Cell Signalling VI

Pregunta	Respuesta
Functions of apoptosis	Embryogenesis - Sculpting limbs/removal of redundant structures Maintain Cell #
What is PCD	Elimination of cells damaged beyond repair
What kinda damage	DNA Damage Repair mech. can't cope w/ the damage Misfloded protein accumulation
Morphological features/ ultrastructure changes	Cell shrinkage Chromatin condensation IC content fragging + Membrane blebbing Formation of AB
Caspases (4)	1. Cys at AS 2. Cleave aspartic acid residues of target proteins. 3. Synthesised as inactive proteins. 4. Undergo proteolytic autocleavage of aspartic acid residues to become active.
Chain reaction (5)	1. Autocleavage 2. Activate effector caspases 3. Cleave nuclear lamin 4. Effector + other caspases 5. Cleave cytosolic proteins.
Hallmark cleavage of Chr. DNA	Cleave protein that prevents endonuclease activity. DNA endonuclease cut into internucleosomal units of 180-200 bp.
Testing for apoptosis	DNA laddering in electrophoresis
What is the key "engulf me" signal?	Phosphotidylserine
MOA	Usually found inner side of mem. Move to outer side during apoptosis (caspase mediated). Phagocytes like macrophages/neutrophils recognise PTS or other apoptopic signals of AB.
Intrinsic molecular pathway of Apoptosis (Mito)	1. Lack of trophic factor-inducing signal i.e. GF/Survival F withdrawal. 2. DNA damage via P53 (Chemo) 3. Protein misfolding (E.R. stress).
What is intrinsic pathway + dependent on?	Release of Cytochrome C from mitochondria
Which molecules promote apoptosis?	Pro BAD BAX BAK
Which molecules inhibit apoptosis?	BCL-2 BCL-XL Block the action of BAX/BAK
How do BAK/BAX work?	Form channels in out mito mem. to release Cytochrome C
Signalling pathway	1. Apoptosis stimulus 2. BAK/BAX + 3. Cytochrome + adaptor protein APAF-1 4. Assembly of adaptor//CCC 5. Recruitment of procaspase 9 6. Formation of apoptosome 7. + of procaspase 9 within apoptosome 8. Caspase cascade leading to apoptosis
GF/SF inhibition of apoptosis	Increase transcription/translation of anti-apoptopic molecules like BCL-2 Stimulation of PKB which Pi and - BAD
Extrinsic Pathway initiation	Receptor mediated Binding of TNF to their R Kills cells targeted by the immune system
Cellular targets	Cancer cells Virus-infected cells Excess lymphocytes at end of immune response
Key features of Death receptors	EC domain Transmembrane domain IC domain containing the Death Domains
Key features of Adaptor	Death Domains interact w/ DD of receptors Death Effector Domains which interact w/ DED domains of initiator procaspases.
MOA	1. Trimeric ligand causes R trimerisation 2. Two cytosolic adaptor proteins FADD + TRADD and procaspase-8 are recruited by the +TNF 3. The 2 procaspase-8 molecules + each other to initiate caspase cascade.

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	Creado por J yadonknow hace alrededor de 6 años