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MCM > Membranes and Transport > Flashcards

Membranes and Transport Flashcards

1
Q

What is the physiological role of a membrane?

A
  1. A membrane serves as the protective barrier of the cells AND organelles.
  2. Gives cell a shape
  3. Separates the intra from extracellular
  4. Semipermeable to diff metabolites
  5. Helps with cell recognition
  6. Anchoring sites
  7. Binding sites for hormones and enzymes
  8. Maintain electrochemical gradient
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2
Q

What is the cell membrane made up of?

A

The cell membrane is made up of 1) lipids, 2) proteins and 3) carbs arranged in a asymmetric bilayer

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3
Q

The cell membrane is primarily made up of _______________

A

Phospholipids

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4
Q

What is the structure of a phospholipid?

A

Phospholipids are amphipathic: they have a hydrophobic tail and a hydrophilic head.

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5
Q

How is the bilayer arranged?

A

Asymmetrically. Both leaflets of the bilayer are different from one another.

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6
Q

The membrane is composed of lipids, proteins and carbs. How are lipids and proteins incorporated into the lipid bilayer?

A 
Lipids and proteins are 
attached, 
embedded or 
anchored to the lipid bilayer. 
The lipid bilayer serves as the foundation.
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7
Q

How are carbs incorporated into the membrane?

A

Carbs are COVALENTLY attached to some membrane lipids or proteins.

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8
Q

What are the three different types of membrane lipids?

A
  1. Phospholipids
  2. Glycolipids
  3. Cholesterol
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9
Q

What are the two types of phosopholipids?

A

There are two types of PL, based on their backbones.

  1. Glycerolphospholipids: have a glycerol backbone
  2. Sphingolipids: have a sphinogosine backbone.
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10
Q

Structure of glycerolphospholipids

A

[Glycerol backbone] with [2 fatty acids] and a [phosphate group with a headgroup attached]

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11
Q

Types of glycerolphospholipids

A
  1. Phosphotidyl serine
  2. Phosphotidyl choline
  3. Phosphotidyl inosital
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12
Q

Structure of a sphingolipid

A

A sphingolipid has a [sphingosine backbone] with a:

[long chain FA] and a [phosphorylcholine]

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13
Q

What is the most common sphingolipid?

A

Sphingomyelin- found in the outer leaflet

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14
Q

Sphingomyelinase

A

Sphingomyelinase has a phosphoryl choline ceremide

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15
Q

What is a glycolipid?

A

A glycolipid is one of the three most common types of lipids. It has a [sphingosine backbone] with [carbohydrate (oligosaccharide) residues].

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16
Q

Where are glycolipids found?

A

Glycolipids are found in the outer leaflet.

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17
Q

Structure of cholesterol

A

Cholesterol is a steroid nucleus with [hydrocarbon side chain] and a hydroxyl (-OH) group.

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18
Q

How does cholesterol interact with the membrane

A

The [hydrocarbon side chain] of cholesterol interacts with the hydrophobic tails of the membrane. Thus, cholesterol is embedded in the membrane in between phospholipids.

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19
Q

Lipid rafts

A

Cholesterol is often present in patches called lipid rafts. These lipid rafts are thought to be important for cell signaling.

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20
Q

______________ is a steroid.

A

Cholesterol is a steroid. Thus, it has a steroid nucleus.

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21
Q

What does it mean that the membrane is arranged in a asymmetric bilayer?

A

This means that the membrane has 2 leaflets: both are different from one another.

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22
Q

The membrane has binding sites for ____________.

A

Hormones and enzymes

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23
Q

Where is sphingomyelin found?

A

Outer leaflet of the membrane bilayer.

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24
Q

Where is phosphotidylcholine found on the membrane?

A

Phosphotidylcholine is a PL. It is found on the outer leaflet.

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25
Q

Where is phosphotidylserine normally found on the membrane?

A

Inner leaflet*

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26
Q

When is ____________ a marker for apoptosis?

A

Phosphotidylserine (PS) is a marker for apoptosis when it is found on the outside leaflet. It serves as a tag.

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27
Q

When PS is found on the outside leaflet, what happens?

A

When PS is found on the outside leaflet, it is a marker for apoptosis. Phagocytes will recognize and remove them.

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28
Q

Bob has Niemann-Pick Dz. What enzyme is he deficient of?

A

Acid-sphingomyelinase (A-SMase).

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29
Q

What does A-SMase do?

A

A-SMase breaks down sphingomyelin.

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30
Q

What is the mechanism of Niemann-Pick Dz?

A

Niemann-Pick Dz occurs when there is a deficiency of Acid-Sphingomyelinase (A-SMase). A-SMase breaks down sphingomyelin. Sphingomyelin will accumulate in the liver, spleen, bone marrow and CNS.

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31
Q

N-P Dz leads to what?

A

In N-P Dz, sphingomyelin is accumulating because we do not have A-SMase to break it down. Thus, we will get enlargement of the spleen, liver and also neurological damage.

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32
Q

How can we tell if someone has N-P Dz?

A

The hallmark is a cherry red spot in the eye.

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33
Q

What are the types of membrane proteins and how are they classified?

A
  1. Integral membrane proteins
  2. Peripheral proteins
  3. Lipid-anchored proteins
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34
Q

Integral membrane proteins

A

Integrated in the membrane. Integral membrane proteins are stabilized by the hydrophobic interactions of the lipids.

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35
Q

Polytopic transmembrane proteins

A

Polytopic transmembrane proteins are integral membrane proteins that span the entire membrane. They weave in and out of the membrane several times and interact with BOTH the intracellular and extracellular portion of the cell.

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36
Q

_____________________ area examples of polytopic transmembrane proteins

A

Ion channels, transporters and enzymes that are responsible for transporting molecules across the membrane and transmit signals from [extracellular]–> [intracellular]

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37
Q

_____________________ are examples of polytopic transmembrane proteins

A

Ion channels, transporters and enzymes that are responsible for transporting molecules across the membrane and transmit signals from [extracellular]–> [intracellular]

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38
Q

What are peripheral proteins?

A

Peripheral proteins are proteins that are attached to the outside of the membrane via [electrostatic interactions]

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39
Q

What are lipid-anchored proteins?

A

Lipid-anchored proteins are proteins that are [tethered] to the membrane via [covalent interactions] with lipids.

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40
Q

[Q:] Tell me about carbs on the membrane

A

Carbs are the membrane are NEVER present by themselves. They are covalently bound to lipids or proteins that face the extracellular side

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41
Q

[Q:} What is an example of a carb on the membrane?

A

Glycocalyx- a carb shell that is located on the surface of cells.

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42
Q

What is glycocalyx important for?

A
  1. Protection
  2. Cell adhesion–> lets cells make stable contact with other cells.
  3. Cell identification–> allows the body to determine if a cell is healthy or not.
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43
Q

_________________ are often glycoslyated

A

Both membrane proteins and lipids.

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44
Q

Another example of carbs on the membranes?

A

Antigens! Antigens are carbs that are found on the surface of red blood cells: they serve as markers for our blood type

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45
Q

What can happen if there is an incompatible transfusion?

A
  1. acute hemolysis
  2. renal failure
  3. Shock
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46
Q

Blood group O Antigen

A

H

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47
Q

Antibody

A

Antibody is an Ig made by the immune sx. They are located in the blood and recognize aliens

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48
Q

Blood group O Antibodies

A

anti-A and anti-B

49
Q

Blood group A Antigens

A

A

50
Q

Blood group A Antibodies

A

Anti-B (Anti-B antibodies will look for B antigens and attack)

51
Q

Blood group B Antigens

A

B

52
Q

Blood group B Antibodies

A

Anti-A antibodies

53
Q

Blood group AB Antigens

A

A and B (meaning, the body will accept both A and B blood)

54
Q

Blood group AB Antibodies

A

None

55
Q

Universal Donor

A

O

56
Q

Universal Acceptor

A

AB

57
Q

What is an Rh factor?

A

Some RBCs can also have Rh factors (D antigens). They are autosomal dominant and you either have them or you don’t.

58
Q

How are Rh factors inherited?

A

Autosomal dominant

59
Q

When are Rh factors a problem?

A

Rh factors can be a problem a pregnancy; when the mom is Rh- and the child is Rh+. The mom will make D-antibodies which can attach the childs RBC’s. This is okay the first pregnancy, but can worsen w pregnancy.

60
Q

Our cell membranes are fluid. But what causes this and why it is important?

A

Proteins and lipids in our cells [rotate] and [move laterally]. This gives our membrane a fluid-like consistency, allowing them to undergo [conformational changes] or to [move], to carry out a specific fx.

61
Q

What factors influence the fluidity of our membrane?

A
  1. Temperature
  2. Lipid composition
  3. Cholesterol
62
Q

Temperature and how it affects membrane fluidity

A

Temp>melting temperature–> more fluid

Temp more rigid

63
Q

Lipid composition and how it affects membrane fluidity

A

If we have more lipids in our membrane that are saturated, more rigid.

If we have more lipids in our membrane that are unsaturated, more fluid.

64
Q

Cholesterol and how it affects membrane fluidity

A

Cholesterol is super cool. It is a balancer. When our membrane is too fluid or too rigid, it can compensate to bring to a more natural state.

Ex. When our membrane is too rigid because of too many saturated FA or tempmelting temp or too many unsaturated FA, it will make it more rigid by filling in kinks.

65
Q

spur cell anemia

A

Spur cell anemia occurs when there is too much cholesterol in the membrane of our RBC. The membranes become too rigid when they pass through the [capillaries of the spleen], they break.

66
Q

What is passive transport?

A

PT is the movement of of molecules DOWN their gradient without the use of NRG.

67
Q

Is passive transport NRG dependent or NRG independent?

A

Passive transport occurs DOWN a gradient without NRG needed.

68
Q

What are the types of passive transport?

A
  1. Simple diffusion

2. Facilitated diffusion

69
Q

What is simple diffusion?

A

Simple diffusion is a type of passive transport. Hydrophobic (non-polar/lipophillic), small polar molecules and uncharged polar molecules can diffuse through the lipid bilayer across the membrane down their gradient.

No protein needed

70
Q

What is facilitated diffusion?

A

Facilitated diffusion is the movement of large polar and charged polar molecules (ions) across the membrane with the help of TRANSmembrane proteins (ion channels or transporters).

Thus, a protein is needed.

71
Q

Types of transmembrane proteins that assist with facilitated diffusion

A

Transporters (uniporters or symporters) or ion channels

72
Q

Ion channels

A

Pores or gates in the membrane that allow [charged] or [polar] molecules to move through the membrane. They open up in response to many things.

73
Q

Which ions are more concentrated OUTSIDE of the cell

A

Na+, Cl- and Ca2+

74
Q

Which ions are more concentrated INSIDE of the cell?

A

K+

75
Q

Ligand-gated ion channels

A

Participate in facilitated diffusion.

How it works: Open and close in response to ligands (usually a NT or a hormone). The ligand will bind to a receptor on the channel, allowing a charged or polar molecule to move down their concentration gradient.

76
Q

Voltage-gated ion channels

A

Participates in facilitated diffusion

How it works: an impulse initiates depolarization, opening up ion channels to allow charged (ions), polar molecules to move down their concentration gradient.

77
Q

Where are VG ion channels located?

A

VG-ion channels are located on EXCITABLE cells, like neurons.

78
Q

What is so GREAT about ion channels?

A

Ion channels transport MILLIONS of molecules/second.

79
Q

Active transport

A

Active transport [uses NRG] and proteins to move things [AGAINST] their gradient.

80
Q

Types of active transport***

A

Primary- uses ATP directly

Secondary AT- Uses the energy stored in the concentration gradient that the primary makes. THUS, it uses ATP indirectly.

81
Q

Secondary AT is coupled to a ____________ transport

A

Primary active transport. It uses the energy from the concentration gradient created by the primary AT.

82
Q

What are the two types of 1 Active Transport

A
  1. P-type Active Transport

2. ABC Type active transport

83
Q

P-type ATPase

A

a type of primary active transport where ATP is hydrolyzed and phosphorylates the ATPase (thus a covalent bond is formed).

Method:

  1. ATP is hydrolyzed
  2. Pi phosphorylates the ASPARTATE residue on the ATPase.
  3. ATPase undergoes a conformational change and opens to transport ions against their gradient.
84
Q

What are examples of P-type ATPases?

A
  1. Na/K ATPases

2. Ca2+ ATPase

85
Q

ABC-type ATPase

A

ATP is hydrolyzed but the ATPase is not directly phosphorylated (no covalent bond is being formed).

86
Q

Secondary AT

A

In Secondary Active transport, a molecule is moved against its concentration gradient. To do this, energy is needed. However, ATP is not used. The energy comes from a concentration gradient that was created via primary active transport, which used ATP. Because ATP does not fuel directly, it is called 2 AT.

87
Q

Examples of 2 AT

A

Na/glucose pump

88
Q

Na/glucose pump

A

glucose is moved against its concentration gradient using te concentration gradient created by moving Na from ^ to low concentration

Both move in the cell. so it uses a symporter.

89
Q

How is the gradient in secondary active transport usually established and maintained?

A

By primary active transport.

90
Q

Voltage gated Na+ channels are examples of what kind of transport?

A

facilitated diffusion

91
Q

Glucose transporters are examples of what kind of transport?

A

facilitated diffusion

92
Q

What is tetrodotoxin?

A

Tetrodotoxin is a poison found in pufferfish. This poison will inactivate Na+ channels. This stops synaptic transmission; causing numbness

93
Q

What is the practical application of tetrodotoxin?

A

lidocaine

94
Q

How can we maintain low levels of Calcium inside the cell?

A

First off, note that Ca2+ is more concentrated outside of the cell. To maintain low levels inside the cell, we use a

Na+/Ca2+ Antiporter.

3 Na+ are moved into a cell, down its concentration gradient while 1 Ca2+ is moved out AGAINST its concentration gradient.

95
Q

In the Na+/Ca2+ pump, how does Ca2+ move against its concentration gradient?

A

It uses the NRG that is created by Na+ moving down its concentration gradient.

96
Q

How is glucose transported from [lumen of the intestine] to the [blood]?

A

Glucose (& other sugars) enter a cell from the lumen of the small intestine via 2 transporters.

  1. SGLT-1- moves [glucose, galactose and Na] inside the cell via secondary active transport mechanism
  2. GLUT5- moves [fructose] inside the cell via facilitated diffusion
97
Q

How do we move glucose, fructose and galactose out of the cell?

A

GLUT2 transporters via facilitated diffusion (bc moving down a concentration gradient.

98
Q

What transporters are used to to take dietary monosaccharides from the lumen of the ER–> bloodstream?

A
  1. SGLT-1: galactose, glucose and Na+ using secondary active transport
  2. GLUT5: fructose using facilitated diffusion
  3. GLUT2: fructose, galactose, and glucose out of the cell–> blood using facilitated diffusion
  4. Na/K ATPase pump
99
Q

Apical

A

faces inward towards a lumen

100
Q

Basolateral

A

does not face a lumen.

101
Q

What transporters for uptake of monosaccharides are located on the apical side of the cell?

A

SGLT-1
&
GLUT5

102
Q

What transporters for uptake of monosaccharides are located on the basolateral side of the cell?

A

GLUT2
&
Na/K ATPase.

103
Q

What processes occur that facilitate dietary monosacchardes uptake?

A

Secondary active transport and facilitated diffusion

104
Q

Summary of monosacharide uptake

A

We need to uptake monosaccharides from the lumen of the intestine–> bloodstream. But how do we do this?

SGLT-1 transports [glucose, galactose, and Na+] into the cell using secondary active transport.

GLUT5 transports [fructose] into the cell using facilitated diffusion.

Once inside the cell, we have a buildup of monosaccharides and Na+ and need to get it out.

GLUT2 transporters move [galactose, glucose and fructose] to the bloodstream and Na+ leaves via Na/K ATPase pumps.

105
Q

A defective transport of ___________ leads to Cystic Fibrosis

A

Chloride (Cl-)

106
Q

CF is caused by a mutation in the _______ gene.

A

CFTR

107
Q

What happens in CF?

A

CF is a mutation of the CFTR gene. It misfolds and never wants to leave the ER. CFTR is a Cl- channel that actively moves Cl- from inside the cell–> outside.

If Cl- never wants to leave the cell, there is a buildup. As a result, our body will try to compensate by channeling in Na+. However, this creates a salt. When Na+ comes in, water also follows. This will decrease the H2O concentration of the surface creating a thick mucous on [AIRWAYS and SWEATDUCTS] that is susceptible to bacterial infection.

Sweat a lot and coughing.

108
Q

CFTR is a gene that acts as a Cl- protein channel. How does it move Cl-.

A

CFTR ACTIVELY moves Cl- from inside to outside.

This makes sense because naturally, Cl- is more concentrated outside of the cell.

109
Q

What are disorders of transporters?****

A
  1. Cystic Fibrosis- CFTR gene which makes Cl- channels
  2. Cystinuria–> cystinuria is a defect in the transporters that are responsible for the uptake of [cystine, arginine, lysine and ornithine].
  3. Hartnups disease–> a defect in the transporters of non-polar, neutral AA (such as trytophan, alanine, leucine, valine and threonone)
110
Q

Cystinuria is a disorder that is due to __________.

A

A defect in the transporter that is responsible for the uptake of

  1. Cystine
  2. Arginine
  3. Lysine
  4. Ornithine
111
Q

What is a result of cystinuria?

A

We have a buildup of the 4 amino acids and develop kidney stones/cystine crystals.

112
Q

Where is the cystine transporters that are affected in Cystinuria located primarily?

A

KIDNEY!

113
Q

What is Hartnups disease?

A

Hartnups disease is a defect in the transporters that deal with non-polar, neutral amino acids such as alanine, leucine, valine, threonine and tryptophan.

Tryptophan is a really important enzyme because it is the precursor to a lot of molecules we use in life. Such as niacin (the precursor to NAD+), melatonin and seratonin. In kids, it causes failure to thrive. In adults, it results in cerebellar ataxia, photodermititis and photosensitivity.

114
Q

Where are the Hartnup transporters found?

A

kidney, small intestine

115
Q

Na/Ca2+ Exchanger is abbreviated

A

NCX

116
Q

What is the role of cardiotonic drugs?

A

Cardiotonic drugs are called cardiac glycosides. They will excite the heart and induce contractions.

117
Q

What are examples of cardiotonic drugs?

A

Oubain

Digoxin

118
Q

How do cardiotonic drugs work?

A

Cardiotonic drugs work by inhibiting Na/K+ ATPases.
-Remember that Na/K+ ATPases will move 3 Na+ out of the cell and 2 K+ in. If they are broken, we cannot get Na+ out of the cell.

A buildup of Na+ in the cell will inhibit NCX, causing secondary buildup of Ca2+. it is this buildup of Ca2+ that will excite the heart bc Ca2+ triggers muscle contraction!

MCM (12 decks)

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