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E3 ubiquitin ligase CHIP facilitates cAMP and cGMP signalling cross-talk by polyubiquitinating PDE9A.
EMBO J
January 2025
Department of Neurology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou University, Zhengzhou, 450000, Henan, China.
The carboxyl terminus of Hsc70-interacting protein (CHIP) is pivotal for managing misfolded and aggregated proteins via chaperone networks and degradation pathways. In a preclinical rodent model of CHIP-related ataxia, we observed that CHIP mutations lead to increased levels of phosphodiesterase 9A (PDE9A), whose role in this context remains poorly understood. Here, we investigated the molecular mechanisms underlying the role of PDE9A in CHIP-related ataxia and demonstrated that CHIP binds to PDE9A, facilitating its polyubiquitination and autophagic degradation.
View Article and Find Full Text PDFGNG2 inhibits brain metastases from colorectal cancer via PI3K/AKT/mTOR signaling pathway.
Sci Rep
January 2025
Department of Gastrointestinal Surgery, Third Xiangya Hospital, Central South University, Changsha, 410006, China.
G-protein gamma subunit 2 (GNG2) plays a vital role in various cellular processes, yet its specific function in colorectal cancer (CRC), particularly in highly invasive cases and brain metastasis, remains unclear. This study identifies GNG2 as a key regulator in metastatic colorectal cancer (mCRC) through bioinformatics analysis and experimental validation. Functional enrichment analyses reveal that GNG2 is related to the PI3K/AKT/mTOR signaling pathway and cell cycle regulation.
View Article and Find Full Text PDFInvolvement of p38 MAPK and MAPKAPK2 in promoting cell death and the inflammatory response to ischemic stress associated with necrotic glioblastoma.
Cell Death Dis
January 2025
Division of Hematology and Oncology, Department of Pediatrics, Penn State College of Medicine, Hershey, PA, USA.
The association of necrosis in tumors with poor prognosis implies a potential tumor-promoting role. However, the mechanisms underlying cell death in this context and how damaged tissue contributes to tumor progression remain unclear. Here, we identified p38 mitogen-activated protein kinases (p38 MAPK, a.
View Article and Find Full Text PDF[Mechanism of chrysophanol in inhibiting ox-LDL-induced macrophage foaminess through NF-κB/HMGB1-PI3K/Akt/mTOR pathway].
Zhongguo Zhong Yao Za Zhi
December 2024
School of Basic Medical Sciences, Guangzhou University of Chinese Medicine Guangzhou 511400, China.
The aim of this study was to investigate the underlying mechanism of chrysophanol(Chr) in reducing inflammation and foam cell formation induced by oxidized low-density lipoprotein(ox-LDL) and to investigate the targets and pathways related to effects of Chr on coronary atherosclerosis, providing a theoretical basis for the development of new clinical drugs. RAW264.7 macrophages were cultured in vitro, and after determining the appropriate concentrations of Chr and ox-LDL for treating RAW264.
View Article and Find Full Text PDF14-3-3θ phosphorylation exacerbates alpha-synuclein aggregation and toxicity.
Neurobiol Dis
January 2025
Center for Neurodegeneration and Experimental Therapeutics, Department of Neurology, University of Alabama at Birmingham, Birmingham, AL 35294, United States of America. Electronic address:
Aggregation of alpha-synuclein (αsyn) plays an integral role in Parkinson's disease (PD) and Dementia with Lewy bodies (DLB). 14-3-3θ is a highly expressed brain protein with chaperone-like activity that regulates αsyn folding. 14-3-3θ overexpression reduces αsyn aggregation, transmission between cells, and neuronal loss, while 14-3-3 inhibition promotes αsyn pathology.
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