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| http://dx.doi.org/10.1016/j.ccell.2020.01.010 | DOI Listing |
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Manganese is a potent inducer of lysosomal activity that inhibits de novo HBV infection.
PLoS Pathog
January 2025
Key Laboratory of Medical Molecular Virology (MOE/NHC/CAMS), Shanghai Institute of Infectious Disease and Biosecurity, School of Basic Medical Sciences, Fudan University, Shanghai, China.
Sodium taurocholate co-transporting polypeptide (NTCP) has been identified as an entry receptor for hepatitis B virus (HBV), but the molecular events of the viral post-endocytosis steps remain obscure. In this study, we discovered that manganese (Mn) could strongly inhibit HBV infection in NTCP-reconstituted HepG2 cells without affecting viral replication. We therefore profiled the antiviral effects of Mn2+ in an attempt to elucidate the regulatory mechanisms involved in early HBV infection.
View Article and Find Full Text PDFSTAT1 Promotes PD-L1 Activation and Tumor Growth in Lymphangioleiomyomatosis.
bioRxiv
December 2024
Division of Pulmonary, Critical Care, and Sleep Medicine, Department of Internal Medicine, University of Cincinnati; Cincinnati, OH 45267, USA.
Lymphangioleiomyomatosis (LAM) is a cystic lung disease that primarily affects women. LAM is caused by the invasion of metastatic smooth muscle-like cells into the lung parenchyma, leading to abnormal cell proliferation, lung remodeling and progressive respiratory failure. LAM cells have TSC gene mutations, which occur sporadically or in people with Tuberous Sclerosis Complex.
View Article and Find Full Text PDF-induced cholesterol accumulation in infected macrophages suppresses autophagy via mTORC1 activation.
Mol Biol Cell
January 2025
Department of Microbiology, Immunology, and Cancer Biology, University of Virginia School of Medicine, Charlottesville, VA 22903.
serovar Typhimurium is a Gram-negative bacillus that infects the host intestinal epithelium and resident macrophages. Many intracellular pathogens induce an autophagic response in host cells but have evolved mechanisms to subvert that response. Autophagy is closely linked to cellular cholesterol levels; mTORC1 senses increased cholesterol in lysosomal membranes, leading to its hyperactivity and suppression of autophagy.
View Article and Find Full Text PDFThe roles of mTORC1 in parathyroid gland function in chronic kidney disease-induced secondary hyperparathyroidism: Evidence from male genetic mouse models and clinical data.
FASEB J
November 2024
Laboratory of Medical Transcriptomics, Nephrology and Internal Medicine B, Hadassah Hebrew University Medical Center and Faculty of Medicine, Jerusalem, Israel.
Secondary hyperparathyroidism (SHP) associated with chronic kidney disease (CKD) contributes to morbidity and mortality, yet the related parathyroid signaling pathways are not fully understood. Previous studies have indicated that the parathyroid mTORC1 pathway is activated in both experimental CKD and hypocalcemia-induced SHP. Furthermore, mice with parathyroid-specific mTOR deficiency (PT-mTOR) exhibit disrupted parathyroid glands, but maintain normal serum PTH levels.
View Article and Find Full Text PDFEnhanced Gαq Signaling in -deficient Cells Is Required for Their Neoplastic Behavior.
Am J Respir Cell Mol Biol
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Research Institute of the McGill University Health Centre, Respiratory Program and Meakins-Christie Laboratories, Montreal, Quebec, Canada.
Article Synopsis
- Inherited or sporadic loss of a specific gene can lead to pulmonary lymphangioleiomyomatosis (LAM), a rare lung disease caused by tumor nodules that display characteristics of neural crest and smooth muscle cells.
- The abnormal growth of these "LAM cells" is linked to increased activity of the mTORC1 protein, which is typically regulated by the TSC1-TSC2 protein complex; while rapamycin slows LAM progression, it does not eliminate the disease, suggesting other processes are involved.
- Recent studies have identified G-protein coupled urotensin-II receptor (UT) signaling as a key player in LAM's cancer-related signaling, revealing that enhanced signaling through UT promotes harmful cell behaviors in
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