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Lecture 1 Oncogenesis
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G-protein coupled receptors, kinase, receptor tyrosine kinases, cancer pathways
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Oncogenesis Week 1Lecture 1
Second messengers are produced inside of
the cell.
Kinases phosphorylate substrates to
activate them. It uses ATP → ADP for this
reaction.
GTPase bound to GDP is inactive/off,
GTPase bound to GTP is active/on.
G-protein receptor, phospholipase-C,
calcium, activation of protein kinases.
→ See PLC.
Nf-kb is an important transcription factor
that can go into the nucleus.
Receptor tyrosine kinases need
dimerization for their activation. They
undergo a conformational change and they
start to cross-phosphorylate.
Phosphorylated tyrosine residues →
activated receptor (ligand is a growth
factor).
SH2 domains → high affinity for
phosphorylated tyrosine residues.
RAS is active if it’s bound to GTP rather than GDP (inactive). GTP Exange Protein (GEP) activates RAS.
GAP = GTPase (GTP → GDP hydrolysis) activating protein → helps Ras to become inactive. Grb2 x SOS
molecule has 1 SH2 and 2 SH3 domains → this recruits Ras. Ras recruits Raf. Raf phosphorylates MEK
and MEK phosphorylates MAPK.
Raf = MAP-kinase-kinase-kinase, MEK = MAP-kinase-kinase, MAPK =MAP-kinase
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