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TRAIL-Induced Apoptosis: From Analysis of the Death-Inducing Signalling Complex (DISC) to Clinical Applicability
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    SPEAKER(S)

Dr. Henning Walczak - German Cancer Research Center, Germany

Dr. Henning Walczak is the Head of the Apoptosis Regulation Research Group, at the Tumor-immunology Program of the German Cancer Research Center in Heidelberg. He is an internationally recognized researcher in the apoptosis field with a special focus on the biochemistry of the death receptor-mediated pathway. The aim of the research conducted in his lab is to identify the molecular mechanisms that allow for specific killing of tumor cells by members of the TNF ligand family and ultimately how to apply them clinically.

Talk Online Publication: Oct 2007

TOPICS COVERED IN TRAIL-INDUCED APOPTOSIS: FROM ANALYSIS OF THE DEATH-INDUCING SIGNALLING COMPLEX (DISC) TO CLINICAL APPLICABILITY

poptosis induction by the TNF-related apoptosis-inducing ligand (TRAIL) - Apoptosis-inducing TNF super-family ligands and receptors - Formation of the deathinducing signalling complex (DISC) - Caspase-8 versus caspase-10 - Synergy of TRAIL with chemotherapeutics - Tumour specificity of TRAIL-induced apoptosis - Regulation of sensitivity versus resistance towards TRAIL-induced apoptosis

How to cite this talk:
Walczak, H. (2007), "TRAIL-Induced Apoptosis: From Analysis of the Death-Inducing Signalling Complex (DISC) to Clinical Applicability", in Hengartner, M. (ed.), Apoptosis: Fundamentals, Pathways, Clinical Applications and Role in Disease, The Biomedical & Life Sciences Collection, Henry Stewart Talks Ltd, London (online at http://hstalks.com/bio)

Direct talk access link:
http://hstalks.com/lib.php?t=HST24.1305_1_2&c=252

    DETAILED SLIDE INDEX

1. Introduction
2. Apoptosis induction by TRAIL
3. TRAIL: a member of the TNF superfamily
4. TNF-related apoptosis-inducing ligand (TRAIL)
5. TRAIL-R belong to the TNF-R superfamily
6. The death receptors
7. The TRAIL system
8. TRAIL DISC formation
9. c-FLIPS/c-FLIPL inhibit TRAIL-mediated apoptosis
10. Caspase 10
11. Caspase-10 is recruited to CD95 and TRAIL
12. Caspase-10 cannot substitute caspase-8
13. Caspase-10 protein expression is lost in tumors
14. Isoforms of caspase-10 and caspase-8
15. No differential cleavage for RIP and TRAF-1
16. Caspase-3 is cleaved by caspase-8 and -10
17. Caspase-8 and -10 generates different proteins
18. Summary and conclusion (caspase-8 versus -10)
19. Death receptors
20. The TRAIL system: can we kill tumor cells?
21. LZ-TRAIL induces apoptosis in tumor cell lines
22. Effect of TRAIL on normal human cells in vitro
23. TRAIL treatment of a subcutaneous tumor
24. Efficacy of TRAIL treatment in tumors
25. Inhibition of etoposide-induced apoptosis by Bcl-x
26. Double hit on tumor cells
27. Safety of TRAIL treatment: alone and in synergy
28. TRAIL versus CD95L in vivo
29. Sensitivity of PHH to TRAIL and to CD95L
30. Sensitivity and resistancy of PHH to TRAIL
31. HepG2 sensitivity to various forms of TRAIL
32. PHH are sensitive to one form of TRAIL only
33. Sensitisation of PHH by chemotherapeutics
34. Summary and conclusion (TRAIL on PHH)
35. What determines TRAIL sensitivity vs. resistance?
36. Sensitivity of various Hep cells to TRAIL
37. Proteasome inhibitors sensitise HC for TRAIL
38. Proteasome inhibition: TRAIL-induced apopotosis
39. Proteasome inhibition results in NF-kB inhibition
40. Proteasome inhibitors: upregulation of TRAIL-R1,2
41. TRAIL upregulation unnecessary for sensitisation
42. Proteasome inhibition enhances TRAIL formation
43. TRAIL sensitisation at the DISC level
44. Crosstalk between the two death pathways
45. Division of apoptosis regulation (DO40)
46. Thank you
47. END