Q@Q Drill time ❹ - cardio69

[ArchivalUser]

Which of the following events is characteristic both Ex & In-TRINSIC pathway of programmed cell death?

a) Caspase 8 activation
b) Cleavage of the proapoptotic factor/BID
c) Activation of caspases 3, 6 and 7
d) Involvement of fas assco death domain protein
e) Activation of caspases 3 and 10


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[ArchivalUser]

Time's UP>

[ArchivalUser]

The activation of caspase can be both intrinsic and extrinsic.

Cell death can occur through both extrinsic death receptor pathway and intrinsic mitochondria pathway, and they both meet at caspase 3 thereby activating other proteases.

From here, and just take a 50/50 guess.

C

[ArchivalUser]

Great

You understand if paint pic of loss of plasma membrane integrity & cellular collapse with extrusion of cytoplasmic contents but then I tell you the cell nuclei remain intact (for ex; due to a virus or some external factor such as MI or trauma). Can you name the “R that dependent kinases” dependent? You know of to cause ↓ mitochondrial ATP, ↑ ROS and rupture of lysosomal membranes in scenario here

[ArchivalUser]

Increased Ca in the cytosol, might cause activation of cellular enzymes, producing ATPase which decreases ATP levels.

Phospholipase which diminishes phospholipids hence causing membrane rupture

Cathepsin D

Nef overexpression

Not sure of this lol

[ArchivalUser]

to be honest. Just wrote down foactors that i think might decrease mitochondria ATP, lysosomal enzymes

[ArchivalUser]

Good try @cross others just watch.

Programmed necrosis/necroptosis -> involves the activity of ubiquitinated/Or deubiquitinate RIP1/K3.
For ex, “necroptosis,” it happens in response to specific stimuli, such as TNF- & TLR-mediated signals. Remember it has blade contrast to apoptosis so, you can say caspase/INdependent

[ArchivalUser]

All I want u to spit -> two unique kinases -> RIP1 & 3

[ArchivalUser]

Thanks

[ArchivalUser]

Glad I could help.