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28 Cards in this Set

  • Front
  • Back
major differences between apoptosis and necrosis
apoptosis- chromatin condense, membrane blebbing, engulfed by nearby cells, clean
necrosis- cell swells, inflammation, messy
Biochemical processes of apoptosis
acidification, DNA degraded, proteolysis, phosphatidylserine flipped out to face ECM
TUNEL staining
stains nuclei that have DNA that have undergone strand breaks
which gene are caspases related to
CED-3 gene
3 major duties of caspases
inactivate survival proteins, activate pro-apoptotic proteins, dismantle cytoskeleton
Describe extrinsic death receptor activation
TNF-alpha ligand binds to receptor with death domain-->trimerization-->FADD adapter-->proCasp gather and activate each other
Describe intrinsic death receptor activation
Bcl-2 promote/inhibit release of cytC--> with Apaf-1 form apoptosome--> proCasp activate each other
Describe activity of some survival proteins
Bcl-2 prevents release of cyt C
inhibition of apoptosome formation
FLIP competitive inhibitor for death domain
Inhibit active caspases
partition coefficient (in relation to solute/solvents)
ratio of concentration of compound in 2 immiscible solvents at equilibrium
carriers are either transporters or active carriers- describe the two
transporters bind solute, undergo conformation change, solute goes down gradient
active carriers either couple down gradient with up gradient process or use ATP
Na-K-Cl cotransporter (NKCC)- what does it do and where is it?
1 Na+, 1 K+, 2Cl- all in same direction, kidney
Na/K pump- what does it do, how does it work
sends 3 Na+ out of the cell when phosphorylated, brings 2 K+ into the cell when dephosphorylated
Nernst equation
membrane potential = (RT/zF)*ln([x]1/[x]2)
What is a membrane's Nernst potential?
equilibrium when electrostatic forces and osmotic forces are balanced (requires energy to keep actual potential different from membrane potential)
Goldman-Hodgkin-Katz equation- what does it give you?
It determines the membrane potential for any cell
inactivation versus deactivation of ion channels
sodium channels are inactivated when "ball" sterically blocks opening of channel
potassium channels are deactivated once the stimulus is removed
Ionotropic vs metabotropic ligand-gated channels
ionotropic- ligand binding provides energy for conformational change
metabotropic- middle step present between binding and channel opening (e.g. G protein)
% of voltage-gated channels open relative to membrane potential
Boltzmann distribution
Describe shunting inhibition relative to "leaky" channels
with more channels open, resistance across membrane drops, leading to smaller voltage change and shorter duration of spike
General anesthetics- idea about mechanism
KNCK K+ channels mediate activity in thalamocortical neurons involved in rest/sleep
Difference between action of benzo and barbiturates on GABAa receptor
benzo- increases probability of channel opening
barbiturates- prolong channel open time
Pathogenesis of long QT syndrome
genes or medication- KCNQ channel disrupted- reduces rate of repolarization
Pathogenesis of epilepsy (one example)
slow inactivation of sodium channels
Describe function of intermediate filaments keratin and lamin
Keratin: protects against tissue splicing
Lamin: protects integrity of nucleus
What do MAPS and +TIPS do?
MAPS stabilize MTs and connect them to capping proteins
+TIPs bind to + end of MTs, anchor MTs to targets (part of search and capture)
Describe actin's role in cell crawling and polarity
ARP complexes generate actin polymerization network that pushes cell forward
actin network directs flow of organelles, vesicles around cell
cilia power stroke relies of activity of which MT motor?
dyneins
Phalloidin/Cytochalasin,
taxol/monastrol- what do they do?
stabilize/destabilize actin/MTs, respectively