It has been reported that intracellular accumulation of reactive oxygen species (ROS) has a significant role in tumor necrosis factor (TNF)-α-induced cell apoptosis and necrosis; however, the key molecules regulating ROS generation remain to be elucidated. The present study reports that knockdown of endogenous receptor for activated C kinase 1 (RACK1) increases the intracellular ROS level following TNF-α or HO stimulation in human hepatocellular carcinoma (HCC) cells, leading to promotion of cell death. Carbonyl reductase 1 (CBR1), a ubiquitous nicotinamide adenine dinucleotide phosphate-dependent enzyme, is reported to protect cells from ROS-induced cell damage. The present study reports that RACK1 is a regulator of CBR1 that interacts with and sustains the protein stability of CBR1. Overexpression of CBR1 reverses the enhanced cell death due to RACK1 knockdown. Taken together, the results of the present study suggest that RACK1 protects HCC cells from TNF-α-induced cell death by suppressing ROS generation through interacting with and regulating CBR1.
Key Laboratory of Plant Nutrition and the Agro-Environment in Northwest China, Ministry of Agriculture and Rural Affairs, College of Natural Resources and Environment, Northwest A & F University, Yangling, Shaanxi 712100, China.
Microplastics (MPs) have been confirmed as a hotspot for antibiotic resistance genes (ARGs) in wastewater. However, the impact of MPs on the transfer of ARGs in wastewater treatment remains unclear. This study investigated the roles and mechanisms of conventional (polystyrene, PS) and biodegradable (polylactic acid, PLA) MPs in the conjugative transfer of ARGs during ultraviolet disinfection.
As many proteins prioritize functionality over constancy of structure, a proteome is the shortest stave in the Liebig's barrel of cell sustainability. In this regard, both prokaryotes and eukaryotes possess abundant machinery supporting the quality of the proteome in healthy and stressful conditions. This machinery, namely chaperones, assists in folding, refolding, and the utilization of client proteins.
Background: Cognitive frailty (), characterized by the coexistence of physical frailty and cognitive impairment, is linked to increased morbidity and mortality in older adults. While has been linked to multiple physiological and lifestyle factors, the underlying biological mechanisms remain poorly understood. This study investigated the risk factors for and explored the relationship between mitochondrial function and in hospitalized patients.
Ovarian cancer remains one of the main causes of human mortality, accounting for millions of deaths every year. Despite of several clinical options such as chemotherapy, photodynamic therapy (PDT), hormonal treatment, radiation therapy, and surgery to manage this disease, the mortality rate is still very high. This alarming statistic highlights the urgent need for innovative approaches to improve both diagnosis and treatment.
Plasma membrane (PM) nanodomains have emerged as pivotal elements in the regulation of plant cellular functions and signal transduction. These nanoscale membrane regions, enriched in specific lipids and proteins, behave as regulatory/signaling hubs spatially and temporally coordinating critical cellular functions. In this review, we first examine the mechanisms underlying the formation and maintenance of PM nanodomains in plant cells, highlighting the roles of PM lipid composition, protein oligomerization and interactions with cytoskeletal and cell wall components.
