3.1: cell signalling Flashcards

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1
Q

what is a ligand

A

molecules produced by signalling cells that interact w receptors

  1. large, hydrophilic, polar charged -> repelled by hydrophobic core of PL
  2. small, hydrophobic, non-polar, uncharged -> diffuse across plasma membrane into cytoplasm
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2
Q

what is a second messenger

A

small, non-protein, water-soluble molecules

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3
Q

why are second messengers small and water soluble

A

rapid diffusion thru cell

quick transduction of signal

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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
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5
Q

function of second messengers

A
  1. relay signals from ligand binding (1st messenger) at cell surface receptors to target molecules in cytosol/nucleus
  2. greatly amplify strength of signal -> large cellular response
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6
Q

cell signalling: ligand-receptor interaction

A
  1. recognition and reversible binding of ligand to specific receptor (complementary 3D conformation)
  2. activation of receptor
  3. ligand-receptor complex
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7
Q

cell signalling: signal transduction

A
  1. conformational change to specific receptor
  2. signal converted and amplified via second messengers & phosphorylation cascade of kinases
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8
Q

cell signalling: cellular response

A

activation of specific cellular activity

  1. regulation of protein/enzyme activity
  2. regulation of protein synthesis via gene expression
  3. apoptosis

etc

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9
Q

homeostasis

A

allow metabolic rxns to occur at optimum rate

  • self regulation
  • negative feedback
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10
Q

advantages of cell signalling system

A
  1. specificity of ligand-receptor int = specific response from specific target cells
  2. activation of gene expression in nucleus
  3. activate many target cells simultaneously = regulation and control of response
  4. signal amplification = one signal molecule -> large cellular response
  5. one signal molecule -> activate multiple pathways = rxns simultaneously
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11
Q

kinase as a molecular switch

A
  • ADDS phosphate grps
  • activates proteins
  • involved in signal amplification
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12
Q

phosphotase as a molecular switch

A
  • REMOVES phosphate grps
  • deactivates proteins
  • signal termination
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13
Q

generally, how can a signal be terminated?

A
  1. dissociation of ligand from receptor
  2. GTPase hydrolyses bound GTP to GDP
  3. phosphodiesterase converts cAMP to AMP
  4. protein phosphotases inactivate kinases via dephosphorylation
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14
Q

RTK: L-R interaction

A
  1. insulin binds to extracellular binding sites of RTK
  2. activates RTK protein
  3. dimerises 2 RTK proteins
  4. intracellular domain of RTK undergoes conformational change
  5. intrinsic tyrosine kinase is activated
  6. tyrosine kinase adds phosphate grp from ATP to tyrosine residues on tail of other RTK via autophosphorylation
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15
Q

RTK: signal transduction

A
  1. activated RTK triggers assembly of relay proteins
  2. relay proteins further recruit and activate other downstream relay molecules and kinases
  3. at each step, each activated kinase phosphorylates and activates a large no of next kinase
    SIGNAL AMP
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16
Q

RTK: cellular response

A
  1. glycogen synthase activated = GLYCOGENESIS ( glucose -> glycogen)
  2. vesicles embedded w glucose transporters fuse w plasma membrane = increase glucose uptake
  3. decrease in glycogenolysis and gluconeogenesis
  4. decrease in blood glucose level back to set pt = NEGATIVE FEEDBACK
17
Q

RTK: signal termination

A
  1. insulin dissociates from RTK = inactivation of RTK
  2. phosphotase dephosphorylates tyrosine residues on RTK tails -> dimer dissociates back into individual RTK proteins
  3. phosphotases inactivate protein kinases by dephosphorylation
18
Q

GPLR: L-R interaction

A
  1. glucagon binds to extracellular site of GPLR
  2. causes conformational change in GPLR
  3. cytoplasmic side of activated GPLR binds inactive G protein
  4. G protein exchanges bound GDP for GTP
  5. activation and dissociation of G protein
  6. dissociated active G protein binds and activated adenlyl cyclase
19
Q

GPLR: signal transduction

A
  1. adenlyl cyclase catalyses conversion of ATP -> cAMP
  2. second messenger cAMP binds and activates a large no of PKA (protein kinase A)
  3. each activated kinase will initiate sequential phosphorylation -> phosphorylation cascade
  4. at each step of the cascade, each kinase can activate a large no of kinases -> signal amplification
  5. activated PKA P+A phosphorylase kinase -> glycogen phosphorylase
20
Q

GPLR: cellular response

A
  1. large no of glycogen phosphorylase activated = glycogenolysis (glycogen -> glucose)
  2. increase in gluconeogenesis
  3. decrease in glycogenesis and glycolysis
  4. increase in blood sugar conc to set pt = NEGATIVE FEEDBACK
21
Q

GPLR: cellular response

A
  1. large no of glycogen phosphorylase activated = glycogenolysis (glycogen -> glucose)
  2. increase in gluconeogenesis
  3. decrease in glycogenesis and glycolysis
  4. increase in blood sugar conc to set pt = NEGATIVE FEEDBACK
22
Q

GPLR: signal termination

A
  1. glucagon dissociates from GPLR
  2. GTPase intrinsic to G protein hydrolyses bound GTP -> GDP
  3. phosphodiesterase converts cAMP -> AMP
  4. phosphotases inactivate protein kinases via dephosphorylation