13086083
Descrição
FlashCards por J yadonknow, atualizado more than 1 year ago
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Criado por J yadonknow
aproximadamente 6 anos atrás
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| Questão | Responda |
| 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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