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Flashcards

Signal Transduction

hazel wilkie Physiology English 58 cards

Cards in this deck (58)

  1. 1what do extracellular signalling molecules do ?- They act on membrane-bound receptors that control signalling proteins via the production of second messengers.
    •These mediate cell activity.
  2. 2what are the two common ways to activate/deactivate signalling proteins?- phosphorylation
    - GTP binding
    (both activates)
    - GDP deactivates
    - dephosphorylation deactivates
  3. 3what is the function of a kinase?adds a phosphate
  4. 4what is the function of a phosphatase?removes a phosphate
  5. 5name the two main types of kinases-tyrosine kinase
    - serine/threonine kinase
  6. 6name the two types of GTP - binding proteins-trimeric G proteins
    -monomeric GTPases
  7. 7what activates G-proteins?ligand binding
  8. 8what does activation of a G-protein lead to?an activated g protein in turn activates or inhibits another protein
    - often this is an enzyme that generates a specific second messenger (intracellular)
  9. 9what a g protein activation and complex formation a part of?- a cycle
  10. 10how many membrane spanning regions do G protein coupled receptors have?7
  11. 11what side of the cell is the amino termini of the GPCR on?extracellular
  12. 12which side of the cell is the carboxyl termini of GPCR on?intracellular (on the face of the plasma membrane)
  13. 13define trimericcomposed of three different subunits
    - alpha beta gamma
  14. 14what are many cell surface receptors coupled to?trimeric signal transducing G proteins that bind either GTP or GDP
  15. 15describe the mechanism of actin of GPCRs1. ligand binds to receptor and this induces a conformational change in the receptor
    2. this activated receptor binds to a G-alpha subunit
    3. this binding induces a conformational change in the G alpha subunit - GDP is displaced by GTP and G alpha dissociated from Gbeta gamma.
    4. the ligand dissociated from the receptor, G alpha bind to the effector protein, activating it.
    5. GTP is hydrolyes to GDP which causes G alpha to dissociate from effector and reassociate with G beta gamma.
    4. effector is inactivated
  16. 16what is the name of the effector in the previous exampleadenylate cyclase
  17. 17what is required for the ligand-induced stimulation of adenylate cyclase?GTP
  18. 18what type of receptor is on the extracellular side of a GPCR?B2 adrenergic (7 TM)
  19. 19name the function of the following G protein (G alpha) classes: Gq Ga GiGq - stimulates phospholipase C
    Ga - stimulates adenylate cyclase, increases cAMP
    Gi - inhibits adenylate cyclase, decreases cAMP
  20. 20what does adenylate cyclase do?produces cAMP
  21. 21what are isoforms?proteins which possess distinct domain structures but catalyse the same reaction
    - Some domains are common (catalytic, membrane localisation)
    - Some domains are unique (regulatory)
  22. 22name an isoformPhospholipase C
  23. 23what does PLC do?liberates IP3 and DAG from PIP2
  24. 24what opens calcium channels?IP3
  25. 25what activates PKC?DAG and calcium
  26. 26what can calcium signals trigger?- many biological processes
    - triggers start of embryonic development in starfish egg and prevents other sperm from entering cell
  27. 27what are most PKC isoforms present as?catalytically inactive, soluble proteins in the cytoplasm
  28. 28what triggers PKC to bind to the cytosolic leaflet of the plasma membrane?rise in calcium levels
  29. 29what does PKC binding to cytosolic leaflet lead to?PKC can then be activated by the membrane associated DAG and/or calcium ions.
  30. 30what does activated PKC then do?it phosphorylates a wide variety of substrate proteins on serine and threonine residues.
  31. 31how can PKC function in a transient way?it has substrates in the cytoplasm and some iso forms can translocate to the nucleus to phosphorylate nuclear proteins
  32. 32how can PKC activation also function 'indirectly' to alter gene expression?because it can phosphorylate nuclear proteins
  33. 33name another type of GPCR signallingbinding of adrenalin to the B2 adrenergic receptor
  34. 34what does the binding of adrenalin to the beta 2 adrenergic receptor cause?1. increases the intracellular concentration of cAM as receptor couples to G alpha s
  35. 35how is cAMP synthesised?within cells from ATP by the enzyme adenylate cyclase
  36. 36how is cAMP degraded?by the enzyme cAMP phosphodiesterase
  37. 37does each receptor have its own adenylate cyclase?- different receptors utilise a common adenylate cyclase
    -adenylate cyclase is an amplifier
  38. 38how does increased cAMP activate the cAMP dependent protein kinase PKA?cAMP binds to the regulatory subunits, exposing the catalytic sites on the catalytic subunits.
  39. 39how does signal transduction affect a signal?it results in amplification of a signal - a small change at the top can have a large change at the bottom
  40. 40what can the catalytic subunit of PKA do?it can phosphorylate substrates on serine or threonine residues.
    - it has substrates in the membrane, cytoplasm and the nucleus.
  41. 41what can PKA do in the nucleus?PKA can activate transcription of genes containing cAMP response elements, or CREs in their promoter.
  42. 42what is CREB? and what does it do?A specific transcription factor - the cAMP response element binding protein.
    it binds to this sequence and activates transcription of downstream genes.
  43. 43when can CREB activate transcription?when it is phosphorylated
  44. 44what does the cholera toxin do once it enters the intestinal tract?- stimulates Galpha s
    - this leads to an over stimulation of cAMP
    - this results in release of water and ions into the lumen of small intestine = rapid fluid loss and dehydration
  45. 45how do pertussis toxin act?acts in the reverse manner to cholera
    - inhibits G alpha i
    - increases cAMP production in the lung epithelia
  46. 46name an enzyme linked receptor?Receptor Tyrosine Kinases (RTKs)
  47. 47what activates RTKS and what does this control?insulin like growth factors active RTKs to control cell proliferation
  48. 48what do RTKs activate?Ras
  49. 49what do Ras regulate?cellular processes: proliferation, cytoskeletal dynamics, membrane trafficking/vesicular transport
  50. 50what is a small GTPase?RTK activating Ras
  51. 51what are small GTPases of the Rac/Rho subfamily are direct targets for?clostridial cytotoxins
  52. 52what is a mutation to the Ras protein found in?Ras proteins are mutated to a constitutively-active (GTP-bound) form in approximately 20% of human cancers.
  53. 53what does Ras activate?the MAPK (mitogen-activated protein kinase) pathway
  54. 54what is EGFR (epidermal growth factor receptor) ?an RTK activated by TGFα (Transforming growth factor alpha)
  55. 55what does EGFR activate?Ras via Grb2/SOS proteins
  56. 56what does EGFR activated Ras, activate?Raf (kinase), which in turn stimulates gene transcription via other kinases (MEK and ERK).
  57. 57what are Mutations in EGFR, Ras and Raf are associated with?tumorigenesis
  58. 58what do these mutations cause?These cause overexpression and/or hyperactivation of the respective proteins

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Physiology (Cells) Flashcards on Signal Transduction, created by hazel wilkie on 01/05/2017.
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hazel wilkie
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