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Recent advancements in Parkinson's disease (PD) drug development have been significantly driven by genetic research. Importantly, drugs supported by genetic evidence are more likely to be approved. While genome-wide association studies (GWAS) are a powerful tool to nominate genomic regions associated with certain traits or diseases, pinpointing the causal biologically relevant gene is often challenging.
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- Protein quality control (PQC) is essential for the function of heart cells, and certain mutations (like R120G in CRYAB and P209L in BAG3) can lead to the buildup of harmful protein aggregates and heart diseases.
- The study explored how these protein aggregates are taken up by mitochondria and removed through a process called mitophagy, especially in mice lacking the TRAF2 protein, which is necessary for mitophagy.
- Results showed that without TRAF2, there was an increase in protein aggregates and misplacement of other proteins, indicating that proper mitophagy is critical for preventing cardiac dysfunction.
Prediction of acute myeloid leukemia prognosis based on autophagy features and characterization of its immune microenvironment.
Front Immunol
December 2024
School of Computer and Control Engineering, Yantai University, Yantai, Shandong, China.
Background: Autophagy promotes the survival of acute myeloid leukemia (AML) cells by removing damaged organelles and proteins and protecting them from stress-induced apoptosis. Although many studies have identified candidate autophagy genes associated with AML prognosis, there are still great challenges in predicting the survival prognosis of AML patients. Therefore, it is necessary to identify more novel autophagy gene markers to improve the prognosis of AML by utilizing information at the molecular level.
View Article and Find Full Text PDFCaMKII suppresses proteotoxicity by phosphorylating BAG3 in response to proteasomal dysfunction.
EMBO Rep
October 2024
Division of Abdominal Tumor Multimodality Treatment, Department of Medical Oncology, Cancer Center and Laboratory of Molecular Targeted Therapy in Oncology, West China Hospital, Sichuan University, Chengdu, Sichuan Province, China.
Protein quality control serves as the primary defense mechanism for cells against proteotoxicity induced by proteasome dysfunction. While cells can limit the build-up of ubiquitinated misfolded proteins during proteasome inhibition, the precise mechanism is unclear. Here, we find that protein kinase Ca/Calmodulin (CaM)-dependent protein kinase II (CaMKII) maintains proteostasis during proteasome inhibition.
View Article and Find Full Text PDFThe BAG3-IFITM2 Axis Enhances Pancreatic Ductal Adenocarcinoma Growth via the MAPK Signaling Pathway.
Carcinogenesis
August 2024
West China School of Basic Medical Sciences and Forensic Medicine, Sichuan University, Chengdu, China.
Pancreatic ductal adenocarcinoma (PDAC), a highly lethal malignancy, exhibits escalating incidence and mortality rates, underscoring the urgent need for the identification of novel therapeutic targets and strategies. The BAG3 protein, a multifunctional regulator involved in various cellular processes, notably plays a crucial role in promoting tumor progression and acts as a potential "bridge" between tumors and the tumor microenvironment. In this study, we demonstrate that PDAC cells secrete BAG3 (sBAG3), which engages the IFITM2 receptor to activate the MAPK signaling pathway, specifically enhancing pERK activity, thereby propelling PDAC growth.
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