Protection of renal cells from cisplatin toxicity by cell cycle inhibitors. - Wikidata - awgldk - TriplyDB

Protection of renal cells from cisplatin toxicity by cell cycle inhibitors.

Protection of renal cells from cisplatin toxicity by cell cycle inhibitors.

http://www.wikidata.org/entity/Q44579261

about

Mechanisms of Cisplatin nephrotoxicity An integrated view of cisplatin-induced nephrotoxicity and ototoxicity Cisplatin-induced Kidney Dysfunction and Perspectives on Improving Treatment Strategies Cellular and Molecular Mechanisms of AKI.Membrane transporters as mediators of Cisplatin effects and side effects.Protection of cisplatin cytotoxicity by an inactive cyclin-dependent kinase.Inhibitors of histone deacetylases suppress cisplatin-induced p53 activation and apoptosis in renal tubular cells.Pathophysiology of cisplatin-induced acute kidney injury.LIN-3/EGF promotes the programmed cell death of specific cells in Caenorhabditis elegans by transcriptional activation of the pro-apoptotic gene egl-1.MicroRNA-34a is induced via p53 during cisplatin nephrotoxicity and contributes to cell survival.TIM2 gene deletion results in susceptibility to cisplatin-induced kidney toxicity.Cdk2-dependent phosphorylation of p21 regulates the role of Cdk2 in cisplatin cytotoxicity Dependence of cisplatin-induced cell death in vitro and in vivo on cyclin-dependent kinase 2 MicroRNA-687 Induced by Hypoxia-Inducible Factor-1 Targets Phosphatase and Tensin Homolog in Renal Ischemia-Reperfusion Injury.Apoptosis and acute kidney injury Dual action of the inhibitors of cyclin-dependent kinases: targeting of the cell-cycle progression and activation of wild-type p53 protein.DNA damage response in cisplatin-induced nephrotoxicity.Cytoplasmic initiation of cisplatin cytotoxicity.Cdk2 phosphorylation of Bcl-xL after stress converts it to a pro-apoptotic protein mimicking Bax/Bak.Mimicking Cdk2 phosphorylation of Bcl-xL at Ser73 results in caspase activation and Bcl-xL cleavage.Metabolomics as an extension of proteomic analysis: study of acute kidney injury.Cisplatin: a review of toxicities and therapeutic applications.The cell cycle and acute kidney injury.CDK4/6 inhibition induces epithelial cell cycle arrest and ameliorates acute kidney injury.Signalling mechanisms involved in renal pathological changes during cisplatin-induced nephropathy.Role of transporters in the distribution of platinum-based drugs.Pharmacotherapeutic options for treating adverse effects of Cisplatin chemotherapy.The Role of Transporters in the Toxicity of Chemotherapeutic Drugs: Focus on Transporters for Organic Cations.Role of protein kinase A signaling pathway in cyclosporine nephrotoxicity.Bone marrow-derived mesenchymal stem cells protect against cisplatin-induced acute kidney injury in rats by inhibiting cell apoptosis.Cisplatin toxicity reduced in human cultured renal tubular cells by oxygen pretreatment.Cisplatin nephrotoxicity: a review of the literature.Overexpression of p18INK⁴C in LLC-PK1 cells increases resistance to cisplatin-induced apoptosis.Identification of the functional domain of p21(WAF1/CIP1) that protects cells from cisplatin cytotoxicity.p38 MAP kinase inhibition ameliorates cisplatin nephrotoxicity in mice.Role of p53 in cisplatin-induced tubular cell apoptosis: dependence on p53 transcriptional activity.Cisplatin-induced cell death is EGFR/src/ERK signaling dependent in mouse proximal tubule cells.Role of p21 and oxidative stress on renal tubular resistance after acute ischaemic injury.PERP, a p53 proapoptotic target, mediates apoptotic cell death in renal ischemia.Inhibition of p21 modifies the response of cortical proximal tubules to cisplatin in rats.

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P2860

Protection of renal cells from cisplatin toxicity by cell cycle inhibitors.

http://www.wikidata.org/entity/Q44579261

description

2003 nî lūn-bûn

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2003年の論文

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name

Protection of renal cells from cisplatin toxicity by cell cycle inhibitors.

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Protection of renal cells from cisplatin toxicity by cell cycle inhibitors.

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type

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Protection of renal cells from cisplatin toxicity by cell cycle inhibitors.

@en

Protection of renal cells from cisplatin toxicity by cell cycle inhibitors.

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prefLabel

Protection of renal cells from cisplatin toxicity by cell cycle inhibitors.

@en

Protection of renal cells from cisplatin toxicity by cell cycle inhibitors.

@nl

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AJPRENAL.00192.2003

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American Journal of Physiology - Renal Physiology

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Protection of renal cells from cisplatin toxicity by cell cycle inhibitors.

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Judit Megyesi

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Peter M Price

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Robert L Safirstein

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P2860

Comparison of the effectiveness of adenovirus vectors expressing cyclin kinase inhibitors p16INK4A, p18INK4C, p19INK4D, p21(WAF1/CIP1) and p27KIP1 in inducing cell cycle arrest, apoptosis and inhibition of tumorigenicity

The p21 Cdk-interacting protein Cip1 is a potent inhibitor of G1 cyclin-dependent kinases

WAF1, a potential mediator of p53 tumor suppression

D type cyclins associate with multiple protein kinases and the DNA replication and repair factor PCNA

Cleavage of the actin-capping protein alpha -adducin at Asp-Asp-Ser-Asp633-Ala by caspase-3 is preceded by its phosphorylation on serine 726 in cisplatin-induced apoptosis of renal epithelial cells

Metabolism of Cisplatin to a nephrotoxin in proximal tubule cells.

Modulation of apoptosis by the cyclin-dependent kinase inhibitor p27(Kip1)

Clinical perspectives on platinum resistance.

Drugs five years later. Cisplatin.

Protein kinase C-alpha and ERK1/2 mediate mitochondrial dysfunction, decreases in active Na+ transport, and cisplatin-induced apoptosis in renal cells.

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10.1152/AJPRENAL.00192.2003

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