Endoplasmic reticulum (ER)-associated degradation (ERAD) is a universally important process among eukaryotic cells. ERAD is necessary to preserve cell integrity since the accumulation of defective proteins results in diseases associated with neurological dysfunction, cancer, and infections. This process involves recognition of misfolded or misassembled proteins that have been translated in association with ER membranes. Recognition of ERAD substrates leads to their extraction through the ER membrane (retrotranslocation or dislocation), ubiquitination, and destruction by cytosolic proteasomes. This review focuses on ERAD and its components as well as how viruses use this process to promote their replication and to avoid the immune response.
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http://dx.doi.org/10.3389/fmicb.2014.00330 | DOI Listing |
J Virus Erad
December 2024
Center of Infectious Diseases, West China Hospital of Sichuan University, Chengdu, 610041, China.
Background: Hepatitis C virus (HCV) eradication with sofosbuvir/velpatasvir (SOF/VEL) represents a significant advancement, offering hope for eliminating the virus in diverse patient populations. But real-world data on its effectiveness and safety remains scarce for patients with chronic hepatitis C (CHC) in China, especially those with HCV GT3b, cirrhosis, hepato-cellular carcinoma (HCC), or HCV/hepatitis B (HBV), HCV/HIV, or HCV/HBV/HIV coinfection.
Methods: In this real-world prospective observational study, we recruited patients from the West China Hospital and Public Health Clinical Center of Chengdu in China.
Am J Physiol Cell Physiol
December 2024
Department of Biological Sciences, University of Pittsburgh, Pittsburgh, PA, USA.
Autosomal dominant polycystic kidney disease (ADPKD) is a common genetic disorder leading to end-stage renal disease. ADPKD arises from mutations in the and genes, which encode polycystin 1 (PC1) and polycystin 2 (PC2), respectively. PC2 is a non-selective cation channel, and disease-linked mutations disrupt normal cellular processes, including signaling and fluid secretion.
View Article and Find Full Text PDFAtherosclerosis
December 2024
Department of Medical Biochemistry, Amsterdam UMC Location AMC, University of Amsterdam, Meibergdreef 9, 1105AZ, Amsterdam, the Netherlands; Amsterdam Gastroenterology Endocrinology Metabolism (AGEM) Institute, Amsterdam UMC, Meibergdreef 9, 1105AZ, Amsterdam, the Netherlands; Amsterdam Cardiovascular Sciences (ACS) Institute, Amsterdam UMC, Meibergdreef 9, 1105AZ, Amsterdam, the Netherlands. Electronic address:
Cholesterol is a vital component of cellular membranes and is an essential molecule in mammalian physiology. Yet dysregulation of hepatic cholesterol metabolism and an increase in plasma cholesterol is linked to development of atherosclerotic cardiovascular disease. Maintaining tight regulation of cholesterol homeostasis is therefore essential, elegantly highlighted by the control of hepatic low-density lipoprotein receptor (LDLR) abundance and associated lipoprotein clearance.
View Article and Find Full Text PDFJ Exp Med
March 2025
Department of Immunobiology, University of Lausanne, Epalinges, Switzerland.
Toll-like receptors (TLRs) are central to initiate immune responses against invading pathogens. To ensure host defense while avoiding aberrant activation leading to pathogenic inflammation and autoimmune diseases, TLRs are tightly controlled by multilevel regulatory mechanisms. Through a loss-of-function genetic screen in a reporter cell line engineered to undergo cell death upon TLR7-induced IRF5 activation, we identified here CCDC134 as an essential factor for TLR responses.
View Article and Find Full Text PDFCell Discov
December 2024
Institute of Biotechnology, Helsinki Institute of Life Science HiLIFE, University of Helsinki, Helsinki, Finland.
The continuous evolution of SARS-CoV-2 has led to the emergence of several variants of concern (VOCs) that significantly affect global health. This study aims to investigate how these VOCs affect host cells at proteome level to better understand the mechanisms of disease. To achieve this, we first analyzed the (phospho)proteome changes of host cells infected with Alpha, Beta, Delta, and Omicron BA.
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