Deletion of p 18 INK 4 c aggravates cisplatin ‐ induced acute kidney injury

[1]  J. Megyesi,et al.  Cytoplasmic initiation of cisplatin cytotoxicity. , 2008, American journal of physiology. Renal physiology.

[2]  Z. Dong,et al.  Cisplatin nephrotoxicity: mechanisms and renoprotective strategies. , 2008, Kidney international.

[3]  R. Kaufman,et al.  The endoplasmic reticulum and the unfolded protein response. , 2007, Seminars in cell & developmental biology.

[4]  M. Peyrou,et al.  Cisplatin, gentamicin, and p-aminophenol induce markers of endoplasmic reticulum stress in the rat kidneys. , 2007, Toxicological sciences : an official journal of the Society of Toxicology.

[5]  Mariela C. Marazita,et al.  Cell cycle inhibitor, p19INK4d, promotes cell survival and decreases chromosomal aberrations after genotoxic insult due to enhanced DNA repair. , 2007, DNA repair.

[6]  S. Muruganandan,et al.  Calpain-induced endoplasmic reticulum stress and cell death following cytotoxic damage to renal cells. , 2006, Toxicological sciences : an official journal of the Society of Toxicology.

[7]  P. Walter,et al.  Intracellular signaling by the unfolded protein response. , 2006, Annual review of cell and developmental biology.

[8]  J. Megyesi,et al.  Dependence of cisplatin-induced cell death in vitro and in vivo on cyclin-dependent kinase 2. , 2006, Journal of the American Society of Nephrology : JASN.

[9]  Afshin Samali,et al.  Mediators of endoplasmic reticulum stress‐induced apoptosis , 2006, EMBO reports.

[10]  A. Hishida,et al.  Inhibition of p21 modifies the response of cortical proximal tubules to cisplatin in rats. , 2006, American journal of physiology. Renal physiology.

[11]  J. Massagué,et al.  Cyclin-dependent Kinase Inhibitors Uncouple Cell Cycle Progression from Mitochondrial Apoptotic Functions in DNA-damaged Cancer Cells* , 2005, Journal of Biological Chemistry.

[12]  Sudhir V. Shah,et al.  p53-dependent Caspase-2 Activation in Mitochondrial Release of Apoptosis-inducing Factor and Its Role in Renal Tubular Epithelial Cell Injury* , 2005, Journal of Biological Chemistry.

[13]  J. Megyesi,et al.  Identification of the functional domain of p21(WAF1/CIP1) that protects cells from cisplatin cytotoxicity. , 2005, American journal of physiology. Renal physiology.

[14]  K. Nath Provenance of the protective property of p21. , 2005, American journal of physiology. Renal physiology.

[15]  Dong Wang,et al.  Cellular processing of platinum anticancer drugs , 2005, Nature Reviews Drug Discovery.

[16]  M. Peyrou,et al.  The Endoplasmic Reticulum in Xenobiotic Toxicity , 2005, Drug metabolism reviews.

[17]  A. Hishida,et al.  The induction of cell cycle regulatory and DNA repair proteins in cisplatin-induced acute renal failure. , 2004, Toxicology and applied pharmacology.

[18]  I. Braakman,et al.  Protein folding and quality control in the endoplasmic reticulum. , 2004, Current opinion in cell biology.

[19]  D. Scadden,et al.  In vivo self-renewing divisions of haematopoietic stem cells are increased in the absence of the early G1-phase inhibitor, p18INK4C , 2004, Nature Cell Biology.

[20]  J. Megyesi,et al.  Protection of renal cells from cisplatin toxicity by cell cycle inhibitors. , 2004, American journal of physiology. Renal physiology.

[21]  A. Aboussekhra,et al.  The tumor suppressor p16INK4a gene is a regulator of apoptosis induced by ultraviolet light and cisplatin , 2004, Oncogene.

[22]  Z. Siddik,et al.  Cisplatin: mode of cytotoxic action and molecular basis of resistance , 2003, Oncogene.

[23]  P. Price,et al.  Lack of a functional p21WAF1/CIP1 gene accelerates caspase-independent apoptosis induced by cisplatin in renal cells. , 2003, American journal of physiology. Renal physiology.

[24]  J. Bonventre,et al.  Animal models of acute tubular necrosis , 2002, Current opinion in critical care.

[25]  J. Megyesi,et al.  Coordination of the cell cycle is an important determinant of the syndrome of acute renal failure. , 2002, American journal of physiology. Renal physiology.

[26]  P. Devarajan,et al.  Cisplatin induces apoptosis in LLC-PK1 cells via activation of mitochondrial pathways. , 2002, Journal of the American Society of Nephrology : JASN.

[27]  K. Mori Tripartite Management of Unfolded Proteins in the Endoplasmic Reticulum , 2000, Cell.

[28]  S. Shankland,et al.  Cell cycle regulatory proteins in renal disease: role in hypertrophy, proliferation, and apoptosis. , 2000, American journal of physiology. Renal physiology.

[29]  M. Razzaque,et al.  Cisplatin-induced apoptosis in human proximal tubular epithelial cells is associated with the activation of the Fas/Fas ligand system , 1999, Histochemistry and Cell Biology.

[30]  T. Weinert DNA Damage and Checkpoint Pathways Molecular Anatomy and Interactions with Repair , 1998, Cell.

[31]  W. Lieberthal,et al.  Mechanisms of death induced by cisplatin in proximal tubular epithelial cells: apoptosis vs. necrosis. , 1996, The American journal of physiology.

[32]  C. Cordon-Cardo Mutations of cell cycle regulators. Biological and clinical implications for human neoplasia. , 1995, The American journal of pathology.

[33]  James M. Roberts,et al.  Inhibitors of mammalian G1 cyclin-dependent kinases. , 1995, Genes & development.

[34]  M. Roussel,et al.  Novel INK4 proteins, p19 and p18, are specific inhibitors of the cyclin D-dependent kinases CDK4 and CDK6 , 1995, Molecular and cellular biology.

[35]  A. Hishida,et al.  Role of the Increase in p 21 in Cisplatin-Induced Acute Renal Failure in Rats , 2001 .

[36]  L. Hengst,et al.  Inhibitors of the Cip/Kip family. , 1998, Current topics in microbiology and immunology.

[37]  J. Megyesi,et al.  Induction of p 21 WAF 1 / CIP 1 / SDI 1 in Kidney Tubule Cells Affects the Course of Cisplatin-induced Acute Renal Failure , 1998 .

[38]  V. Godfrey,et al.  CDK inhibitors p18 INK4c and p27 Kip1 mediate two separate pathways to collaboratively suppress pituitary tumorigenesis , 1998 .