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Lecture

Notes taken during lecture

4 Pages
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Department
Biology
Course Code
BIO120H1
Professor
Jean Jiang Nash

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LECTURE 20
P27 inhibits g1-s
Apoptosis = programmed cell death
Important for development
Digits separated is because interdigital cells died apoptosis important
No tail because during embryogenesis, tail was regressed or asorbed by apoptosis
Also important for protecting cells and you from cancer or some mutated state
oExcessive myc production, for instance, drives cell into s-phase
oCell can tell when it has too much myc
oActivates Arf protein binds to mdm2
oP53 stops cell cycle and waits if condition corrected, then cell continue
living but if not correction made, then programmed cell death is caused
Necrosis = accidental cell death
V. damaged cell
Spill contents out
Causes inflammation in body/ multicellular organisms
Apoptosis
By neatly shrinking the cell
Collapsing the cytoskeleton
Fragmenting the DNA
Signalling to macrophages for cell removal by engulfment
Guts of the cell never exposed to extracellular environment packaged into
vesicles that are engulfed
How does cell activate its program of cell death?
oInvolves caspases proteases
oCysteine caspases cysteins in active sites
oProcaspase precursor proteins
oBy other caspases
oLeads to amplified cascade of caspase activity
oProtocaspase has couple of cleavage sites
oActive caspase cleaves off pro domain
oGet together tetramer is the active caspase
Formed by products of cleavage of two caspases
First activated caspase activates cleave and activate executioner caspases
Executioner caspases cleave other proteins, not caspases
Initatior cleaves caspases
Once DNAs activated chromosomes chopped up
Negative at op and positive at bottom agarose gel
Small at bottom
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Description
LECTURE 20 P27 inhibits g1-s Apoptosis = programmed cell death Important for development Digits separated is because interdigital cells died apoptosis important No tail because during embryogenesis, tail was regressed or asorbed by apoptosis Also important for protecting cells and you from cancer or some mutated state o Excessive myc production, for instance, drives cell into s-phase o Cell can tell when it has too much myc o Activates Arf protein binds to mdm2 o P53 stops cell cycle and waits if condition corrected, then cell continue living but if not correction made, then programmed cell death is caused Necrosis = accidental cell death V. damaged cell Spill contents out Causes inflammation in body multicellular organisms Apoptosis By neatly shrinking the cell Collapsing the cytoskeleton Fragmenting the DNA Signalling to macrophages for cell removal by engulfment Guts of the cell never exposed to extracellular environment packaged into vesicles that are engulfed How does cell activate its program of cell death? o Involves caspases proteases o Cysteine caspases cysteins in active sites o Procaspase precursor proteins o By other caspases o Leads to amplified cascade of caspase activity o Protocaspase has couple of cleavage sites o Active caspase cleaves off pro domain o Get together tetramer is the active caspase Formed by products of cleavage of two caspases First activated caspase activates cleave and activate executioner caspases Executioner caspases cleave other proteins, not caspases Initatior cleaves caspases Once DNAs activated chromosomes chopped up Negative at op and positive at bottom agarose gel Small at bottom www.notesolution.com
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