Functions of Channels and Transporters Flashcards
how do ion channels differ from aqueous pores? (2)
ion channels show ion selectivity
ion channels are not continuously open
how many different types of ion channels are there?
more than 100
in what types of cells are ion channels found? (3)
animal cells
plant cells
microorganisms
ion channel: K+ leak channel
typical location:
function:
plasma membrane of most animal cells
maintenance of resting membrane potential
ion channel: voltage gated Na+ channel
typical location:
function:
plasma membrane of nerve axon
generation of axon potentials
ion channel: voltage gated K+ channel
typical location:
function:
plasma membrane of nerve cell axon
return of membrane to resting potential after initiation of action potential
ion channel: voltage gated Ca2+ channel
typical location:
function:
plasma membrane of nerve terminal
stimulation of neurotransmitter release
ion channel: Ach receptor (ach-gated Na+ and Ca2+ channel)
typical location:
function:
plasma membrane of muscle cell (at neuromuscular junction)
excitatory synaptic signaling
ion channel: GABA receptor (GABA gated Cl- channel)
typical location:
function:
plasma membrane of many neurons (synapses)
inhibitory synaptic signaling
ion channel: stress-activated cation channel
typical location:
function:
auditory hair cell in inner ear
detection of sound vibrations
a small flow of ions carries sufficient charge to cause a large change in the
membrane potential
the ions that give rise to the membrane potential lie in a thin, less than – nm, surface layer close to the membrane
1 nm
the ions that give rise to the membrane potential are held there by their — on either side of the membrane
counterions
for typical cell, 1 microcoulomb of charge (6x10^12 monovalent ions) per square centimeter of membrane, transferred from one side of the membrane to the other, changes the membrane potential by roughly
1V
for example, that in a spherical cell of diameter 10 um, the number of K+ ions that have to flow out to alter the membrane potential by 100 mV is only about 1/100,000 of the total number of
k+ ions in the cytosol
as k+ leaks out through leak channels, it leaves behind a
negative charge known as membrane potential
when is the membrane potential at zero?
when there is an exact balance of charges on each side of the membrane so that each positive ion is balanced by a negative counterion
when is there a nonzero membrane potential?
when a few of the positive ions cross the membrane from right to left, leaving their negative counterions behind
electrochemical gradients are measured by the charge on the
inside of the membrane
the Na+K+ ATPase pump helps maintain — — across the cell membrane
osmotic balance
the Na+ concentration inside the cell is
low
Na+K+ pumps – into the cell
K+
the plasma membrane also has K+ leak channels, which allow
K+ to move freely in and out of the cell
foe every molecule of ATP hydrolyzed inside the cell, the pump moves
3 Na+ out
2 K+ in
ouabain
inhibitor of the Na+K+ ATPase
binds to the extracellular domain of the ATPase so K+ cant bind
ouabain and K+ compete for
the same site on the extracellular side of the pump
because of the leak channels, K+ comes almost to
equilibrium
how does K+ come to almost equilibrium?
the electrical force exerted by the excess of negative charges attracting K+ into the cell is balanced by the tendency of K+ to leak out through the leak channels down its concentration gradient
suppose there is no voltage gradient across the plasma membrane. the high intracellular concentration of K+ will cause it to flow out of the cell through the leak channels. as K+ moves out, this leaves behind an unbalanced negative charge creating a membrane potential. once the membrane potential reaches a certain point, K+ will
no longer move out of the cell
the equilibrium condition defines the
resting membrane potential
resting membrane potential is about
-70 mV
which equation can we use to calculate the resting membrane potential?
the nerst equation
for the nerst equation, we much know the ratio of
internal and external ion concentrations
the nerst equation is dependent on the
inside and outside concentrations of the ion
voltage gated channels open and close based on
changes in membrane potential
ligand-ligand (extracellular and intracellular ligand) channels open and close based on
the binding of a particular molecule to the binding site of the channel
stress activated channels open and close based on
physical force
ex. hair cells involved in hearing because of the movement of sound waves through the channel
what is the axon length?
less than 1 mm to more than 1 m
an action potential is triggered by a brief pulse of current, which
depolarizes the membrane
the membrane cannot fire a second action potential until the Na+ channels have
returned to the closed conformation
until then, the membrane is refractory to stimulation
an action potential can only travel away from the site of depolarization because
Na+ channel inactivation prevents the depolarization from spreading backward
on myelinated axons, clusters of Na+ channels can be —- apart from each other
millimeters
when the membrane potential is depolarized, the channel opens and begins to conduct ions. if the depolarization is maintained, the open channel adopts an — conformation
inactive
inactive conformation
the pore is occluded by the N-terminal 20 amino acid “ball” which is linked to the channel proper by a segment of unfolded polypeptide chain that serves as the “chain”
when an action potential reaches the nerve terminal in the presynaptic cell, it stimulates the terminal to release its
neurotransmitter
the neurotransmitter molecules are contained in synaptic vesicles and are released to the cell exterior when the vesicles fuse with the — — of the nerve terminal
plasma membrane
the released neurotransmitter binds to and opens the transmitter-gated ion channels concentrated in the plasma membrane of the postsynaptic target cell at the
synapse
the resulting ion flows alter the — — of the target cell, thereby transmitting a signal from the excited nerve
membrane potential
cystic fibrosis
mutations in CFTR gene which is a chloride channel
hereditary disease of ion channels and carrier proteins mentioned in class
cystic fibrosis
tetrodotoxin blocks
sodium channels
saxitoxin blocks
voltage gated sodium channels
lidocaine and novocaine anesthetics block
sodium ion channels
used in extracting teeth, fillings, etc
iberiotoxin (eastern indian scorpion) blocks
potassium channels
heteropodatoxin (brown spider) blocks
potassium channels
— is produced by puffer fish, which are prepared and served in Japan
tetrodotoxin
antiepileptic drugs target molecules of the
excitatory synapse
ABC transporters
ATP-binding cassette
ABC transporters are a superfamily of — membrane proteins
integral
what are ABC transporters responsible for?
ATP-powered translocation of molecules such as sugars, amino acids, lipids, ions, polysaccharides, peptides, proteins, toxins, drugs, antibiotics, xenobiotics, and other metabolites
what are the 4 ABC transporter domains?
2 hydrophobic
2 ATP binding
when is the interface between ATP-binding domains closed? when is it open?
closed: when ATP is bound
open: when ATP is hydrolyzed
instances of ABC transporters of clinical importance? (3)
- cause of drug resistance which develops in many human cancers
- mutations in ABC chloride carrier is a cause of cystic fibrosis
- cause of drug resistance, which frequently develops in malaria parasite
— of secretory vesicles is another mechanism to get material (proteins) across a lipid bilayer membrane which are unable to pass through the bilayer directly themselves
exocytosis
receptor mediated endocytosis from class
LDL binds to the LDL receptor which leads to the clustering of clathrin to form a clathrin coated vesicle through endocytosis.
the vesicle is uncoated of clathrin
the vesicle fuses with an endosome
the endosome fuses with a lysosome
cholesterol is released inside of the cell
how is the LDL receptor returned to the plasma membrane?
a vesicle containing the receptor pinches off as a secretory vesicle, which returns the LDL receptor to the plasma membrane
what are the possible fates for transmembrane receptor proteins following endocytosis? (3)
- recycling
- transcytosis
- degradation
eventually, all of the internal membranes produced by the invaginations are digested by — and — in lysosomes
proteases
lipases
the invagination is essential to achieve complete digestion of endocytosed — proteins
membrane
if it were not for the invagination. lysosomal hydrolyases could not digest the cytosolic domains of transmembrane proteins (because of the outer membrane of the multivesicular body becomes continuous with the lysosomal membrane) such as the
EGF receptor
if it werent for the pinching of the vesicles, we wouldnt be able to save
receptors
the transferrin cycle
after endocytosis, iron is released from the receptor-ferrotransferrin complex in the acidic late endosome compartment. the apotransferrin protein remains bound to its receptor at this pH and they recycle to the cell surface together where the neutral pH of the exterior medium causes release of the iron-free apotransferrin
many bacteria have developed resistance to antibiotics because there has been mutations in the —, which are responsible for
transporters
transporting the antibiotic into the cell
