Mitochondrial density determines the cellular sensitivity to cisplatin-induced cell death. - Wikidata - wikimedia - TriplyDB

Mitochondrial density determines the cellular sensitivity to cisplatin-induced cell death.

Mitochondrial density determines the cellular sensitivity to cisplatin-induced cell death.

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Mechanisms of Cisplatin nephrotoxicity Oxidative Stress Resistance in Metastatic Prostate Cancer: Renewal by Self-Eating Cisplatin induces a mitochondrial-ROS response that contributes to cytotoxicity depending on mitochondrial redox status and bioenergetic functions Increased distributional variance of mitochondrial DNA content associated with prostate cancer cells as compared with normal prostate cells Tempol, a superoxide dismutase mimetic agent, ameliorates cisplatin-induced nephrotoxicity through alleviation of mitochondrial dysfunction in mice Computational modeling of apoptotic signaling pathways induced by cisplatin Reduced mitochondrial DNA content associates with poor prognosis of prostate cancer in African American men.Species diversity regarding the presence of proximal tubular progenitor cells of the kidney.Cytoplasmic initiation of cisplatin cytotoxicity.A Comprehensive Review on the Genetic Regulation of Cisplatin-induced Nephrotoxicity Evidence against protective role of sex hormone estrogen in Cisplatin-induced nephrotoxicity in ovarectomized rat model.SIRT1 contributes in part to cisplatin resistance in cancer cells by altering mitochondrial metabolism Minimal systems analysis of mitochondria-dependent apoptosis induced by cisplatin Novel Anticancer Platinum(IV) Complexes with Adamantylamine: Their Efficiency and Innovative Chemotherapy Strategies Modifying Lipid Metabolism.Effects of Fennel Essential Oil on Cisplatin-induced Nephrotoxicity in Ovariectomized Rats.Regulation of mitochondrial respiratory chain biogenesis by estrogens/estrogen receptors and physiological, pathological and pharmacological implications.Common Chemical Inductors of Replication Stress: Focus on Cell-Based Studies.Canonical and new generation anticancer drugs also target energy metabolism.The ability of mannitol to decrease cisplatin-induced nephrotoxicity in children: real or not?Anticarcinogenic action of quercetin by downregulation of phosphatidylinositol 3-kinase (PI3K) and protein kinase C (PKC) via induction of p53 in hepatocellular carcinoma (HepG2) cell line.Effect of creatine and pioglitazone on Hk-2 cell line cisplatin nephrotoxicity.Cisplatin nephrotoxicity: a review of the literature.Mitochondrial density contributes to the immune response of macrophages to lipopolysaccharide via the MAPK pathway.Resveratrol induces SIRT1- and energy-stress-independent inhibition of tumor cell regrowth after low-dose platinum treatment.Effects of thymoquinone against cisplatin-induced cardiac injury in rats.Deoxycholic acid can induce apoptosis in the human colon cancer cell line HCT116 in the absence of Bax.TNF-alpha/cycloheximide-induced apoptosis in intestinal epithelial cells requires Rac1-regulated reactive oxygen species.Increased mitochondrial DNA induces acquired docetaxel resistance in head and neck cancer cells.L-thyroxine modifies nephrotoxicity by regulating the apoptotic pathway: The possible role of CD38/ADP-ribosyl cyclase-mediated calcium mobilization.Effects of Cisplatin in neuroblastoma rat cells: damage to cellular organelles.Cisplatin as an anti-tumor drug: cellular mechanisms of activity, drug resistance and induced side effects Modulation of PKC signaling and induction of apoptosis through suppression of reactive oxygen species and tumor necrosis factor receptor 1 (TNFR1): key role of quercetin in cancer prevention.Bioenergetics of acquired cisplatin resistant H1299 non-small cell lung cancer and P31 mesothelioma cells.Berberine attenuates oxidative stress and hepatocytes apoptosis via protecting mitochondria in blunt snout bream Megalobrama amblycephala fed high-fat diets.Association of mitochondrial dysfunction with oxidative stress and immune suppression in Blunt Snout Bream Megalobrama amblycephala fed a high-fat diet.Cisplatin-induced injury of the renal distal convoluted tubule is associated with hypomagnesaemia in mice.The protective effect of thiamine pyrophosphate, but not thiamine, against cardiotoxicity induced with cisplatin in rats.Mitochondrial NADP+-dependent isocitrate dehydrogenase deficiency increases cisplatin-induced oxidative damage in the kidney tubule cells.Effects of creatine in a rat intestinal model of ischemia/reperfusion injury Benfotiamine, a Lipid-Soluble Analog of Vitamin B, Improves the Mitochondrial Biogenesis and Function in Blunt Snout Bream () Fed High-Carbohydrate Diets by Promoting the AMPK/PGC-1β/NRF-1 Axis

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Mitochondrial density determines the cellular sensitivity to cisplatin-induced cell death.

http://www.wikidata.org/entity/Q46656360

description

2005 nî lūn-bûn

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2005年の論文

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2005年学术文章

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2005年學術文章

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name

Mitochondrial density determin ...... cisplatin-induced cell death.

@en

Mitochondrial density determin ...... cisplatin-induced cell death.

@nl

type

label

Mitochondrial density determin ...... cisplatin-induced cell death.

@en

Mitochondrial density determin ...... cisplatin-induced cell death.

@nl

prefLabel

Mitochondrial density determin ...... cisplatin-induced cell death.

@en

Mitochondrial density determin ...... cisplatin-induced cell death.

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Mitochondrial density determines the cellular sensitivity to cisplatin-induced cell death

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Anwarul Md Haque

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Eisuke Sato

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Manabu Nishikawa

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Masayasu Inoue

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Masayuki Mashimo

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Wei Qian

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P2860

Sequence and organization of the human mitochondrial genome

A role for mitochondrial enzymes in inherited neoplasia and beyond

Minocycline up-regulates Bcl-2 and protects against cell death in mitochondria

The biochemistry of apoptosis

Mitochondria and apoptosis

Human cells lacking mtDNA: repopulation with exogenous mitochondria by complementation

Mitochondrial control of cell death

Mitochondrial DNA damage is more extensive and persists longer than nuclear DNA damage in human cells following oxidative stress

Repair of DNA damage in mitochondria.

Mitochondria as the central control point of apoptosis.

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