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Cardiomyocyte S1PR1 promotes cardiac regeneration via AKT/mTORC1 signaling pathway.

Theranostics

January 2025

State Key Laboratory of Cardiovascular Diseases and Medical Innovation Center, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, 200120, China.

Lower vertebrates and some neonatal mammals are known to possess the ability to regenerate cardiomyocyte and fully recover after heart injuries within a limited period. Understanding the molecular mechanisms of heart regeneration and exploring new ways to enhance cardiac regeneration hold significant promise for therapeutic intervention of heart failure. Sphingosine 1-phospahte receptor 1 (S1PR1) is highly expressed in cardiomyocytes and plays a crucial role in heart development and pathological cardiac remodeling.

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Dipeptidase 1 (DPEP1), initially identified as a renal membrane enzyme in mature human kidneys, plays a pivotal role in various cellular processes. It facilitates the exchange of materials and signal transduction across cell membranes, contributing significantly to dipeptide hydrolysis, glucose and lipid metabolism, immune inflammation, and ferroptosis, among other cellular functions. Extensive research has delineated the complex role of DPEP1 in oncogenesis and tumor progression, with its influence being context dependent.

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The therapeutic potential of bitter leaf ( Del.) has been established both empirically and in various scientific investigations. However, the molecular pathways related to its possible anti-inflammatory and antioxidant properties remain unclear.

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The endonuclease activity of MCPIP1 controls the neoplastic transformation of epithelial cells via the c-Met/CD44 axis.

Cell Commun Signal

January 2025

Department of General Biochemistry, Faculty of Biochemistry, Biophysics and Biotechnology, Jagiellonian University, Krakow, Poland.

The RNase activity of MCPIP1 is essential for regulating cellular homeostasis, proliferation, and tumorigenesis. Our study elucidates the effects of downregulation of MCPIP1 expression and an RNase-inactivating mutation (D141N) on normal epithelial kidney cells, indicating that MCPIP1 expression is a key factor that suppresses neoplastic transformation. We observed that either expression downregulation or mutation of MCPIP1 significantly increased its clonogenicity and altered the expression of cancer stem cell (CSC) markers and factors involved in epithelial-to-mesenchymal transition (EMT).

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Background: Clear cell renal cell carcinoma (ccRCC) is the most common malignant urological tumor, and regrettably, and is insensitive to chemotherapy and radiotherapy, resulting in poor patient outcomes. DBF4 plays a critical role in DNA replication and participates in various biological functions, making it an attractive target for cancer treatment. However, its significance in ccRCC has not yet been explored.

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