, Hangzhou 311121, China.
Endoplasmic reticulum (ER) stress and the unfolded protein response (UPR) play critical roles in tumorigenesis, cancer progression, and drug resistance. Persistent activation of the ER stress system enhances the survival capacities of malignant tumor cells, including increased proliferation, invasion, and resistance to treatment. Dysregulation of ER function and the resultant stress is a common cellular response to cancer therapies and may lead to cancer cell death.
View Article and Find Full Text PDFDistinct UPR and Autophagic Functions Define Cell-Specific Responses to Proteotoxic Stress in Microglial and Neuronal Cell Lines.
Cells
December 2024
Departamento de Bioquímica y Biología Molecular, Facultad de Farmacia, Universidad de Sevilla (US), 41012 Sevilla, Spain.
Autophagy is a catabolic process involved in different cellular functions. However, the molecular pathways governing its potential roles in different cell types remain poorly understood. We investigated the role of autophagy in the context of proteotoxic stress in two central nervous system cell types: the microglia-like cell line BV2 and the neuronal-like cell line N2a.
View Article and Find Full Text PDFMitochondrial Dysfunction in Cardiac Disease: The Fort Fell.
Biomolecules
November 2024
Department of Cardiology, Hygeia Hospital, 15123 Athens, Greece.
Myocardial cells and the extracellular matrix achieve their functions through the availability of energy. In fact, the mechanical and electrical properties of the heart are heavily dependent on the balance between energy production and consumption. The energy produced is utilized in various forms, including kinetic, dynamic, and thermal energy.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!