Proteasome inhibition by chronic oxidative stress in human trabecular meshwork cells.

[1]  F. Sierra,et al.  Models of accelerated ageing can be informative about the molecular mechanisms of ageing and/or age-related pathology , 2003, Mechanisms of Ageing and Development.

[2]  J. Campisi.  Cellular senescence and apoptosis: how cellular responses might influence aging phenotypes , 2003, Experimental Gerontology.

[3]  W. Hur,et al.  Expression of wild-type and truncated myocilins in trabecular meshwork cells: their subcellular localizations and cytotoxicities. , 2002, Investigative ophthalmology & visual science.

[4]  E. Stone,et al.  Myocilin glaucoma. , 2002, Survey of ophthalmology.

[5]  Bertrand Friguet,et al.  Impairment of proteasome structure and function in aging. , 2002, The international journal of biochemistry & cell biology.

[6]  J. Louie,et al.  Proteasome function and protein oxidation in the aged retina. , 2002, Experimental eye research.

[7]  B. Halliwell.  Hypothesis: Proteasomal Dysfunction , 2002 .

[8]  E. Porta.  Pigments in Aging: An Overview , 2002, Annals of the New York Academy of Sciences.

[9]  T. Grune,et al.  Proteolytic Response to Oxidative Stress in Mammalian Cells , 2002, Biological chemistry.

[10]  Randy L. Johnson,et al.  Targeted Disruption of the Myocilin Gene (Myoc) Suggests that Human Glaucoma-Causing Mutations Are Gain of Function , 2001, Molecular and Cellular Biology.

[11]  K. Davies,et al.  Age-related changes in protein oxidation and proteolysis in mammalian cells. , 2001, The journals of gerontology. Series A, Biological sciences and medical sciences.

[12]  K. Davies,et al.  Protein oxidation and 20S proteasome-dependent proteolysis in mammalian cells , 2001, Cellular and Molecular Life Sciences CMLS.

[13]  D. Allan Butterfield,et al.  Brain protein oxidation in age-related neurodegenerative disorders that are associated with aggregated proteins , 2001, Mechanisms of Ageing and Development.

[14]  P. Palmberg.  Risk factors for glaucoma progression: Where does intraocular pressure fit in? , 2001, Archives of ophthalmology.

[15]  T. Borrás,et al.  Inefficient processing of an olfactomedin-deficient myocilin mutant: potential physiological relevance to glaucoma. , 2001, Biochemical and biophysical research communications.

[16]  K. Davies.  Degradation of oxidized proteins by the 20S proteasome. , 2001, Biochimie.

[17]  J. Schuman,et al.  Activation of a tissue-specific stress response in the aqueous outflow pathway of the eye defines the glaucoma disease phenotype , 2001, Nature Medicine.

[18]  G. Chang,et al.  Protein oxidation and turnover. , 2000, Journal of biomedical science.

[19]  C. Franceschi,et al.  Fibroblast cultures from healthy centenarians have an active proteasome , 2000, Experimental Gerontology.

[20]  B. Friguet,et al.  Age-related alterations of proteasome structure and function in aging epidermis , 2000, Experimental Gerontology.

[21]  W. Markesbery,et al.  Decreased levels of proteasome activity and proteasome expression in aging spinal cord , 2000, Neuroscience.

[22]  B. Friguet,et al.  Increase of oxidatively modified protein is associated with a decrease of proteasome activity and content in aging epidermal cells. , 2000, The journals of gerontology. Series A, Biological sciences and medical sciences.

[23]  D. Epstein,et al.  Genes upregulated in the human trabecular meshwork in response to elevated intraocular pressure. , 2000, Investigative ophthalmology & visual science.

[24]  D. Vollrath,et al.  A cellular assay distinguishes normal and mutant TIGR/myocilin protein. , 1999, Human molecular genetics.

[25]  F. Bardag-Gorce,et al.  Changes in 20S proteasome activity during ageing of the LOU rat , 1999, Molecular Biology Reports.

[26]  M. Figueiredo-Pereira,et al.  Ubiquitin, cellular inclusions and their role in neurodegeneration , 1998, Trends in Neurosciences.

[27]  R. G. Allen,et al.  Relationship between donor age and the replicative lifespan of human cells in culture: a reevaluation. , 1998, Proceedings of the National Academy of Sciences of the United States of America.

[28]  J. Karlsson,et al.  Proteolytic cleavage of N-Succ-Leu-Leu-Val-Tyr-AMC by the proteasome in lens epithelium from clear and cataractous human lenses. , 1998, Experimental eye research.

[29]  A. Spector,et al.  The aqueous humor is capable of generating and degrading H2O2. , 1998, Investigative ophthalmology & visual science.

[30]  T. Reinheckel,et al.  Degradation of oxidized proteins in mammalian cells , 1997, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[31]  A. Goldberg,et al.  Lactacystin and clasto-Lactacystin β-Lactone Modify Multiple Proteasome β-Subunits and Inhibit Intracellular Protein Degradation and Major Histocompatibility Complex Class I Antigen Presentation* , 1997, The Journal of Biological Chemistry.

[32]  J. Alvarado,et al.  The cellular basis of aqueous outflow regulation. , 1997, Current opinion in ophthalmology.

[33]  D. Epstein,et al.  Effect of age on superoxide dismutase activity of human trabecular meshwork. , 1996, Investigative ophthalmology & visual science.

[34]  H. Quigley.  Number of people with glaucoma worldwide. , 1996, The British journal of ophthalmology.

[35]  K. Davies.  Oxidative stress: the paradox of aerobic life. , 1995, Biochemical Society symposium.

[36]  A. Goldberg,et al.  Inhibitors of the proteasome block the degradation of most cell proteins and the generation of peptides presented on MHC class I molecules , 1994, Cell.

[37]  K. Davies,et al.  Exposure of hydrophobic moieties promotes the selective degradation of hydrogen peroxide-modified hemoglobin by the multicatalytic proteinase complex, proteasome. , 1994, Archives of biochemistry and biophysics.

[38]  K. Davies,et al.  Protein modification by oxidants and the role of proteolytic enzymes. , 1993, Biochemical Society transactions.

[39]  H. A. Quigley,et al.  Open-angle glaucoma. , 1993, The New England journal of medicine.

[40]  W. M. Grant,et al.  Outflow facility studies in the perfused human ocular anterior segment. , 1991, Experimental eye research.

[41]  D. Epstein,et al.  Hydrogen peroxide removal by the calf aqueous outflow pathway. , 1988, Investigative ophthalmology & visual science.

[42]  D. Epstein,et al.  Superoxide dismutase and catalase of calf trabecular meshwork. , 1985, Investigative ophthalmology & visual science.

[43]  D. Epstein,et al.  Glutathione peroxidase of calf trabecular meshwork. , 1984, Investigative ophthalmology & visual science.

[44]  D. Epstein,et al.  Glutathione in calf trabecular meshwork and its relation to aqueous humor outflow facility. , 1983, Investigative ophthalmology & visual science.

[45]  R Holliday,et al.  Autofluorescence as an index of ageing in human fibroblasts in culture , 1982, Bioscience reports.

[46]  J. R. Smith,et al.  Colony size distributions as a measure of in vivo and in vitro aging. , 1978, Proceedings of the National Academy of Sciences of the United States of America.

[47]  T. Grune.  Oxidative stress, aging and the proteasomal system , 2004, Biogerontology.

[48]  P. Jenner,et al.  Oxidative stress in Parkinson's disease , 2003, Annals of neurology.

[49]  R. Kopito,et al.  Impairment of the ubiquitin-proteasome system by protein aggregation. , 2001, Science.

[50]  Keith K. Green,et al.  Free radicals and aging of anterior segment tissues of the eye: a hypothesis. , 1995, Ophthalmic research.

[51]  Stuart K. Williams,et al.  Isolation and culture of human trabecular meshwork cells by extracellular matrix digestion. , 1995, Current eye research.

[52]  W. M. Grant,et al.  Chandler and Grant's Glaucoma , 1986 .