Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
32 Cards in this Set
- Front
- Back
Describe how energy from ATP hydrolysis is used by P-Type, primary active ATPases to transport ions such as sodium potassium and calcium across membranes
|
w
|
|
understand the catalytic cycle of Na/K atpase and know similarities and diff of it to Ca atpase
|
w
|
|
specific drugs that inhibit p-type atpases
|
w
|
|
wilsons and multidrug resistance/ new atpase transporters
|
w
|
|
descr the basic secondary active transport mechanism (alt access model)
co transporters Counter transporters |
w
|
|
what are the two main classes of transport proteins?
|
Carrier proteins and channel proteins
|
|
Carrier proteins
|
carriers/permeases/transporters
BIND solute and undergo conf change 2 classes: Primary active:NA K atpoase Secondary Active: NA/CA exchange |
|
Channel proteins
|
do NOT really bind substrates
|
|
Name the three vital P-Type atp-ases
|
P-Type ATPases: a large family of related proteins that transport ions, most usually cations, across biological membranes in nearly all species
Na/K Ca H/K also under the non-heavy metal transporters |
|
Name the three primary active transporters
|
Non-heavy metal transporters
Heavy metal transporters ABC (ATP binding cassette) transporters |
|
Primary active transporters
catalytic subunit (alpha) has two parts |
1) alpha helices that traverse mem
2) large cytosol part (bulk of enz) has three domains P (phos) N (nt binding) A (actuator) |
|
Na/K-ATPase aka the Na pump
|
in virtually every cell
for every ATP pumps 3 Na out and 2 K in electrogenic (moves more pos out of the cell than in Inhibited by: cardia glycosides(steroids) ouabain and digitalis) |
|
Describe E1 of the Na/K pump
|
E1 - LOW energy state, has Na binding sites, is open to the Cytosol
steps: E1 + ATP E1-P*(Na)3 (high energy) ATP hydrol->P of the alpha subunit -> conf change and Na is encased E2-P?: ECM side opens |
|
Describe the E2 state of the Na/K pump
|
E2 - has K binding site, is open to the ECM
Steps: E2-P + 3 Na (with ECM side open)( low affinity ) --> Na leaves 2 K from ECM bind E2-P ( high affinity) P leaves E2 encases K (high energy conformation) ATP binds E2 returns it to E1 (LOW affinity, K in E1) and K is released |
|
explain osmotic balance through the Na pump
|
neg charged anions in cytosol, accompanying cations to balance this draw water into the cell,
is Na out of cell and accompanying Cl- kept out my mem pot |
|
Ca-ATPase pump
high or low Ca in cell name the two primary active transporters how many Ca's pumped per ATP |
LOw inside cell
two primary active transporters PM (plasma mem)(calmodulin binding to C terminus) SR (moves Ca into organelles) 1-2 Ca per ATP |
|
Post albers E1 E2 transport cycle of Ca
|
E1 + 2Ca --> E1*2Ca
--> E1 ATP 2Ca -->E1-P 2Ca --> --> E2P --> E2 -(spontaneous)->E1 (low E) |
|
Ca binding E1
water problem |
(-) charged aa's in the alpha helix have high affinity for Ca when exposed to cytosol, lots of water in the cation binding vestibule, cations are surrounded by water, need to strip it in order to get through the plasma membrane, water carries cations to aa residues, ATP binds, causing M1 to get bent in half and pushes the water out
in occluded state no water! |
|
ATP binding to E1-Ca
|
closes the three domains (A N P)
A pulls on M1 and M2 displacing water and trapping Ca in mem. N domain closes in on the P domain, so asp can be P'd by ATP |
|
Cation dissocation from E2
|
The major E1 to E2 conformational transition disrupts Ca coordination
alpha helices undergo twisting in the E2 form to completley disrupt the Ca binding sites, twists make E2 a low affinity binding for Ca therefore it will be released |
|
H/K atpase (proton pump)
|
found in parietal cells(HCl)
60% seq ID with Na/K both have beta subunit vital for targeting of the pump to the Plasma Membrane |
|
Omeprazole -
|
inhibits activity of proton pump
|
|
Wilsons disease
|
AR disease of copper metabolism
|
|
Menkes disease
|
inborn Cu deficiency, high [Cu] in organs damages liver and CNS, cirrhosis, mottor problems and psych disturbances
|
|
MDR ATP-ases
|
multi-drug resistance
ABC transporter pg 199 |
|
Secondary active transport
what is it?/ how different from primary? 2 types |
two or more molecule mvmt is coupled, ATP NOT used directly
2 types cotransport countertransport |
|
Cotransport
dir of solute flow? 3 ex? |
all solutes in same dir
ex) Na/gluc Na aa Na/K 2Cl |
|
Na gluc and Na aa
location binding sites specificity |
location - luminal membraneof small intestines and proximal tubule
2 binding sites on ECM side (one for na and one for gluc for Na aa, each protein (5) is responsible for a spec subset of aa's based on molecular specificity SEE PAGE 200 |
|
Na/K Cl transporter
important location |
important in kidney and intestine
|
|
CounterTRansport
|
solutes move in opp dir
ex) Na/Ca - downhill mvmt of na into cell drives Ca out of cell, 3 Na for each Ca, ELECTROGENIC - 3 pos enter cell, 2 pos leave it and Na/H - inward mvmt of 1 Na , outward mvmt of 1 H |
|
cardia glycosides
|
inhibit the sodium pump, increase Na on inside.
ouabain and digitalis changes sodium gradient change the driving force for Ca expulsion out of cardiac myosite |
|
Ca overview
|
E1, calcium binds
E1*Ca ATP binds clam shell closes(water leaves) E2P Ca leaves E2 phosphate leaves E1 |