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68 Cards in this Set

  • Front
  • Back
How does actin polymerize?
-at the barbed end ATP actin is added and hydrolyzed immediately
-70 s later the Pi is released
-depolymerization takes place at the pointed end
What are Arp 2 and 3 for?
They mimic an actin dimer, and when they bind actin, filament elongation is accelerated because the rate-limiting step (getting to the stable nucleus) is overcome.
What are WASPs (or NPFs) for?
They activate Arps.
What is Wiskott-Aldrich Syndrome?
-deficiency in WASPs (necessary for platelet formation and leukocyte migration)
-recurrent infections
What are the homologs of WASP?
-N-WASP (ubiquitous)
-Wave/Scar-1 (ubiquitous, but highest in brain)
-Wave-2 (widely expressed, especially in peripheral blood lymphocytes)
-Wave-3 (mainly in brain)
What is ActA?
A WASP homolog that some bacteria use to hijack the host skeleton.
What do RhoA-GTPases do?
-non-muscle myosins
-actin filament stabilizing proteins
What are the main members of the RhoA-GTPase family?
Which bacterial toxins target RhoA-GTPases?
-Salmonella: SopE, Sop E2 (activate RhoA-GTPases)
-Clostridium: C3 toxin (ADP ribosylates RhoA-GTPases, inactivating)
-Clostridium: cytotoxin (glycosylates RhoA-GTPases, inactivating)
What structures are formed by actin assembly?
-lamellipodia (cell migration)
-filipodia (sense direction)
-stress fibers/cellular cortex (contractile and deformation abilities)
-microvilli (surface area)
What is villin?
An actin binding protein that links filaments in microvilli. For tightly packed bundles.
What is fimbrin?
An actin binding protein that is enriched in filipodia. For tightly packed bundles.
What is α-actinin?
An actin binding protein that is enriched in stress fibers. For loosely packed bundles.
What is spectrin?
An actin binding protein that forms meshwork in erythrocytes, allowing them to deform. For loosely packed bundles.
What is filamen?
An actin binding protein that is enriched in lamellipodia. For loosely packed bundles.
What is spherocytosis?
Abnormal spectrin → spherical red blood cells
What is focal segmental glomerulosclerosis?
-renal insufficiency disease
-podocyte (a kidney cell) has defective α-actinin which binds actin too tightly
-reduced filipodia extensions
Which actin binding proteins prevent random polymerization?
-Cap Z (caps barbed ends)
-gelsolin, cofilin (severs existing filaments)
-profilin, thymosin (sequester monomers)
How is uncontrolled actin depolymerization prevented?
-pointed end capping proteins (e.g. tropomodulin)
-barbed end capping proteins
How are kinesin, myosin, microtubules, and microfilaments involved in vesicular trafficking?
-kinesin bound cargo is trafficked on microtubules
-then handed off to myosin to travel on microfilaments
What is the purpose of using drugs that stabilize microtubules?
-will not inhibit transport
-blocks cell division
What are the other cellular sources of energy besides ATP?
-creatine phosphate
-acetyl phosphate
What are the products of glycolysis? (starting with 1 glucose)
-2 ATP
-2 pyruvates
What are the products of the citric acid cycle? (starting with 2 acetyl CoA)
-1 GTP
-1 FADH2
What each produced in each turn of the fatty acid cycle? (using 2 carbons)
-1 acetyl CoA
-1 FADH2
What processes occur in the matrix of the mitochondria?
-citric acid cycle
-fatty acid oxidation
What processes occur across the mitochondrial inner membrane?
-electron transport oxidation reactions
-ATP synthesis
-metabolite transport
What processes occur across the mitochondrial outer membrane?
molecules less than 5 kD cross freely
What processes occur in the intermembrane space of mitochondria?
-phosphorylation of nucleotides other than ATP
-FA conversion to FA-CoA
What is the difference between mitochondria with plate-like cristae and those with tubular cristae?
Platelike: ATP production, with cytochromes, dehydrogenases, flavoproteins, ATP synthase
Tubular: steroid production, with steroid synthesizing enzymes
What does it mean if the cristae are condensed?
active ATP production
Why is cardiolipin important?
-4 fatty acid lipid
-makes up high proportion of mitochondrial inner membrane
-makes membrane less permeable to ions
How many electrons are released with the conversion of NADH to NAD+?
What is the electron transport chain?
NADH → NADH dehydrogenase complex → ubiquinone → cytochrome b-c1 complex → cytochrome c → cytochrome oxidase complex → O2
How does ATP synthase work?
-F0 (10-14 membrane proteins) is in the membrane, it rotates 120°
-F1 is in the matrix, catalyzes ADP + Pi = ATP
-3 ATP per 360° rotation, requires 12 protons
What transporters are in the inner membrane?
-ATP/ADP antiporter (ATP out, ADP + Pi in)
-Pi/OH antiporter
-pyruvate/OH antiporter
What is different and similar in the energy utilized during sprinting vs. slow running?
-phosphocreatine → creatine
-muscle glycogen → lactate
Slow running:
-muscle glycogen → lactate
-glucose, fatty acids, ketone bodies → CO2 + H2O
What stimulates and inhibits AMPK? What does it do?
Stimulate: AMP
Inhibit: ATP
It blocks ATP consumption and stimulates catabolism.
How does oligomycin work?
-blocks H+ channel
How does dinitrophenol work?
-proton ionophore
-uncouples metabolism from ATP production
-produces heat
How does cyanide work?
blocks cytochrome oxidase → blocks oxidative phosphorylation
How does rotenone work?
-blocks electron transport
How does antimycin work?
-anti-fungal agent
-blocks proton pump
How may defects in oxidative phosphorylation explain insulin resistance?
-fat accumulation in muscle cells interferes with insulin action
-decreased insulin stimulated glucose uptake, decreased glycogen synthesis
-insulin secretion is regulated in part by ATP
What is the lag time between discovery between efficacious forms of treatment and their incorporation into patient care?
15-20 years
What are the three key elements of evidence-based medicine?
-clinical expertise
-research evidence
-patient preferences
What are the four fundamental skills of evidence-based medicine?
-ask a clinically relevant question
-acquire the best available evidence
-appraise the evidence
-apply the evidence to patient care
What are foreground questions? What are the 3-4 essential components?
-asks for specific knowledge about a disorder
-comparison (if relevant)
What are examples of "synopses" sources?
-ACP Journal Club
-Clinical evidence
What are examples of "syntheses" sources?
-Cochrane library
-Specialty websites
What are examples of "studies" sources?
-National Library of Medicine
What are Levels I, II, and III of evidence?
Level I: randomized controlled trials
Level II: non-randomized trials, observational, case-control
Level III: expert opinion
In which organs and under which conditions do cells experience large external osmotic challenges?
-upper GI tract
-renal medulla
-diabetes mellitus
What is the difference between acute and long term volume regulation?
Acute: ion transporter activation
Long term: osmolyte alteration
What type of junction separates the cell into apical and basolateral domains?
tight junction
What are the membrane equivalents to an electric circuit?
-ion channel = resistor
-membrane potential = battery
-lipid bilayer = capacitor
How is the time constant of the electrotonic potential calculated?
Rm (resistance) x Cm (conductance)
What is the time constant of the electrotonic potential?
the amount of time needed for the potential to reach 63% of the maximum
How is the space constant of the electrotonic potential calculated?
(d x Rm / Ri)^(1/2)
d = axon diameter
Rm = membrane resistance
Ri = internal resistance
What is the space constant of the electrotonic potential?
The distance that the potential has traveled when it is reduced in amplitude by 63%.
How does glucose uptake trigger insulin release in β-cells of the pancreas?
-glucose is converted to ATP by mitochondria
-ATP closes a K+ channel which prevents K+ from leaving the cell
-membrane slowly depolarizes (becomes less negative inside)
-opens a voltage-gated Ca2+ channel
-insulin release is triggered
What happens to the action potential if extracellular [Na+] is decreased?
-action potential starts more slowly
-amplitude is smaller
What type of information is encoded by an electrotonic potential?
What type of information is encoded by an action potential?
What is the general structure of the acetylcholine receptor? How does binding of acetylcholine change the structure?
A pentamer with 2 α subunits, a β, a γ, and a δ subunit. There is a pore which is blocked by Leu side chains of M2 helices. Binding of acetylcholine causes twisting of M2 helices so that the channel opens.
Why can't Na+ pass through the K+ channel?
Na+ is smaller, so it binds water more tightly. It is difficult for Na+ to lose enough water molecules to fit in the channel.
How does intracellular [Ca2+] affect the slow after-hyperpolarization?
as [Ca2+] increases, the time of the after-hyperpolarization also increases
What is the difference between the after-hyperpolarization caused by voltage-dependent delayed rectifier (A-type) K+ channels and the Ca2+ dependent K+ channels?
A type: fast AHP
Ca2+ dependent: slow AHP