physio mini 1b

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  1. proteins involved in Gprotein linked cAMP cascade
    • H2O sol hormone + receptor (7tmd) = Gprotein(ac)
    • Gp(a) splits = alpha su + (delta and gamma su)
    • (alpha)GDP-> (a)GTP
    • aGTP + ACi = ACa
    • ACa+ ATP= cAMP
    • cAMP + PKAi= PKAa
    • PKAa+ CREBi= CREBa
    • CREBa + CREBbp+ CREB binding element= tx
  2. pseudoparathyroidism
    clinical- pt shows signs of PTH def: hypoCa and tetany, but PTH levels are normal

    cause- PTHr mutation, abnormal Gs protein so AC is not activated enough
  3. Toxic thyroid nodules
    • TSH from pituitary raises cAMP in thyroid causing hormone production and cell proliferation
    • -problem- BENIGN tumors in thyroid overproduce hormones
    • -cause- activating mutation on TSHr, Gs mutation that blocks its GTPase activity(which would deactivate)
  4. cholera toxin
    • catalyzes covalent modification of a s/u on Gs. abolishing GTPase activity leaving it in a permanently active state. leading to increased cAMP, which causes watery diarrhea
    • **also attack ZO-1 of desmosome, leading to leakage beside cells
  5. pertussis toxin
    modifies a/s/u of Gi protein, inactivating it and leading to fluid accumulation in the lung via increased cAMP(but this time due to inavtivation of inhibitory G and not permanent activation of activating G
  6. DAG and IP3 as second messengers
    • H2O sol hm + r = activated Gs
    • Gs splits = Gs a/s/u +( b/s/u + g/s/u)
    • a/s/u-GDP ==> a/s/u-GTP
    • a/s/u + PLCi = PLCa
    • PLCa + PIP2 = IP3 free + DAG
    • IP3 to ER opens Ca ch= increase Ca IC
    • Ca + DAG + PKCi = PKCa
  7. NMDAr
    ligand gated ion channel in the brain that opens in response to glutamate
  8. calmodulin
    Ca++ dependent enzyme activator, often activat PKs
  9. Ca channel blockers
    inhibit VOLTAGE gated Ca channels
  10. ADH response in liver
    Glycogen breakdown
  11. Thrombin (hormone)
    cleaves a piece of the Thrombin-r permanently activating it
  12. cGMP cascade
    • **no G protein involved**
    • membrane bound GC are activated directly by hormones
  13. NO
    can activate cytoplasmic GC
  14. ANF
    • ANF + ANFr = GC (activated ANFr is GC)
    • GTP + GC = cGMP
    • cGMP + PKGi = PKGa (PO4ates proteins)
    • **ANF causes increased Na excretion in the kidneys and relaxation of vascular SM**
  15. cAMP and cGMP in vascular SM
    act as Ca antagonists, causing relaxation (vasodilation)
  16. signalling thru a GF
    • GF (dimer) binds a GFr (w/ tyr kin dom) = TKa
    • GFr autoPO4, where IC signalling proteins bind to PO4 an activate (allosterically), then relay signal
    • -*signal proteins have an SH2 domain that bind PO4*
  17. insulin receptor
    similar to GHr, but a IRS(insulin receptor substrate) protein binds the autoPO4 receptor, which itself then PO4s and then the SH2- containing signal proteins bind and activate
  18. GF signalling and activation of IP3 system
    • a PLC alpha will also activate when GFr becomes PO4ed,
    • PIP2----->IP3 (via PLC)
  19. RAS
    G protein that mediated the effects of GF using mitogenic signalling cascade that activates kinases
  20. phosphodiestrase
    • cAMP----> AMP
    • *inhibited by caffeine*
  21. PLC gamma
    • activates in response to autoPO4 GFr
    • -IP3 cascade then ensues
  22. MAP kinase activaiton
    • GF causes autoPO4 of GFr
    • Ras activated by GFr
    • Ras activates protein kinases
    • protein kinases PO4 and activate MAP kinases
  23. PKB activation
    • GF binds GFr and causes autoPO4
    • GFr activates PI3K
    • the 3-PO4 inosities activate PKB
  24. G protein coupled receptor deactivation
    PO4 causes G protein to release and also attracts arrestin. which destines it for lysosomal degradation
  25. BARK
    beta-r kinase that PO4 and activated beta-r and prevent G protein coupling
Card Set
physio mini 1b
physio mini1b
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