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5 Written questions

5 Multiple choice questions

  1. over-activated RSK2.
    Too much ATF4 ~> osteoclacin ~> too many osteoblasts
  2. Regulator of osteocalcin promoter
    activated by RSK2 kinase
    knockout leads to osteogenesis (smaller/thinner bone)
    Without, have trouble importing amino acids (high protein diet can fix)
  3. Chondrocyte, osteoblast, osteoclast
    Growth Formation Resorption
  4. Runx2 ~> osteocalcin ~> osteoblast.
    Twist inhibits Runx2
    without it, no bone!
    (Runx2 is also for chondrocytes)
  5. Delay: Msx2, Runx2 haploinsufficiencies
    Acceleration: FGF, MSX2 activating mutations. twist haploinsufficiency

4 True/False questions

  1. Proliferation of chrondrocytesRunx2 ~> IHH ~> Proliferation
    Twist inhibits Runx2 as well
    However, IHH also induces PTHrP which inhibits IHH.
    This elongates the proliferative stage so you have enough cells before entering hypertrophy.


  2. Cleidocranial dysplasiaover-activated RSK2.
    Too much ATF4 ~> osteoclacin ~> too many osteoblasts


  3. Jansen blomstrands chrondroplaysiaPTHrP mutation in receptor
    Severe dwarfism.
    But aren't little people soooooo cute?


  4. Coffin-LowryInactivated RSK2.
    ATF4 isn't turned on
    can't import AA or fully differentiate osteoblasts
    treated with high protein diet


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