Cell Biology Exam 2

Src was used as a protein to report the effect of stretch on signaling through adhesions. How was this done?
A. The serine phosphorylation of Src was shown to increase with stretch
B. FRET between the the terminal portions of Src containing two different fluorescent proteins was shown to change.
C. Src was shown to become tyrosine phosphorylated upon stretch
D. Signaling through Src was not affected by stretch
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Src was used as a protein to report the effect of stretch on signaling through adhesions. How was this done?
A. The serine phosphorylation of Src was shown to increase with stretch
B. FRET between the the terminal portions of Src containing two different fluorescent proteins was shown to change.
C. Src was shown to become tyrosine phosphorylated upon stretch
D. Signaling through Src was not affected by stretch
FRET between the the terminal portions of Src containing two different fluorescent proteins was shown to change.
Which of the following WOULD be expected when the PDGF binds to PDGF receptors (Receptor Tyrosine Kinase type)?
A. A change in conformation takes place on the cytoplasmic portion of the receptor
B. Receptors cross phosphorylate each other on serine residues
C. Proteins with SH3 domains will bind to the receptor phosphotyrosines D. A small monomeric G protein will be activated
D. A small monomeric G protein will be activated
In which way does signaling through integrins differ from RTKs.
A. Activation of Src
B. Activation of PLCgamma C. Activation of Ras
D. Activation of PI-3 kinase
A. Activation of Src
10. In signaling through receptor tyrosine kinases, what is the specific role of SOS?
A. It binds to and activates MEK
B. It acts as a GEF for Ras.
C. It causes MAP kinase to move into the nucleus
D. It recruits GRB2 to the receptor
B. It acts as a GEF for Ras.
Which of the following would be unlikely candidate for being a protooncogene? A. A mutated constitutively active Ras
B. A mutated constitutively active protein kinase A
C. A mutated and constitutively active Raf
D. A mutated and constitutively active MAP kinase
B. A mutated constitutively active protein kinase A
Which of the following is NOT an action of calcium we have seen
A. Activation of synaptotagmin in nerve terminals
B. Smooth muscle contraction
C. G protein activation
D. Activation of calcineurin.
C. G protein activation
Which of the following about cyclic AMP (cAMP) is NOT ture?
A. Has the same effect in every cell.
B. Normally activates PKA
C. Can increase due to activity of adenylyl cyclase D. Has similar effects in smooth muscle to that of cGMP
A. Has the same effect in every cell.
Which is NOT related to blocking apoptosis due to RTK signaling
A. AKT
B. PI-3 Kinase
C. PLC-gamma
D. FOXO
C. PLC-gamma
Which is the correct sequence of the ras pathway A. Ras => SOS=>Raf=>MEK=>MAP kinase=>Jun
B. SOS => Ras=>Raf=>MEK=>MAP kinase=>Jun
C. SOS => Raf=>Ras=>MEK=>MAP kinase=>Jun
D. SOS => Ras=>MEK=>Raf=>MAP kinase=>Jun
B. SOS => Ras=>Raf=>MEK=>MAP kinase=>Jun
Which is NOT a property of Cadherin-based junctions
A. The basis for cells of particular tissues binding to each other
B. Link actin to fibronectin
C. Tissue movements based contraction of the adherens junction
D. Formation of desmosomes
B. Link actin to fibronectin
Uncoupling of mitochondria would do all the following except A. Make the matrix more acidic B. Make the membrane potential go more positive C. Increase the amount of ATP production D. Increase the amount of oxygen utilizationC. Increase the amount of ATP productionWhich is NOT true concerning conduction A. Propagation is faster than passive spread of depolarization B. Potassium ions carry the depolarization along the inside of the membrane C. Conduction is sped up by myelination which reduces capacitance D. Passive spread is limited to short distances because potassium is permeableA. Propagation is faster than passive spread of depolarizationIn tryosine kinase receptors which IS true A. Mutation of a single receptor gene is typically enough to cause cancer B. The receptor can activate via phosphorylation of its own tyrosines or by being phosphorylated by a neighboring (dimerized) receptor C. Multiple signaling pathways are initiated from a single receptor. D. The most dangerous and difficult to deal with mutation in the signaling pathway would be one that results in a constitutively active receptor.D. The most dangerous and difficult to deal with mutation in the signaling pathway would be one that results in a constitutively active receptor.In secretion at the nerve terminal, which is NOT true A. Vesicles are bound to the target membrane by SNARES B. NSF forces the vesicle to fuse with the target membrane C. Secretion is regulated by calcium D. The last step in the fusion of secretory vesicles depends on synaptotagminB. NSF forces the vesicle to fuse with the target membraneWhich of the following is NOT a component of or feature of apoptosis A. DNA ladders B. Endo G in the nucleus C. Inactivation of caspases D. SMAC/Diablo in the cytoplasmC. Inactivation of caspasesWhich is NOT true of integrin bases adhesions A. They exibit bidirectional signaling B. They are associated with a circular band of actin surrounding the cell C. Throught their association with actin they transmit stress from stress fibers through the membrane to components of the basal lamina or other adhesions. D. They are present in focal adhesionsB. They are associated with a circular band of actin surrounding the cellWhich of the following is NOT true of the threshold potential A. It is the threshold between no sodium channels opening and all sodium channels opening B. In resting cells it is a function of potassium leak channels C. Depolarizations below the threshold potential are normally opposed by potassium efflux. D. It depends or varies with the density of sodium channels.A. It is the threshold between no sodium channels opening and all sodium channels openingFor production of ATP in the mitochondria all of the following occur EXCEPT - A. Oxygen is reduced to water in complex 4 B. 2 carbon acetate units are oxidized to CO2 in the citric acid cycle C. FADH2 donates electrons to complex 1 D. Protons are pumped by complexes I, III and IV.C. FADH2 donates electrons to complex 1In signaling through cadherin based junctions which is NOT true? A. Mutation of APC is a step towards colon cancer. B. Beta catenin is freed up when adhesions are lost C. Free beta catenin is normally ubiquitinated D. Adherens junction are associated with intermediate filamentsD. Adherens junction are associated with intermediate filamentsThe Goldman equation weighs the Nernstian value of each ion gradient by the permeability of the membrane to each ion. A. True B. FalseTrueMalignant cells are those that can escape the basal lamina A. True B. FalseTrueExperiments shown in class support the idea that cell survival depends only on how many integrins are engaged with fibronectin. A. True B. FalseFalseVertebrates primarily speed up conduction along their nerve cells through high diameter axons A. True B. FalseFalseWhen released from the mitochondria ubiquinone is important in triggering apoptosis. A. True B. FalseFalseA tensegrity structure is a method for making a rigid structure with the least amount of building materials. A. True B. FalseTrueOpening Chloride channels is a form of excitatory stimulus in a post-synaptic cell. A. True B. FalseFalseAn action potential at a synapse in the presynaptic cell always leads to an action potential in the post synaptic cell A. True B. FalseFalseCaffeine affects cells in a way that is similar to activating b-adrenergic receptors. A True B. FalseTrueCholera toxin works by preventing the Gs alpha subunit from hydrolyzing GTP A. True B. FalseTrueGive two different ways that phosphatidyl inositol lipids are used in signalingPhosphatidyl Inositol can be phosphorylated, ie PI3K can phosphorylate PIP2 into PIP3, which can be bound by proteins with PH domains. Phosphotidyl Inositol 4,5 bisphosphate can be cleaved into different signaling molecules, ie PLC can cleave PIP2 into IP3 and DAG.Describe an assay that could show that a cell underwent apoptosisTUNEL assay. The assay adds fluorophores to the free ends of DNA. In an apoptotic cell, with lots of free ends on fragmented strands of DNA, you see fluorescence.Concerning proton motive force... How is it generatedETC pumping protons across the inner membrane.Concerning proton motive force... Two components of PMFpH and electrical gradientConcerning proton motive force... using the _________ equation you can convert the _______ component of PMF to __________ (number)1. Nernst 2. pH 3. -60 mVUsing antibodies, how could you show that RTKs activate by clustering?Whole antibodies (which bind to RTKs) can activate RTKs while antibody fragments (Fabs) do not. Adding a second crosslinking antibody to the Fabs will activate the receptors.How could FRET be used as a tool to measure the levels of cAMP in the cell? (3 points)PKA becomes activated with elevated levels of cAMP. You could attach a FRET pair to the regulatory and catalytic subunits of PKA. When cAMP levels are low you see FRET. When cAMP levels are high you do not see FRET.Explain the steps beween signaling through the alpha adrenergic receptor and the effect on smooth muscleAlpha Adrenergic Receptor -> Gq -> PLCbeta -> IP3 -> Ca influx -> CAM -> MLCK -> Myosin Light Chain -> Muscle Contraction in smooth muscle.Explain why activation of cell growth through RTKs requires activation of a survival pathway. Include in your answer the molecular components involved in this survival signalTo ensure that there is an authentic signal coming from the receptor by requiring multiple pathways to fire off simultaneously. Pathways in RTKs can often trigger both growth and apoptosis. Eg MAPK phosphorylates FOXO, sending it to the nucleus and leading to apoptosis. A survival pathway is required to counteract that. Eg, Akt phosphorylates FOXO to keep it in the cytoplasm which blocks apoptosis.Two classes of caspasesInitiator and ExecutionerHow are caspases activated?1) Being clustered and autoactivated 2) Being cleaved by another caspaseProteins involved in apoptosisBAK and BAXWhat do BAK and BAX (apoptosis proteins) doForm a pore in outer membraneTrigger to start BAK and BAX in apoptosisDNA damage, free radicals, UV, high calciumWhat does Tunel Assay show in apoptosisCleavage of DNA into fragmentsDeath receptors and cytochrome C have what similar effectBoth cluster caspases to activateHow are cytochrome C and ubiquinone similar and different?Similar: Shuttle electrons between complexes Different: Ubiquinone is 1, 2 and 3 while cytochrome C is between 3 and 4Which is worth more in ATP: NADH or FADH2NADH since FADH2 enters after the first proton pumping stepWhat gets oxidized and reduced in MitochondriaCarbon compounds get oxidized and oxygen gets reducedWhat happens to matrix because of electron transport systempH becomes basic, develops a negative membrane potentialNernst equation is used for whatConverting pH gradient into mVWhat is required for adherent cells to surviveCells must attach, spread, and be under tensionFibronectin links ______________ to ______________Integrins to basal laminaHow are signalling through integrins similar to signalling through RTKsBoth activate RAS pathway, and activate PI-3 Kinase pathwayHow is Cadherens related to tissue formationCadherens show homotypic adhesion, will bind if show same cadherinWhat activates the RAS signaling pathwaySOS as a GEF for RASWhat pathway leads to growthRasGTP -> Raf1 -> Mek -> MAP Kinase -> Jun + Fod -> AP1How does receptor activation lead to calcium elevationReceptor activates phospholipase C which activates IP3 which opens calcium channels in the EREffects of calcium elevationCan activate calcineurin which then lets MFAT into nucleus It activates transcription of Fos which is part of AP1Difference between protooncogene and OncogeneA protooncogene is a normal cellular protein involved in growth control. When mutated a protooncogene can become an oncogene that drives tumor formation.Enzyme involved in smooth muscle contraction regulationMyosin light chain kinaseWhat does Myosin Light Chain Kinase doPhosphorylates myosin regulatory light chainsWhat G protein is involved in stimulation of beta adrenergic receptorsGsWhat does the protein Gs doActivates Adenylyl cyclaseWhat secondary messenger is involved in the stimulation of beta adrenergic receptorscAMPWhat does cAMP do to affect smooth muscleActivates pKa and phosphorylates MLCK causing inhibitionWhat G protein is involved in stimulation of alpha adrenergic receptorsGqWhat does the protein Gq do?Activates phospholipase CWhat secondary messengers are involved in stimulation of alpha adrenergic receptorsIP3 and calciumWhat do IP3 and calcium do to affect smooth muscleCalcium binds to calmodulin to activate myosin light chain kinaseHow to speed up conductionIncreased axion diameters radius resulting in lower axial resistance Myelination which reduces capacitanceinhibitory neurotransmitterseither open K+ or CL- channels. Opening K+ channels makes the potential go more negative and raises the threshold. Opening chloride channels makes it easier for chloride entry to nullify sodium entry.What is the Hodgkin cycle?the relationship between a stimulus, opening sodium channels, sodium influx and membrane depolarization. a positive feedback loop because each step in the cycle promotes or facilitates the next step in a continuous loop.Why do action potentials start at the axon hillock and not other parts of the neuron such as dendrites or soma?The axon hillock has a much larger density of voltage gated sodium channels than on the cell body or dendrites. Therefore and depolarization will reach threshold first at the axon hillock.the relationship between the potassium ion concentrations inside versus outside to the chloride concentration inside versus outside[K]in / [K]out = [Cl]out / [Cl]inHow does the Nernst equation and the Goldman equation differ?The Nernst equation gives the maximum potential that could develop for a given ion gradient assuming that there is only only ion permeable and we are at equilibrium. The Goldman equation determines the real membrane potential of the cell by weighing the contribution of each ion gradient based on the permeability of that ionHow does the potassium channel lets potassium ions through but not sodium ionsIn order for ions to go through they must lose their bound water molecules. In order to do this the channel must provide a binding site that is equivalent to having the bound water molecules. Sodium ions without its bound water is much smaller than potassium and does not fit well in the channel binding site.