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BIOC 303 > 3.1 Transporters (Passive and Active Transport) > Flashcards

3.1 Transporters (Passive and Active Transport) Flashcards

1
Q

why do we study channels, transporters and receptors

A

30% of total human genome encodes for membrane proteins and 90% of all pharmaceuticals target membrane proteins

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2
Q

passive transport

A

facilitated diffusion

  • down concentration gradient
  • use of a channel or a transporter
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3
Q

active transport

A
  • uphill against electrochemical gradient

- coupled to source of metabolic energy (either chemical reaction of downhill transport of another molecule)

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4
Q

simple diffusion

A

passive transport:

diffusion of nonpolar compounds down concentration gradient

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5
Q

facilitated diffusion

A

passive

  • for: large molecules (sugar, AA, vitamins)
  • depends on: transporter, [substrate]
  • transport is saturable and specific
  • relatively slow
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6
Q

in facilitated diffusion, are any chemical bonds made/broken?

A

no

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7
Q

in facilitated diffusion, which has more affinity for the transporter: substrate inside or outside

A

neither, they have the same affinity to the binding site of the passive transporter

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8
Q

graph of GLUT1 activity (label axises and line)

A

slide 8

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9
Q

why would you want a low Km

A

ensures that the transporter works even at low substrate concentrations, especially important if it’s something that the cell really needs

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10
Q

what kind of transporter is the glucose transporter

A

passive transporter (facilitated diffusion)

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11
Q

steps of glucose transport (4)

A

1) glucose binds to T1
2) binding lowers Ea and triggers transition to T2
3) Glucose released from T2 to cytoplasm
4) Ea rises and transporter returns to T1 conformation

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12
Q

how many conformations does the glucose transporter exist in

A

2

  • T1: glucose-binding site on outside
  • T2: glucose-binding site on inside
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13
Q

what is Km

A

concentration of solute when the transport rate is half its maximum

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14
Q

what does Vmax measure

A

rate which the carrier can flip its two conformations

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15
Q

GLUT1

A

PM of RBC

- Km = 1.5 mM (blood [glucose]=5mM)

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16
Q

why does glucose not get transport back out even though it is a passive transport system

A

as soon as glucose transported into the cell, it is phosphorylated to glucose-6P which has no affinity to GLUT1

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17
Q

GLUT2

A

liver and B cells of pancreas

  • Km = 20 mM
  • transports glucose out of hepatocytes to replenish blood glucose (don’t want to it to use up a lot of glucose)
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18
Q

GLUT3

A

neuronal cells

  • Km = 0.15 mM
  • needs constant influx of glucose so very high affinity
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19
Q

GLUT4

A

skeletal muscle

- Km = 5 mM

20
Q

draw the activity graphs for GLUT1 with GLUT2,3,4

A

slide 13?

21
Q

which GLUT is regulated by insulin

A

GLUT4 (found in skeletal muscle, fat, heart)

22
Q

how is GLUT4 regulated by insulin

A
  • normally GLUT4 is sequestered in secretory vesicles in the cytosol
  • after a rich meal, blood glucose levels exceeds 5 mM and triggers the release of insulin from pancreas
  • insulin receptor triggers movement of vesicles to PM
  • GLUT4 more abundant at the PM
  • glucose uptake increases
  • when insulin release slows down, GLUT4 reabsorbed into secretory vesicles again
23
Q

what is type 1 diabetes and what happens?

A

diabetes mellitus

  • insulin not released
  • GLUT4 stays in vesicles
  • glucose in the blood not transported into the cell so blood sugar remains high
24
Q

active transport types

A

1) coupled: uphill transport of one solute coupled to downhill transport of another
2) ATP-driven: couples uphill transport to hydrolysis of ATP

25
Q

coupled transport energy source

A

electrochemical gradient of another solute

26
Q

symporters

A

coupled transporter

- transport in same direction (co-exchangers)

27
Q

antiporters

A

coupled transporter

- coupled transport in opposite direction (exchangers)

28
Q

what is the main driving force of active transport

A

Na+

29
Q

concentration gradient of Na+ across membrane

A

high Na+ on outside, low Na+ on inside

30
Q

SGLT Transporter

A

active transport protein
- transport of glucose to cytosol coupled with 2 Na+ transport from the intestinal lumen (low glucose) to cytosol (high glucose)

31
Q

with the SGLT transporter, what happens when one of the solutes is at low concentration

A

the other solute will fail to bind to the transporter

32
Q

what is the equation for deltaGtotal

A

deltaGtotal = deltaGc + deltaGm

33
Q

how is the movement of Na+ ions across the PM membrane governed

A

two forces acting in the same direction:

  • membrane potential electric potential (outside of PM more positive than inside (-70 mV)) so Na+ will move in to “balance” the - membrane potential
  • ion concentration gradient (concentration of Na+ much higher outside)
34
Q

where is SGLT found

A
  • internal mucosa of small intestine

- proximal tubule of nephron

35
Q

how can the amount of active transport be increased at the physiological level

A

microvilli (such as in small intestine) to increase SA so you can have a greater number of transporters

36
Q

lactose permease LacY

A

symporter, active transport protein

- proton-driven cotransport of lactose from outside to inside

37
Q

lactose permease LacY structure

A

12 TMS helices clustered into two symmetrical loves

- substrate binding site is a central cavity

38
Q

how is the proton gradient re-established (move H+ back outside) for the lactose permease LacY

A

during fuel oxidation by a proton pump

39
Q

lactose permease LacY mechanism

A

rocking motion between two domains, powered by contribution of charged amino acids

40
Q

steps of lactose transport

A

1) loading of H+ to negative E269
2) binding favors binding of lactose
3) presence of both substrates favor interaction between (+)R144 and (-)E269
4) pairing of (-)E269 destabilizes H+ and releases lactose
5) H+ released too
6) no more substrates to stabilize the (+)R144 and (-)E269 interaction and lactose permease LacY returns to original conformation

41
Q

can lactose escape the cell

A

yes, because the lactose permease LacY mechanism is fully reversible. BUT, lactose generally broken down by B-galactosidase in the cytosol

42
Q

AE1

A

“Anion-exchanger” Antiporter active transporter in respiratory cells
- transports out HCO3- from inside cell to outside with import of Cl-

43
Q

why is there HCO3- inside erythrocytes and why does it need to be moved

A

waste CO2 from tissue is released from resp tissues, enters plasma and then RBC

  • CO2 converted to HCO3- because it is more soluble in plasma so it can be better carried to the lung
  • in the lungs, HCO30 re-enters the RBC and converted to CO2, then exhaled
44
Q

why is the import of Cl- into erythrocyte cytoplasm beneficial

A

1) transport HCO3- out for better transport of CO2 to lung

]2) acidifies RBC cytoplasm to allow for release of O2

45
Q

describe AE1 transporter action in the lungs

A

Cl- from inside transported out while HCO3- imported back in

BIOC 303 (14 decks)

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