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117 Cards in this Set
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- Back
- 3rd side (hint)
Function of Na+ channels
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generating and propagating action potentials in excitable cells
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function of K+ channels
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control of excitability and shaping of electrical signals
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Function of Ca++ channels
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neurotransmitter release, muscle contraction and intracellular signalling pathways
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hyperkalemic periodic paralysis
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an Na+ chanenelopathy revealed when extracellular K+ is raised. Channel doesn't inactivate properly and action potential can't develop.
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tetrodotoxin (TTX)
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neurotoxin that is highly specific blocker of voltage-gated Na+ channels. Leads to respiratory paralysis and is found in puffer fish
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local anesthetics- novacain, lidocain
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block voltage gated Na channels in axon and prevent conduction of nerve impulses
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Lamber-eaton Myasthenic Syndrome (LEMS)
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autoimmune disease that impairs calcium influx and reduces transmitter relase at neuromuscular junction resulting in muscle weakness
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None
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halothan
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anestheic that opens the leak K+ channels
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nifedipin and verapamil
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drugs used in the treatment of cardiovascular disease by blocking Ca++ channels
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3,4 Diaminopyridine
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drug used to treat LEMS by blocking K+ channel and prolongs the action potential
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acetylcholine receptors
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ligand gated channels at neuromuscular junction involved in excitatory neurotransmission
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glutamate receptors
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ligand gated channels at CA3-CA1 hippocampal synapse
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GABA receptors
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ligand gated channels at hippocampal synapses
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Nicotinic acetylcholine receptor
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ligand gated channel at neuromuscular junction that bind Ach and allows Na+ and K+ flux and induces depolarization which increases Ca++ and results in muscle contraction
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hyperpolarized
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a membrane potential which becomes more negative
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depolarized
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a membrane potential which becomes less negative
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acetylcholinesterase
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breaks Ach into acetate and choline and terminates signal
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congenital myasthenic syndrome
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this is a slow channel syndrome present at birth that is caused by mutations on Ach receptors causing weakness, rapid fatigue, and muscle atrophy
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D-Tubocurarine
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competetive inhibitor of Ach that causes paralysis and death by asphyxiation
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Vercoronium, Pancuronium, and Rocuronium
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synthetic chemicals that cause parlaysis by competitively inhibiting Ach receptors. Used in surgical procedures
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α bungarotoxin
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snake toxin that binds competetively and irreversibly to Ach receptors
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None
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Succinycholine
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Ach R agonist that binds and causes depolarization and is used as a muscle relaxant
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Nicotine
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Ach R agonist that binds at same sites as ACh and can cause muscle contraction
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Myasthenia Gravis
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autoimmune neuromuscular disease caused by the destruction of peripheral NACh receptors causing muscle weakness, movement defecit and fatigue
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Picrotoxin
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noncompetetive blocker of GABA
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Benzodiazapine
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anxiolytic drug that increases GABA activity and is used for anxiety disorders and insomnia
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Barbituates
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anticonvulsant and sedative drug that increases GABA activity. Used for epilepsy, anesthesia and anxiety
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Hormone response elements
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DNA sequences where steroid receptor complexes bind and regulate rate of transcription
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Gs
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G-protein that stimulates AC and activates protein kinase A
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Gi
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G-protein that inhibits AC and inhibits protein kinase A
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Gq
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G-protein that is coupled to Phospholipase C which increases DAG, and in turn IP3 and Ca++ and activates protein kinase C
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Cholera toxin
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bacterial toxin that stimulates Gs and causes and excess production of cAMP
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Pertussis Toxin
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bacterial toxin that inhibits Gi and causes excess cAMP
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None
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Sos
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guanine nucleotide exchange factor for Ras that is attracted by Grb2 in the signaling event of tyrosine kinase receptor
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GTPase activating proteint (GAP)
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hydrolyzes GTP and inactivates Ras
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Restriction Point
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the point in G1 when the cell cycle stops being GF dependent
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Oncogene
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a mutated protein of the cell cycle control system that is constituitively activated, Ras, myc, fos, jun
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Tumor supressor gene
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protein that inhibits cell cycle progression- Rb, p53
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Akt pathway
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signaling effect of neurotrophins binding to receptor tyrosine kinase that prevents cell death
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What passes K+ ions but not Na+ or Cl- ions?
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a potassium channel
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changing the cell potential from -80 to 0 mV opens a voltage gated K+ channel. When the channel opens K + ions will flow in which direction
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out of the cell
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a chef preparing puffer fish might find his lips becoming numb because
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tetrodotoxin in the fish inhibits Na+ channels
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If changing the cell potential from -80 to 0 mV opens a voltage gated Ca++ channel, calcium ions will flow in which direction?
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into the cell
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the voltage gated calcium channel pore is formed from:
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a single α subunit consisting of 4 repeated structural units each of which has 6 transmembrane domains
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Voltage gated calcium channels mediate what phase of the cardiac action potential?
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the plateau phase (phase 2)
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Nifedipine and Verapamil block what ion channels to treat cardiovascular disease?
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Calcium channels
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When recording single Na+ channel currents, why are openings only observed at the beginning of a voltage shift to 0 mV
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Na+ channels inactivate after they open.
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Acetylcholine-activated currents at the neuromuscular junction are terminated by
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acetylcholinesterase
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acetylcholine receptor ion channel is opened by
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acetylcholine
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what single channel property is altered in slow channel syndrome?
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open time is increased
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Vecuronium iss used to prepare a patient for surgery because
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It produces paralysis
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the binding of glutamate to NMDA receptors opens an ion channel that passes
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Na+, K+ and Ca++ ions
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why is NMDA current absent at hyperpolarized potentials?
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Mg++ enters the channel and blocks it
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If a cell's resting potential is -80 nV, but it is at -60 mV because of excitatory synaptic activity what happens if a GABA-mediated synaptic current occurs
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the membrane potential will hyperpolarize slightly (become more negative)
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GABA receptors are targets for
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barbituates
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what does ion specificity depend on
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pore size and strength of interaction with pore site
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what is the resting potential of an excitable cell? And are the channels open or closed?
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negative. Closed
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what is the nernst potential for K+
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-105 mV
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what will K+ normally do when the channel is opened?
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move out
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What is the nernst potential fo Na+
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61 mV
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What will Na+ normally do when the channel is opened?
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move in
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what are the 3 molecular configurations for ion channels
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heteromer, homomer, and a single polypeptide
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which channels mediate fast signalling
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ligand gated
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where are ligand gate channels found
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central and peripheral nervous systems
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what are ligand gate channels called
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ionotropic receptors
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3 major classes of Glutamate receptors
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Kainate, AMPA, and NMDA
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Which class of receptors have many coregulators
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NMDA Glutamate receptors
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Which class of receptors is rapid desensitization a characteristic of?
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AMPA Glutamate receptors
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When is NMDA current absent
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at hyperpolarized potentials
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Which Glu receptor allows Calcium to pass?
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NMDA Glutamate receptors
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What inhibits NMDA
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zinc
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Examples of blockers of Glutamate receptors
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NBQX, D-AP5. D-AP 7, ketamine, PCP, MK 801
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What is the main inhibitory neurotransmitter in the CNS
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GABA
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What kind of channel are GABA- receptors?
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Chloride
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What does GABA receptor openings cause to membrane potential?
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hyperpolarization
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What do GABA receptors have binding sites for
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barbituates, benzodiazepines, and potentiators
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Steroids bind to…
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intracellular receptors that affect gene transcription
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None
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G-protein coupled receptors are made up of
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a single subunit with 7 transmembrane domains
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Gq is a heterotrimeric G protein that couples to
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phospholipase C. It stimulates PLC, increases DAG, increases IP3, increases intracellular calcium and activates PKC
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Once cAMP is generated its signaling effects are terminated rapidly because it is destroyed by …
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phosphodiesterase
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IP3 receptors are primarily located …
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in the membrane of the ER
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Albuterol, a bronchodilator used to treat asthma, acts at what G-protein coupled receptor
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beta adrenergic receptor, as an agonist
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Cholera toxin kills by dehydrating the body through massive diarrhea and vomiting. It does this by attacking the cells of the uppers section of the small intestine and…
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stimulating Gs, causing an excess production of cAMP
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Ligand binding to receptors eventually leads to loss of receptors. This is mediated by what process?
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phosphorylation of GRK, binding of β-arrestin to the phosphorylated sites, and recruitment of β-arrestin of endocytosis proteins such as clathrin
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The insulin receptor is a
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tyrosine kinase receptor
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the unliganded epidermal growth factor tyrosine kinase receptor is made of a
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a single subunit with 1 transmembrane domain
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Activation of Ras leads to the following cascade
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activation of Raf, phosphorylation and activation of MAP kinase kinase, phosphorylation and activation of MAP kinase
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Growth factor binding to tyrosine kinase receptors stimulates progression of the cell cycle at what stage
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G1
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The primary cyclin that responds to growth factor stimulation is
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Cyclin D
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PI3 kinase catalyzes
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phosphorylation of PIP2 to form PIP3
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What are the 4 major receptor signalling classes?
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steroid, g-protein coupled, receptor tyrosine kinases and guanylate cyclase nitric oxide signaling
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Family I steroid receptor signaling
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steroid enters the PM, binds to receptor and releases heat shock proteins, enter the nucleus and binds to DNA as dimer to up or downregulate transcription of mRNA
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Family II steroid receptor signaling
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steroids enters the PM, enters the nucleus and binds to receptor, complex binds to DNA as hetero or homo-dimer to up or downregulate transcription
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None
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What facilitate the binding of steroid receptors to DNA sequences?
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zinc finger
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Steroid-steroid receptor examples
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androgens and vitamin D
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What do androgens regulate?
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male sexual differentiation and pubertal changes
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where can HREs of androgens be found
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in laryngeal myosin, prostate specific antigen
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What can agonists of androgens treat?
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hypogonadism
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what do antagonists of androgens treat?
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prostate cancer
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What does Vitamin D regulate?
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bone mineralization, Ca++ and PO4 homeostatis
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What causes rickets
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a deficiency in vitamin D
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Where are vitamin d HRE's?
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calbindin
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What does the binding of a ligand to G-protein couple receptor do?
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facilitates the exchange of GTP for GDP and the α and βγ to dissociate
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How is a G-protein couple receptor signal terminated
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GTP is hydrolyzed to GDP and the α subunit dissociates
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How do cells respond to persistent stimulation by a drug?
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by decreasing the number of receptors available to respond to a drug
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3 steps of developing tolerance
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desensitization, internalization and down regulation
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What does the binding of a ligand to a receptor tyrosine kinase cause?
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dimerization
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What is the binding site for Grb2
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the P-tyrosines of the receptor tyrosine kinase
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How does GTP-Ras stimulate the MAP kinase cascade?
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interacting with Raf kinase (Map kinase kinase kinase)
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What does MAP kinase lead to?
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early gene transcription and eventual activation of cyclins to stimulate cell division
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What happens to cells deprived of Growth Factor
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arrest at G0
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Growth factors effect on cyclin D
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1) induce transcription 2) stabilize 3) promote translocation to nucleus 4) promote assembly with Cdk 4 and 6
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dephosphorylated Retinoblastoma protein
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binds regulatory protein that favor proliferation
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phosphorylated Rb
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releases proteins so the cell proliferate
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What causes unregulated proliferation
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expression of oncogene, loss of tumor supressor gene, Growth factors always activated
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Functions of neurotrophin
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stimulate axonal and dendritic outgrowth and synapse formation; potentiates synaptic function; and promotes cell migration
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Where do neurotrophins bind
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receptor tyrosine kinases, with 3 signaling effects
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