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1. Introduction
2. Talk outline
3. Normal eye illustration
4. Mouse lens cataract range
5. Normal clear lens vs. cataract lens
6. Lens brunescence and clarity vary independently
7. Lens development: a model for aging research
8. Protein precipitation disease
9. Cataract prevalence increases with age
10. The retina
11. The structure of the human retina
12. Photo-oxidative stress to the retina
13. The life cycle of the RPE
14. Progress of retinal degeneration
15. Distorted central vision due to AMD
16. View through AMD-damaged retina
17. AMD prevalence increases exponentially by age
18. AMD and cataract will increase within two decades
19. Loss of sight - second greatest fear of the elderly
20. Therapeutic opportunities
21. Etiology, environmental factors, pathophysiology
22. The eye deals with different kinds of stress
23. Smoking and AMD
24. Proteins are damaged upon oxidative stress
25. Oxidative damage to lens proteins
26. Formation of protein carbonyls
27. Oxidation reactions and sequela reaction products
28. Cataract, decreased P-SH and increased carbonyl
29. Glycoprotein vs. age in human lens
30. Lens protein distribution with age
31. Modifications to proteins/proteases in older tissues
32. Active proteases remove damaged proteins
33. Ubiquitin pathway selectivity for substrates
34. The ubiquitin-proteasome pathway (UPP)
35. Ubiquitin chain linkage and function
36. Oxidatively modified proteins in HLEC
37. Could we isolate ubiquitin conjugates?
38. K6W-Ub is conjugation competent
39. Selectivity of ubiquitination for oxidized proteins
40. Impairing the UPP by expression of K6W-Ub
41. Protease inactivation and damaged proteins
42. Lens clearity depends on a functional Ub pathway
43. Glutathiolation and gammaC-crystallin degradation
44. Glutathiolation enhances protein degradation rate
45. Proteolysis of GSH-modified gamma-C-crystallin
46. Degradation of glutathiolated gamma-C-crystallin
47. Glutathiolation and CAIII degradation
48. Minor CAIII structural alteration upon GSH
49. E1 and E2 are thiol enzymes
50. Thiolation of E1 following exposure to H2O2
51. Control of the UPP by GSSG:GSH
52. Oxidative inactivation of the proteasome
53. Protein deamidation progresses with age
54. Methylglyoxal reacts with Lys and Arg of proteins
55. Glycation/MGO decreases degradation
56. Clinical relevance
57. Simple sugars might cause cataract and AMD
58. High dietary glycemic index - risk for early ARM
59. Antioxidants can delay aging
60. What happens upon aging in the Ub pathway?
61. Summary

Topics Covered

• Description of cataract and AMD as the ultimate protein misfolding diseases
• Lens development: a model for aging research
• Photo-oxidative stress to the retina
• Etiology
• Environmental factors
• Pathophysiology
• Protein quality control
• Ubiquitin pathway selectivity for oxidatively modified, glutathiolated, deamindated and glycated substrates
• Clinical relevance

Links

Series:

• Free Radicals and the Oxygen Paradox

Categories:

• Biochemistry

Therapeutic Areas:

• Ophthalmology

Talk Citation

Taylor, A. (2017, October 21). Ubiquitin dependent degradation of proteins modified by oxidation, deamidation and glycation: role in vision [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved November 23, 2024, from https://doi.org/10.69645/SJOK9608.
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Publication History

• Published on November 1, 2007
• Reviewed on October 21, 2017

Financial Disclosures

• Prof. Allen Taylor has not informed HSTalks of any commercial/financial relationship that it is appropriate to disclose.