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10 resultat
Taxol, a microtubule-stabilizing antineoplastic agent, induces expression of tumor necrosis factor alpha and interleukin-1 in macrophages.
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Taxol, a naturally occurring diterpene with antitumor activity, induces tubulin polymerization to generate abnormally stable and nonfunctional microtubules. Previously, we showed that taxol has lipopolysaccharide (LPS)-like effects on macrophages. As LPS is a potent inducer of macrophage cytokine
Taxol, a microtubule stabilizer, improves cardiac functional recovery during postischemic reperfusion in rat in vitro.
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OBJECTIVE
Microtubule disruption contributes to cellular and organic dysfunction, and is implicated in ischemia/reperfusion (I/R) injury. The purpose of this study was to explore the effects of taxol, a microtubule stabilizer, on cardiac functional recovery during reperfusion.
METHODS
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Taxol, a microtubule-stabilizing antineoplastic agent, differentially regulates normal and tumor-bearing host macrophage nitric oxide production.
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Taxol, a potent antitumor chemotherapeutic, promotes in vitro cytotoxic antitumor activities by normal host macrophage (M phi s). Because tumor growth induces functional changes among M phi populations, we determined whether fibrosarcoma growth (Meth-KDE) modified M phi responsiveness to the
CD14 is not involved in Rhodobacter sphaeroides diphosphoryl lipid A inhibition of tumor necrosis factor alpha and nitric oxide induction by taxol in murine macrophages.
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Taxol, a microtubule stabilizer with anticancer activity, mimics the actions of lipopolysaccharide (LPS) on murine macrophages in vitro. Recently, it was shown that taxol-induced macrophage activation was inhibited by the LPS antagonist Rhodobacter sphaeroides diphosphoryl lipid A (RsDPLA). To
Lipopolysaccharide and tumor necrosis factor-alpha induce lipopolysaccharide receptor expression on bone marrow cells by different mechanisms.
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Two cell types, monocytes/macrophages and neutrophilic granulocytes, play a prominent role in the pathogenic effects of endotoxins during Gram-negative infections. We previously established that nanomolar concentrations of LPS induce the expression of new specific LPS-binding sites (LpsR) in bone
Stabilization of apoptotic cells: generation of zombie cells.
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Apoptosis is characterized by degradation of cell components but plasma membrane remains intact. Apoptotic microtubule network (AMN) is organized during apoptosis forming a cortical structure beneath plasma membrane that maintains plasma membrane integrity. Apoptotic cells are also characterized by
Stabilization Of Apoptotic Cells: Generation Of Zombie Cells.
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Apoptosis is characterized by degradation of cell components but plasma membrane remains intact. Apoptotic microtubule network (AMN) is organized during apoptosis forming a cortical structure beneath plasma membrane that maintains plasma membrane integrity. Apoptotic cells are also characterized by
Taxol and lipopolysaccharide activation of a murine macrophage cell line and induction of similar tyrosine phosphoproteins.
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Taxol, a unique antimitotic drug, is thought to exert its antitumor activity by binding to and promoting the assembly of microtubules. Studies on the mechanism of action of Taxol have focused mainly on this ability to induce microtubule polymerization. Recent evidence suggests that Taxol affects
Heat shock protein 90 mediates macrophage activation by Taxol and bacterial lipopolysaccharide.
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Taxol, a plant-derived antitumor agent, stabilizes microtubules. Taxol also elicits cell signals in a manner indistinguishable from bacterial lipopolysaccharide (LPS). LPS-like actions of Taxol are controlled by the lps gene and are independent of binding to the known Taxol target, beta-tubulin.
Molecular effects of paclitaxel: myths and reality (a critical review).
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Recent studies on paclitaxel (Taxol), a microtubule-stabilizing agent and effective anti-cancer drug, have identified numerous cellular and molecular effects, such as induction of cytokines and tumor-suppressor genes, indirect cytotoxicity due to secretion of tumor necrosis factor, vast activation
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