exam 2 lecture 11 Flashcards

1
Q

mechanism for ligand-gated ion channel

A

first messenger ligand binds to channel function, channel opens to allow Na+, K+, Ca2+ to cross

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2
Q

the 2 domains in the channels and what they are

A

extracellular- bind to the first messenger ligand
transmembrane- the pore for ions to flow

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3
Q

mechanism for neural signaling through channels

A

neurotransmitter ligands released from excited presynaptic neuron into synaptic cleft, then binds to channel induced ion flow to cause postsynaptic siganl

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4
Q

first messenger examples

A

serotonin, GABA, nicotine, acetylcholine, glutamate, glycine

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5
Q

clinical relevance of ligand gated ion channels

A

involved in blood pressure regulation and cardiovascular disease

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6
Q

ligand gated ion channel example

A

nicotine acetylcholine receptor

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7
Q

mechanism for nicotine acetylcholine receptors

A

ace binds to extracellular LBD and causes channel to widen from 3-8 angstroms to have sodium flow and depolarize post-synaptic membrane

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8
Q

receptor tyrosine kinases are what type of receptors

A

enzyme linked

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9
Q

receptor tyrosine kinases mechanism

A

ligand binds and induced dimerization to active catalytic activity

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10
Q

the activated cytoplasmic domains on the receptor tyrosine kinases do what to form binding sites

A

they autophosphorylate, the phosphorylate themselves onto tyrosine

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11
Q

what are some examples of receptor tyrosine kinases

A

insulin, growth factor receptors

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12
Q

how do receptor tyrosine kinases terminate signaling

A

receptor internalization- the ligand dissociated and leads to the dimer going back to single form

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13
Q

what does dysfunction of receptor tyrosine kinases cause

A

cancer

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14
Q

besides receptor internalization, another way to terminate the signaling from receptor tyrosine kinases could be

A

protein phosphatase as part of a protein phosphorylation cycle

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15
Q

growth factor receptors bind what and initiate what

A

binds growth factor ligands and initiates the mitogen-activated protein kinase (MAP) cascade

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16
Q

mechanism of MAP kinase cascade

A

growth factor binds and phosphorylates activating Ras protein, then GTP Ras activates MAP3K which triggers cascade

17
Q

Ras mutations lead to what

A

cancer

18
Q

what are the 3 Ras genes

A

HRas, KRas, NRas

19
Q

what are the two parts of the Ras structure

A

hypervariable region-localized at membrane
Gdomains

20
Q

what are the subunits of the G domain in KRas

A

switch 1, switch 2, p-loop (mutation spot)

21
Q

KRas is active and inactive when

A

active when GTP bound
inactive when GDP bound

22
Q

Ras is activated how

A

by growth factors binding to RTK or by cell receptors

23
Q

T/F Ras binds SPECIFIC effectors and activates MULTIPLE pathways

A

TRUE

24
Q

Guanine nucleotide exchange factors (GEFs) do what

A

increase rate of GDP dissociation and slow hydrolysis to promote cancer

25
Q

what proteins hydrolyze activated Ras

A

GTPase-activating proteins GAPs

26
Q

KRas mutation effects

A

decrease GTPase activity, increased affinity for GTP, KRas always active

27
Q

G-protein-coupled-receptors (GPCRs) have how many regions

A

7 alpha helical transmembrane regions

28
Q

GPCRs signal through what

A

heterotrimeric G-proteins

29
Q

T/F transient association with an agonist bound GPCR increases GDP release from Galpha

A

True

30
Q

Which subunit of trimeric G protein should be similar in structure to the monomeric G protein

A

G alpha

31
Q

what are the three subunits of heterotrimeric GPCRs

A

G alpha, G beta, G gamma

32
Q

which subunit has GTPase activity

A

G alpha