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caspases
Caspases
  • Protease- cut specific tetrapeptides
  1. Procaspase activation - form dimer
  2. Proteolytic cascade
    1. Initiator caspases cleave executioner
    2. Breakdown nuclear lamins, cleave DNase inhibitor
    3. All or nothing
Bcl2
Bcl2 & related
    1.  pro and anti apoptotic proteins (Bcl2 = anti)
    2. e/ contain BH domain - interact
    3. Balance sway = Trigger intrinsic pathwy
 
necrosis vs apoptosis
Necrosis vs apoptosis
Stuff Necrosis Apoptosis Cell volume Increased Decreased Chromatin Fragmented Condensed Plasma membrane Lyse Intact* Inflammation Frequent No Role Pathologic Planned*** Cell fate Lysis Digested DNA Degraded Cleaved** * phosphatidylserine to outside = indication **cleaved in ~200bp increments ***developing embryo, more neurons  created than necessary
extrinsic
Extrinsic pathway
    1. Initiated by other cells -ie killer T cells
    2. Fas ligand bind to Fas receptor
    3. FADD + procaspase 8/10 bind to receptor -->DISC
    4. DISC activates caspase 8/10 -> activate executioner casp.
      1. Close proximity
    5. apoptosis
 
intrinsic
Intrinsic pathway
    1. Internal cellular decision - injury, stresses, dna damage, lack O2
    2. Release of cytochrome c from mitochondria
    3. Assemble apotosome w/ initiator procaspases 9
    4. Close proximity -> activate caspase 9 -> cascade
    5. apoptosis
 
tumor suppressor genes
Tumor suppressor genes
  • Normally help cell undergo apop
    • P53, BRCA1/2, many others - LOH
  • LOH lead to excessive growth -> tumor
proto-oncogenes
Proto-oncogenes
  1. Normal geneto promote division
    • Bcl2, cyclin D1, EGFR
  2. Single mutation = gain of function
    • Excessive growth -> cancer (oncogene)
  3. In absence of GF no signal tranduced to nucleus
    • Oncogene = activation of pathway
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