Printable Handouts

PDF

Navigable Slide Index

1. Introduction
2. Heat shock genes and proteins discovery
3. Heat shock elements and transcription factor 1
4. Conditions for activation of HSF-1
5. 5 different heat shock protein families
6. Some families are nor HSF-1 regulated
7. HSPs are molecular chaperones
8. HSPs and folding of nascent proteins
9. Heat-induced HSP up-regulation
10. HSP70 and toxicity protection
11. HSPs and mutant proteins
12. HSPs: expansion and functional diversification
13. Interaction between different HSP families
14. HSP70 machines
15. Functional specificity via different HSP70s
16. Functional specificity via different NEFs
17. Functional specificity via different DNAJs
18. Functional classification of DNAJ proteins
19. Promiscuous client binding in DNAJ proteins
20. Ydj1 and Sis1/DNAJB1 generally promote refolding
21. DNAJB2 directs clients to degradation
22. Selective client binding
23. DNAJs without client binding for tethering HSP70
24. DNAJC2
25. Functional specificity beyond DNAJs
26. The HSP70 machine and folding diseases
27. PolyQ diseases
28. Recognizing HSPs in polyQ disease
29. DNAJB6/8 suppressors of poly-Q aggregation
30. DNAJB6/8 protect against poly-Q toxicity
31. Deletion of SSF-SST region of DNAJB8
32. DNAJB6 / DNAJB8 interact with HDACs
33. HDAC4 is required for DNAJB6/8 function
34. DNAJB8 acetylation
35. C-terminal lysines involved in activity of DNAJB8
36. DNAJB6 prevents polyQ aggregation in vitro
37. DNAJB6/8 prevent polyQ aggregation in cells
38. A model of prevention of polyQ aggregation
39. HSPB expansion and functional diversification
40. HSPB alpha-crystalline domain
41. Human HSPB family
42. Refolding vs. polyQ aggregation
43. Canonical mechanism of refolding
44. Non-canonical mechanism of refolding
45. Summary
46. Acknowledgements
47. References

Topics Covered

• Heat shock proteins
• Regulation and chaperone activity
• Several protein families with many different members
• DNAJ family
• Regulation of differentiation of HSP machines to drive client specificity and differential client processing
• Involvement in folding, proteasomal degradation, autophagy
• Potent suppressors of protein deposit diseases, e.g. CAG repeat diseases

Links

Series:

• Protein Homeostasis

Categories:

• Biochemistry
• Cell Biology

Talk Citation

Publication History

• Published on February 2, 2012

Financial Disclosures

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