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FOM - WLB > Week 5 Drewes - Membrane Transport, Cell Signaling > Flashcards

Week 5 Drewes - Membrane Transport, Cell Signaling Flashcards

1
Q

What type of molecules can passively move through a membrane via simple diffusion?

A

O2, CO2, EtOH, Steroids

Anything lipid soluble.

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2
Q

Does facilitated diffusion transport down a concentration gradient or against?

A

Down gradient (high to low)

  • Type of passive transport.
  • Done via:
    • Pore
    • Gated channel
    • Carrier protein
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3
Q

What does a graph of simple diffusion look like (rate of transport versus concentration of transported molecule)?

A

Simple diffusion is linear.

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4
Q

What does a graph of carrier-mediated or facilitated diffusion look like (rate of transport versus concentration of transported molecule)?

A

Hyperbola with max velocity (Vmax) and Km

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5
Q

What tissues are GLUT1 transporters found in?

A

Red Blood Cells

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6
Q

What kind of tissues are GLUT4 transporters found in?

A

Fat, muscle, and heart (insulin sensitive tissues)

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7
Q

Where are aquaporins found?

A

Kidneys, brain, and the eyes

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8
Q

How many transmembrane segments do *most *GLUT transporters have?

A

12

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9
Q

What drives active transport?

A

ATP Hydrolysis

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10
Q

In the equation for active transport, deltaG = RTln(C2/C1), what is C2 and what is C1?

A

C2 = concentration of moving ions

C1 = starting ion concentration

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11
Q

How much energy does the Na+/K+ pump cost the cell?

A

1 ATP

(for 3Na+ out/2K+in)

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12
Q

What kind of cells have a Na+/K+ pump?

A

Cardiac, intestinal epithelial

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13
Q

Digoxin slows heart rate by what mechanism?

A

steroid that binds and inhibits Na+/K+ ATPase

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14
Q

What drives the Na+/glucose symporter?

A

High extracellular [Na+]

  • indirectly requires ATP (2° active transport)
  • gradient due to activity of Na+/K+ ATPase (hydrolyzes ATP, 1° active transport)
  • 2 Na+ down concentration gradient, Glucose against concentration
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15
Q

Can simple diffusion have competitive inhibition?

A

No, not carrier-mediated transport.

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16
Q

How do GLUT4 receptors respond to insulin?

A

Insulin binds to cell membrane of muscle/adipose tissue

-causes vesicles with GLUT4 receptors to fuse with membrane and take in glucose at faster rates

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17
Q

What are ABC Transporters?

A

ATP-Binding Cassette Transporters

  • 49 Types
    • ATPases
  • cassette = sequence of AA’s that bind ATP
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18
Q

Why are ABC transporters important?

A
  • Drug resistance genes in cancer
    • Chemotherapy resistance
    • increased efflux
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19
Q

What is the most common cause of cystic fibrosis?

A

A mutation in the chloride pump (CFTR)

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20
Q

What symptoms are characteristic of Cystic Fibrosis?

A
  • Lung infections
    • mucous flows incorrectly
  • Pancreatic dysfunction
  • Infertility
  • Salty skin
    • secrete Cl-
    • without exercise
21
Q

What voltage-gated ion channels have 24 transmembrane proteins (four subunits, 6 proteins each) with intracellular and extracellular loops?

A

Na+Channel

Ca2+Channel

22
Q

What do Ionophores do?

A

Carry ions from one side of the membrane to another without using a channel.

-forms a crude pore/”ferry”

23
Q

What medicinal uses do ionophores have?

A

Can be used as antibacterials and antivirals.

24
Q

What ion channel is formed from 6 transmembrane proteins only?

A

K+channel

25
Q

What causes a voltage-gated channel to open?

A
  • Change in membrane potential → OPEN
    • allows ionmovement
    • voltage dependent
26
Q

What are the modes of cell-signaling?

A
  1. Hormone signaling (ex. Endocrine)
  2. Adjacent target cell (ex. Paracrine)
  3. Same cell target (ex. Autocrine)
  4. Contact dependent (ex. Justacrine)
27
Q

What is Endocrine signaling?

A

Hormone secreted into blood.

Blood vessel transports signal to target cells.

Whole body signalling.

28
Q

What is Paracrine signalling?

A

A secretory cell releases a signal into the interstitial fluid for an adjacent cell to receive.

Affect something within the neighborhood.

29
Q

What is Autocrine signalling?

A

Signal secreted and recognized by target sites on the same cell (itself).

30
Q

What is Juxtacrine signalling?

A

Cell exposes signal to surrounding cells that it is in contact with.

Signal never released, just simply exposed on cell surface (membrane-bound signal molecule).

31
Q

How is Nitric oxide synthesized?

A

dehydration of Arginine

32
Q

What are four common neurotransmitters discussed in class?

A
  1. Acetylcholine
  2. Histamine
  3. Nitric oxide (NO, gaseous NT)
  4. g-Aminobutyric acid (GABA)
33
Q

What are the three main classes of cell-surface receptors?

A
  1. Ion channel receptors (ligand-gated)
  2. Enzyme-linked receptors (kinases/bind kinases)
  3. Heptahelical receptors (2nd messengers, 7TM, G-protein)
34
Q

How do general hetertrimeric G-proteins function in Heptahelical receptor signalling.

A
  1. Hormone binds to receptor
  2. G-protein exchanges GTP for GDP and dissociates (subunits separate)
  3. Active G-protein subunit hydrolyzes GTP to make cAMP (which goes on to amplify signal)
  4. Subunit becomes inactive with GDP
35
Q

Where does cAMP come from?

A
  • Adenyl cyclase changes ATP → cAMP when bound to active G-protein
    • ATP - 2P’s = cAMP
    • takes off two phosphate groups
36
Q

How do G-proteins activate ion channels?

A
  • signal binds to receptor
    • activates g-protein
  • Active g-protein binds to ion channel → OPEN
  • G-protein becomes inactive when dephosphorylated → ion channel CLOSES
37
Q

How are IP3, Ca2+ used as secondary messengers?

A
  • Signal binds to receptor → activates G-protein
  • Active g-protein activates phospholipase
    • changes 4,5-BP → IP3
  • IP3 opens Ca2+channel in ER → Ca2+ released into cytoplasm
  • Ca2+ activates PKC
38
Q

What occurs in muscle cells when Ca2+ is released as a secondary messenger after IP3 opens the ER channel?

A

Muscle contraction

(accelerated Ca2+ release >> malignant hyperthermia)

39
Q

What receptior is associated with malignant hyperthermia?

A

Ryanodine Receptor

(accelerated Ca2+ release > involuntary muscle contraction > ATP hydrolysis > HEAT!)

40
Q

How do Tyrosine Kinase Receptors relay the cell signal?

A
  • Signal binds → Tyrosine Kinase Receptor dimerizes and is activated (phosphate groups added)
  • Intracellular signaling proteins bind to tyrosine kinase receptor and become activated (phosphorylated)
    • signal relayed by ACTIVATED signaling proteins into the cell’s interior
    • relay races! yay
41
Q

What effect does Tyrosine Kinase Receptors have on Ras proteins?

A
  • Activated Tyrosine Kinase Receptor phosphorylates Ras → active Ras
    • done via adaptor protein and Ras-activating protein
  • Active Ras starts MAP Kinase Kinase Kinase
    • MAP KKK → MAP KK
    • MAP KK → MAP K
    • MAP K → change gene regulation & expression by phosphorylation of particular proteins
42
Q

What happens if a mutated form of Ras cannot hydrolyze ATP?

A

CANCER

  • continuous transmission of signal along multiple pathways in abscence of signal molecule
  • leads to increased:
    • DNA replication
    • Proliferation
    • Differentiation
  • Non-active Tyrosine Kinase Receptor
43
Q

RSV

A

RSV (Rous Sarcoma Virus) → Src gene (g-protein)

Mutated src (oncogene) → DNA replication, Cell proliferation, & Differentiation

44
Q

How does STAT (JAK-STAT) become a transcription factor?

A
  • Receptors bind cytokines → dimerize → bind JAK
  • JAK → cross phosphorylates itself and receptor
  • Phosphorylated receptor → phosphorylates STAT
  • Phosphorylated STAT → enters nucleus
    • Activates transcription!
45
Q

What is the difference between an Ionotropic Effect and a Metabotropic Effect?

A
  • Ionotropic effect:
    • open/close ion channel
    • short effect
    • ex. NT at synaptic cleft
  • Metabotropic effect:
    • initiate G-protein signal cascade
    • long effect
    • ex. insulin/glucagon response
46
Q

How does Nictric Oxide (NO) act as an intracellular chemical messenger?

A
  • ACh activates NO synthase in endothelial cells
    • converts Arginine → NO
  • NO rapidly diffuses across membranes and binds to quanylyl cyclase
    • produces cGMP
  • cGMP causes rapid relaxation of smooth muscle
    • vessel relaxation → increased blood flow
      • (VIAGRA)
47
Q

How does Viagra allow increased blood flow?

A
  • NO bound to quanylyl cyclase → cGMP
    • increased/prolonged production of cGMP causes smooth muscle relaxation
      • increased blood flow → ERECTION!
    • inhibits breakdown of cGMP
48
Q

How does the threonin/serine kinase receptor lead to transcription?

A
  • Growth factor binds to Type II receptor
    • forms dimer with Type I receptor
  • Type II phosphorylates Type I
  • Type I receptor phosphorylates R-SMAD
  • R-SMAD joins with Co-SMAD
    • migrates to the nucleus
      • DNA promoter
        • Transcription
          • mRNA
            • Protein!
49
Q
A

FOM - WLB (20 decks)

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