3.1: cell signalling Flashcards
1
Q
what is a ligand
A
molecules produced by signalling cells that interact w receptors
- large, hydrophilic, polar charged -> repelled by hydrophobic core of PL
- small, hydrophobic, non-polar, uncharged -> diffuse across plasma membrane into cytoplasm
2
Q
what is a second messenger
A
small, non-protein, water-soluble molecules
3
Q
why are second messengers small and water soluble
A
rapid diffusion thru cell
quick transduction of signal
4
Q
why are second messengers non-protein and small
A
- less sensitive to pH/temp
- less easily degraded
- synthesised in shorter time
- less resources needed than larger molecules
5
Q
function of second messengers
A
- relay signals from ligand binding (1st messenger) at cell surface receptors to target molecules in cytosol/nucleus
- greatly amplify strength of signal -> large cellular response
6
Q
cell signalling: ligand-receptor interaction
A
- recognition and reversible binding of ligand to specific receptor (complementary 3D conformation)
- activation of receptor
- ligand-receptor complex
7
Q
cell signalling: signal transduction
A
- conformational change to specific receptor
- signal converted and amplified via second messengers & phosphorylation cascade of kinases
8
Q
cell signalling: cellular response
A
activation of specific cellular activity
- regulation of protein/enzyme activity
- regulation of protein synthesis via gene expression
- apoptosis
etc
9
Q
homeostasis
A
allow metabolic rxns to occur at optimum rate
- self regulation
- negative feedback
10
Q
advantages of cell signalling system
A
- specificity of ligand-receptor int = specific response from specific target cells
- activation of gene expression in nucleus
- activate many target cells simultaneously = regulation and control of response
- signal amplification = one signal molecule -> large cellular response
- one signal molecule -> activate multiple pathways = rxns simultaneously
11
Q
kinase as a molecular switch
A
- ADDS phosphate grps
- activates proteins
- involved in signal amplification
12
Q
phosphotase as a molecular switch
A
- REMOVES phosphate grps
- deactivates proteins
- signal termination
13
Q
generally, how can a signal be terminated?
A
- dissociation of ligand from receptor
- GTPase hydrolyses bound GTP to GDP
- phosphodiesterase converts cAMP to AMP
- protein phosphotases inactivate kinases via dephosphorylation
14
Q
RTK: L-R interaction
A
- insulin binds to extracellular binding sites of RTK
- activates RTK protein
- dimerises 2 RTK proteins
- intracellular domain of RTK undergoes conformational change
- intrinsic tyrosine kinase is activated
- tyrosine kinase adds phosphate grp from ATP to tyrosine residues on tail of other RTK via autophosphorylation
15
Q
RTK: signal transduction
A
- activated RTK triggers assembly of relay proteins
- relay proteins further recruit and activate other downstream relay molecules and kinases
- at each step, each activated kinase phosphorylates and activates a large no of next kinase
SIGNAL AMP
16
Q
RTK: cellular response
A
- glycogen synthase activated = GLYCOGENESIS ( glucose -> glycogen)
- vesicles embedded w glucose transporters fuse w plasma membrane = increase glucose uptake
- decrease in glycogenolysis and gluconeogenesis
- decrease in blood glucose level back to set pt = NEGATIVE FEEDBACK
17
Q
RTK: signal termination
A
- insulin dissociates from RTK = inactivation of RTK
- phosphotase dephosphorylates tyrosine residues on RTK tails -> dimer dissociates back into individual RTK proteins
- phosphotases inactivate protein kinases by dephosphorylation
18
Q
GPLR: L-R interaction
A
- glucagon binds to extracellular site of GPLR
- causes conformational change in GPLR
- cytoplasmic side of activated GPLR binds inactive G protein
- G protein exchanges bound GDP for GTP
- activation and dissociation of G protein
- dissociated active G protein binds and activated adenlyl cyclase
19
Q
GPLR: signal transduction
A
- adenlyl cyclase catalyses conversion of ATP -> cAMP
- second messenger cAMP binds and activates a large no of PKA (protein kinase A)
- each activated kinase will initiate sequential phosphorylation -> phosphorylation cascade
- at each step of the cascade, each kinase can activate a large no of kinases -> signal amplification
- activated PKA P+A phosphorylase kinase -> glycogen phosphorylase
20
Q
GPLR: cellular response
A
- large no of glycogen phosphorylase activated = glycogenolysis (glycogen -> glucose)
- increase in gluconeogenesis
- decrease in glycogenesis and glycolysis
- increase in blood sugar conc to set pt = NEGATIVE FEEDBACK
21
Q
GPLR: cellular response
A
- large no of glycogen phosphorylase activated = glycogenolysis (glycogen -> glucose)
- increase in gluconeogenesis
- decrease in glycogenesis and glycolysis
- increase in blood sugar conc to set pt = NEGATIVE FEEDBACK
22
Q
GPLR: signal termination
A
- glucagon dissociates from GPLR
- GTPase intrinsic to G protein hydrolyses bound GTP -> GDP
- phosphodiesterase converts cAMP -> AMP
- phosphotases inactivate protein kinases via dephosphorylation
