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The small GTPase Ras, which transmits extracellular signals to the cell, and the kinase Aurora-A, which promotes proper mitosis, can both be inappropriately activated in human tumors. Here, we show that Aurora-A in conjunction with oncogenic Ras enhances transformed cell growth. Furthermore, such transformation and in some cases also tumorigenesis depend upon S194 of RalA, a known Aurora-A phosphorylation site. Aurora-A promotes not only RalA activation but also translocation from the plasma membrane and activation of the effector protein RalBP1. Taken together, these data suggest that Aurora-A may converge upon oncogenic Ras signaling through RalA.
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http://dx.doi.org/10.1128/MCB.00916-08 | DOI Listing |
Cell Mol Life Sci
September 2025
Department of Gastroenterology, The Second Hospital of Shandong University, Jinan, China.
Metabolic associated steatohepatitis (MASH) is a severe form of metabolic dysfunction-associated steatotic liver disease (MASLD) characterized by hepatocellular injury, inflammation, and fibrosis. Despite advances in understanding its pathophysiology, the molecular mechanisms driving MASH progression remain unclear. This study investigates the role of long non-coding RNA Linc01271 in MASLD/MASH pathogenesis, ant its involvement in the miR-149-3p/RAB35 axis and PI3K/AKT/mTOR signaling pathway.
View Article and Find Full Text PDFJ Extracell Vesicles
September 2025
Division of Sports Medicine and Adult Reconstructive Surgery, Department of Orthopedic Surgery, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, Jiangsu, China.
Osteoarthritis (OA), the prevalent debilitating joint disorder, is accelerated by dysregulated intercellular crosstalk, yet the role of fibroblast-like synoviocyte (FLS)-derived extracellular vesicles and particles (EVPs) in disease progression remains to be elucidated. Here, integrative analysis of clinical specimens, animal models, and publicly available datasets revealed significant alterations in exosomal pathways within OA synovium. Proteomic profiling revealed distinct molecular signatures in EVPs derived from inflammatory and senescent FLSs, reflecting the pathophysiological status of their parent cells.
View Article and Find Full Text PDFZhong Nan Da Xue Xue Bao Yi Xue Ban
May 2025
Department of Geriatric Pulmonary and Critical Care Medicine, Xiangya Hospital, Central South University; National Clinical Research Center for Geriatric Disorders (Xiangya Hospital), Changsha 410008.
Objectives: Non-small cell lung cancer (NSCLC) is associated with poor prognosis, with 30% of patients diagnosed at an advanced stage. Mutations in the and genes are important prognostic factors for NSCLC, and targeted therapies can significantly improve survival in these patients. Although tissue biopsy remains the gold standard for detecting gene mutations, it has limitations, including invasiveness, sampling errors due to tumor heterogeneity, and poor reproducibility.
View Article and Find Full Text PDFJ Invest Dermatol
September 2025
Department of Surgery, University of California San Diego, La Jolla, CA, United States; Department of Dermatology, University of California San Diego, La Jolla, CA, United States. Electronic address:
Normal cutaneous wound healing is a multicellular process that involves the release of small extracellular vesicles (sEVs) that coordinate intercellular communication by delivery of sEV payloads to recipient cells. We have recently shown how the pro-reparative activity of inflammatory cell sEVs, especially macrophage and neutrophil-derived sEVs, in the wound bed is dysregulated in impaired wound healing. Here we show that loss of Rab27A, a small GTPase that has a regulatory function in sEV secretion, reduces the release of neutrophil and macrophage-derived sEVs.
View Article and Find Full Text PDFSci Rep
September 2025
Biochemistry Sector, Chemistry Department, Faculty of Science, Helwan University, Cairo, 11795, Egypt.
Background: Ovarian cancer (OC) is a leading cause of cancer deaths in women. Comprehensive molecular studies are required to understand OC pathogenesis. KRAS and NOXA genes are involved in tumorigenesis and disease progression.
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