• A shorter telomere is the key factor in preventing cultured human mesenchymal stem cells from senescence escape
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• A shorter telomere is the key factor in preventing cultured human mesenchymal stem cells from senescence escape
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• SWATH™-and iTRAQ-based quantitative proteomic analyses reveal an overexpression and biological relevance of CD109 in advanced NSCLC
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• Davallialactone Reduces Inflammation and Repairs Dentinogenesis on Glucose Oxidase–induced Stress in Dental Pulp Cells
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• Davallialactone Reduces Inflammation and Repairs Dentinogenesis on Glucose Oxidase–induced Stress in Dental Pulp Cells
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• Davallialactone Reduces Inflammation and Repairs Dentinogenesis on Glucose Oxidase–induced Stress in Dental Pulp Cells
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• Wogonin-enhanced reactive oxygen species-induced apoptosis and potentiated cytotoxic effects of chemotherapeutic agents by suppression Nrf2-mediated signaling in HepG2 cells.
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• Wogonin-enhanced reactive oxygen species-induced apoptosis and potentiated cytotoxic effects of chemotherapeutic agents by suppression Nrf2-mediated signaling in HepG2 cells.
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• Wogonin-enhanced reactive oxygen species-induced apoptosis and potentiated cytotoxic effects of chemotherapeutic agents by suppression Nrf2-mediated signaling in HepG2 cells.
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• Wogonin-enhanced reactive oxygen species-induced apoptosis and potentiated cytotoxic effects of chemotherapeutic agents by suppression Nrf2-mediated signaling in HepG2 cells.
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• Wogonin-enhanced reactive oxygen species-induced apoptosis and potentiated cytotoxic effects of chemotherapeutic agents by suppression Nrf2-mediated signaling in HepG2 cells.
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• A novel protein extracted from foxtail millet bran displays anti-carcinogenic effects in human colon cancer cells
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• A novel protein extracted from foxtail millet bran displays anti-carcinogenic effects in human colon cancer cells
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• A novel protein extracted from foxtail millet bran displays anti-carcinogenic effects in human colon cancer cells
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• Exogenous High Mobility Group Box 1 Inhibits Apoptosis and Promotes the Proliferation of Lewis Cells via RAGE/TLR4‐Dependent Signal Pathways
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