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CELL PROLIFERATION AND CELL DEATH, effector caspase 3, cytochrome c…
CELL PROLIFERATION AND CELL DEATH
TYPES OF CELLS
LABILE CELLS
constantly dividing and self-renewing
e.g. keratinocytes and epithelial cells
STABLE CELLS
usually divide slowly but rapidly in response to stimuli
PERMANENT
do not divide, regenerate from stem cells
CELL NUMBER AND SIZE AND TISSUE GROWTH
HYPERPLASIA
increase in number of cells
HYPERTROPHY
increase in size of cells
BOTH
INTERPHASE
G1 PHASE or GROWTH 1
cyclins are stimulated to Cyclin-Dependent Kinases CDKs
cells grow in size
increased energy and protein production
increased organelle formation
S PHASE or SYNTHESIS
DNA replication occurs
G2
preparation for M phase
M PHASE
consists of Pro, Meta, Ana, Telo
cytokinesis occurs
replication of cell cytoplasm
CELL CYCLE CONTROL
CDKs
activation of proteins through phosphorylation
stay inactive when not bound by cyclins
CYCLINS
proteins that are cyclically produced during the cell cycle
form cyclin-CDK complex
ROLE OF Rb PROTEIN
binds to E2F transcription factors
prevents progression from from G1 to S
CELL DEATH
APOPTOSIS
cell shrinks
forms blebs without inflammation
blebbing causes cell to break into apoptotic bodies
these are phagocytosed
chromatin gets condensed and fragmented
organelles clump together
no inflammatory response
programmed cell death
NECROSIS
cell swells
significant inflammation
cell membrane breaks down
nucleus shrinking, fragmentation and dissolution
organelles break down
cell ruptures and breaks down
release of enzymes
FACTORS LEADING TO APOPTOSIS
withdrawal of positive signals
RECEIPT OF NEGATIVE SIGNALS
increased level of oxidants within cell
DNA damage by UV light, X-rays and chemotherapeutic drugs
death activators
TNF-α, FasL
interference in cell death pathway
failure to replicate
incorrect mechanistic signalling activation
EXTRINSIC AND INTRINSIC APOPTOTIC SIGNALS
EXTRINSIC PATHWAY
death ligands bind to
death receptors
activates initiator caspase 8
INTRINSIC PATHWAY
initiated by DNA damage and p53
chemical stress causes mitochondrial membrane to become leaky
initiator caspase 9
effector caspase 3
apoptosis
cytochrome c activates caspase cascade