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1. Trabid patient mutations impede the axonal trafficking of adenomatous polyposis coli to disrupt neurite growth

2. Mitochondrial E3 ubiquitin ligase MARCHF5 controls BAK apoptotic activity independently of BH3-only proteins

3. Physiological restraint of Bak by Bcl-x(L) is essential for cell survival

5. Activation mechanism of PINK1n (vol 602, pg 328, 2022)

6. Therapeutic targeting of mitophagy in Parkinson's disease

7. Activation mechanism of PINK1

12. Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)

13. Dynamic reconfiguration of pro-apoptotic BAK on membranes

14. Too much death can kill you: inhibiting intrinsic apoptosis to treat disease

15. Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition).

16. Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)1.

17. VDAC2 and the BCL-2 family of proteins

18. Mesenchymal stromal cell apoptosis is required for their therapeutic function

19. A new crystal form of GABARAPL2

20. Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)

22. MCL-1 is essential for survival but dispensable for metabolic fitness of FOXP3+regulatory T cells

23. Mechanism and inhibition of the papain-like protease, PLpro, of SARS-CoV-2

24. Robust autoactivation for apoptosis by BAK but not BAX highlights BAK as an important therapeutic target

26. Parkin inhibits BAK and BAX apoptotic function by distinct mechanisms during mitophagy

27. VDAC2 enables BAX to mediate apoptosis and limit tumor development

28. Huntingtin Inclusions Trigger Cellular Quiescence, Deactivate Apoptosis, and Lead to Delayed Necrosis

29. Disordered clusters of Bak dimers rupture mitochondria during apoptosis

32. Bid chimeras indicate that most BH3-only proteins can directly activate Bak and Bax, and show no preference for Bak versus Bax

33. Mitochondria and apoptosis: emerging concepts.

34. Two roads to death - Bax targets mitochondria by distinct routes before or during apoptotic cell death

35. Bid chimeras indicate that most BH3-only proteins can directly activate Bak and Bax, and show no preference for Bak versus Bax

43. Bak apoptotic function is not directly regulated by phosphorylation

44. Granzyme B triggers a prolonged pressure to die in Bcl-2 overexpressing cells, defining a window of opportunity for effective treatment with ABT-737

45. Translocation of a Bak C-Terminus Mutant from Cytosol to Mitochondria to Mediate Cytochrome c Release: Implications for Bak and Bax Apoptotic Function

48. Mitochondrial permeabilization relies on BH3 ligands engaging multiple prosurvival Bcl-2 relatives, not Bak

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