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