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membranes and lipids Flashcards

1
Q

describe the 2D fluid mosaic of membrane structure

A

lipids form bilayer in 2D sea which proteins float in and can move around

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2
Q

describe the formation of the lipids in the bilayer

A

headgroups of the lipids are hydrophilic and (polar) are on the outside
lipid tails are hydrophobic (non polar) and stay in the middle of the layer

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3
Q

what is the most abundant phospholipid in cells and what are they derived from

A

glycerophospholipids derived from glycerol-3-phosphate

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4
Q

give examples of different types of lipids

A 
PIP
glycerophospholipids 
sphingolipids
glycosphingolipids
sterols 
cholesterol
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5
Q

what are fatty acid chains and why are they unique

A

they are made by acetate and added via CoE A

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6
Q

what are sphingolipids made from

A

sphenoid base, N acyl chain and head group

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7
Q

what characteristic of sphinoglipids allows them to interact with polar molecules or cholesterol

A

can form hydrogen bonds

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8
Q

explain the structure and role of glycopsphingolipids (glycolipds)

A

composed mainly of sugars
make around 5% of outer leaflet of the membrane
they play an important role in cell to cell adhesion and can act as recognition sites

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9
Q

what are gangliocydes

A

they are abundant in the brain, they are a sphingosine plus sugar groups which can present receptors - they attach to lipid rafts and only found on the outer surface of the membrane

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10
Q

where is cholesterol found in animal membranes

A

between the lipid molecules

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11
Q

what is a lipid raft

A

they are subdomains of the plasma membrane which contains high concentrations of cholesterol and glycosphingolipids

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12
Q

what are the functional significances of lipid rafts

A

can attach receptors

can drift

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13
Q

what are caveolae

A

a type of lipid raft which invaginate the cell membrane which can contain many proteins and can be used for taking up nutrients

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14
Q

what is lipid bilayer asymmetry

A

the fact that the monolayers that make up the bilayer an have different structures within them

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15
Q

why does lipid interdigitation occur

A

due to lipid length asymmetry which reduces the lipid bilayer thickness

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16
Q

what are translocaze enzymes

A

flip phospholipids across the membrane

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17
Q

what do scrambles enzymes do

A

randomise the normal distribution and oppose translocaze enzymes

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18
Q

what does phosphatidylserine do in apoptosis and blood clotting

A

acts as a pro coagulation surface. it is externalised by collagen and thrombin mediated activity
externalisation of phos.. can also lead to recognition of cell and therefore apoptosis

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19
Q

what causes membrane curvature

A

the relative size of the head group and the tail affect the shape fo the bilayer and the curvature

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20
Q

why is spontaneous negative curvature a bad thing

A

can lead to bilayer disrupting properties which can lead to fusion and non-bilayer intermediates

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21
Q

what is the role of desaturates

A

introduce double bonds into fatty acids

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22
Q

what are the three types of membrane proteins

A

integral (intrinsic) membrane protein (span inside and out)
lipid linked membrane protein
peripheral (extrinsic membrane protein (only found on one side)

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23
Q

what is the structure of integral membrane proteins

what is the problem with extracting them

A

can be single or multiple transmembrane segments - these regions are mainly made up of amino acids and hydrophobic side chains

extracting them will disrupt the membrane using organic solvents or detergents

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24
Q

what are PIP lipids

A

head group phosphorylation at position 3 4 and 5
PIP(4,5)2 is most abundant
found in the inner leaflet of the membrane
they usually face inside of the cell and are signalling molecules for cascade pathways

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25
Q

give an example of an integral membrane protein - simple and multiple

A

glycophorin A - single domain
extra cellular domain is glycosylated
bacteriorhodopsin - multiple domain - 7 transmembrane domains

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26
Q

how are proteins bound to lipids in the membrane

A

covalently linked to lipid which is inserted into the membrane

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27
Q

give some examples of lipid bound proteins

A

prion protein
trial proetins
signalling proteins
insulin receptor

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28
Q

where do peripheral proteins interact (they can be readily removed by high salt concentration and soluble in aqueous solution)

A

only with the hydrophilic heads and with other proteins via ionic interactions

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29
Q

what are some examples of peripheral membrane proteins

A 
cytoskeletal proteins such as:
spectrin - form long filaments 
actin - joins spectrin filaments 
ankyrn - bridges spectrin and band 3 
band 4.1 - stabilises spectrin-actin interaction
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30
Q

what is the role of peripheral membrane proteins in RBC’s

A

maintains shape and rigidity and restricts lateral motion of integral membrane proteins

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31
Q

what is hereditary spherocytosis / elliptocytosis

A

mutations in genes encoding spectrin and ankyrin result in abnormal shape which become degraded by the spleen and results in anaemia

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32
Q

what is the role of amyloid b peptide in alzheimers

A

amyloid beta peptide forms plaques in the brain causing neuronal atrophy which causes loss of part of brain dealing with memory

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33
Q

where are carbohydrates found in the cell membrane

A

either watched to proteins or attached to the bilayer ie glycoprotein or glycolipid - they are found near exclusively on the extracellular face of the cell

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34
Q

what is the difference between O linked and N linked glycoproteins

A

O linked - carb attached to serine or threonine - often shorter
N linked sugars - often large and unbranched - connected to asparagine

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35
Q

why are carbs important to the cell

A

stabilises proteins and used in intracellular recognition eg blood group antigens on RBC

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36
Q

what is amyloid precursor protein and what is it cleaved by - what does it lead to

A

integral membrane protein with transmembrane spanning domain which is cleaved by beta secretase, then by sAPPB and Y secretase - leads to AB42 leads to formation of senile plaques

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37
Q

where do senile plaques tend to from in alzheimers

A

cholesterol rich lipid rafts which produces amyloid beta protein

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38
Q

what is the relevance of ApoE4 in Alzheimers

A

it is involved in cholesterol transport and is more prevalent in alzheimer’s patients

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39
Q

what do statins do

A

lower amyloid beta production in cells and cholesterol content

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40
Q

what is prenylation and where does it occur

A

it is the addition of hydrophobic molecules to a protein or compound. it occurs at cysteine residues at C terminus and allows proteins to be inserted into the membrane

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41
Q

what is palmitolyation

A

covalent attachment of fatty acids to a cysteine residue

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42
Q

which molecules can pass through a pure lipid bilayer the easiest

A

gases

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43
Q

what is a pure bilayer permeable to

A

water, gases, small polar molecules and hydrophobic molecules (benzene)

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44
Q

what is the rate of diffusion proportional to and what is the movement direction

A

the concentration gradient

from areas of high to low concentration

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45
Q

what is facilitated diffusion

A

occurs down the gradient - no energy required and is dependant on integral membrane proteins
similar kinetics to enzymes

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46
Q

what are ionophores types
give examples
(facilitated diff)

A

they can be carrier or channel forming
carrier - carry across the membrane to shield from hydrophobic area eg antibiotic vanomycin (specific to K+)
channel forming - channel that allows free flow of ions eg antibiotic grimicidin specific to Na+ and K=

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47
Q

what are ion channels and what are they used for

facilitated diff

A

allow rapid and gated movement of Na+ and K=
ions flow down gradient
nerves, signal transduction

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48
Q

how does glucose cross the barrier

A

attaches to GLUT-1 which undergoes conformational change and allows diffusion of glucose into the cell - dependant on glucose conc

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49
Q

what happens to glucose uptake in RBC

A

converted to G6P by hexokinase

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50
Q

what are aquaporins

A

water channel proteins - responsible for water flow - its is a tetrameter with 4 pores fro H20 to pass
28KDa with 6 trasndomain a helices

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51
Q

what are the two types of active transport

A

ATP driven

Ion driven

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52
Q

what are some examples of ATP driven transport

A

Na+/K+ ATPase
which maintains high k+ inside the cells and low Na+ inside the cell
3 Na out and 2 K in - works against concentration gradient

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53
Q

what is ion driven active transport, give examples

A

movement of a molecule coupled with an ion
symport - both in one direction eg Na+ glucose transporter
antiport (opposite direction) eg Na+ Ca2+

54
Q

what are the two different types of exocytosis

A

constitutive - occurs in all cells constantly for secreted proteins and plasma membrane proteins
regulated - occurs via specific signal eg release of insulin or neurotransmitters

55
Q

explain exocytosis at the nerve terminal

A

calcium dependant - impulse means ca into cell causes synaptic vesicles to fuse with membranes and release neurotransmitter

56
Q

give three examples of endocytosis

A

phagocytosis
pinocytosis
receptor mediated endocytosis

57
Q

describe process of phagocytosis by dendritic cells, neutrophils and macrophages

A

pathogen engulfed by pseudopodia and ingested into vacuole which fuses with lysosome then foreign antigens displayed on membrane

58
Q

describe receptor mediated endocytosis

A

Receptor-mediated endocytosis is the selective uptake of macromolecules from the extracellular fluid via clathrin-coated pits and vesicles. The ligand being taken up must first bind to a specific cell surface receptor. The receptor-molecule complexes accumulate in a clathrin coated pit and then endocytosed in a clathrin-coated vesicle

59
Q

describe gluoce transport in the intestinal epithelium

A
  • Na+/glucose transporter only in apical membrane, glucose transporter only in basolateral
  • Movement of glucose from gut into epithelial cell driven by movement of Na+ ions down conc. gradient through Na+/glucose symporter
  • Glucose diffuses across basolateral membrane into blood stream
  • Conc. of Na+ ions maintained at low level in cell by Na+/K+ ATPase in basolateral membrane
  • As glucose moves through epithelial cell, water follows by osmosis
60
Q

what is an oral rehydration therapy

A

contains water salts such as Na K and glucose
needed as with cholera can’t just have water as uptake of glucose is dependant on Na+ which then allows water to flow back into cells

61
Q

what are the three stages of remote cell signalling

A

1) reception of extracellular signal by cell
2) transduction of signal from outside to inside the cell
3) response, activation of cellular response

62
Q

what is contact signalling and give an example

A

juxtacrine - where cell displays plasma membrane bound molecules
eg T helper cell activated by antigen presenting cell which causes activation if the correct binding shape

63
Q

what are the 3 types of cell signalling

A

paracrine - remote cell signalling
contact signalling (juxtacrine)
contact signalling via gap junctions

64
Q

describe the process of cell communication via gap junctions and give an example

A

cytoplasms are directly joined by connexion proteins to adjacent cells eg cardiac myocyte cells

65
Q

what are the four main types cells communicate around the body

A

autocrine - acts on itself
paracrine - signal acts on nearby cells
endocrine - released into blood and distant target
neuronal - nerve impulses - uses neurotransmitters

66
Q

what is the difference between lipid hormones and hydrophilic hormones give examples

A

hydrophilic bind to the cell surface but lipid hormones act on the inside
hydrophilic - catecholamines and peptide hormones
lipid base - steroids
thyroid hormones
sterol hormones

67
Q

what are the 4 receptor classes and what are the sub class differences

A 
ligand gated ion channel 
g protein coupled receptors 
kinase linked receptors 
nuclear hormone receptors 
nuclear hormone receptors are the only ones that act intracellularly
68
Q

describe how ligand-gated binding channels work

A

works very fast, binding of ligand causes conformational change to allow specific ions to flow through and alter the cells electrochemical gradient. electrons flow down gradient.
these channels typically open in response to change in membrane potential

69
Q

describe how GPCR’s work

A

they are integral membrane proteins which are coupled with intracellular effector system. transmembrane regions. when a hormone binds to a specific GPCR receptor - conformational change facilitating inside cell with G protein which inhibits or activates down stream proteins or DNA

70
Q

describe how kinase linked receptors work

A

they have a single transmembrane helix with a large extracellular binding domain and an intracellular catalytic domain. the receptor itself is an enzyme which directly effects gene expression by affecting phosphorylation of different tyrosine

71
Q

describe how nuclear hormone receptors work

A

they are present in the cytosol or nucleus - hormones diffuse across the cell membrane and interact with receptors which then causes translocation into the nucleus to form a hormone receptor complex which binds to regions of DNA affecting transcription

72
Q

what does the RAS affect

A

Controls BP, blood volume and electrolyte homeostasis

73
Q

describe the mechanism of the RAS

A

it is stimulated by decrease in blood volume, blood pressure or Na+
Renin from the kidney cleaves angiotensin 1 from angiotensinogen which is made in the liver. ACE then cleaves to angiotensin 2
this causes vasoconstriction of arterioles, retains water and salts in he blood so blood volume increases and is controlled by negative feedback

74
Q

where is ACE found

A

membrane bound in the pulmonary and renal epithelium

75
Q

give some examples of monoamines

A 
noraA
adren
dopamine
histamine 
serotonin
76
Q

give some examples of amino acids

A

glutamate
aspartate
glycine
GABA

77
Q

give some examples of peptides

A

endorphins, substance P, neurokinins

neurotensin

78
Q

what does AG2 target and what are the effects

A 
receptors are al GPCRs
AT1 - vasoconstriction 
increased NA release
Na reabsorption 
aldosterone growth 
AT2 - antihypertrophic 
antihyperssensitive
opposes AT1 effects
79
Q

give an example of a lipid neurotransmitter

A

anandamide

80
Q

describe the life cycle of a neurotransmitter

A

synthesis in nerve terminal
storage in synaptic vesicles
release into synaptic cleft by exocytosis in response to action potential
receptor activation on post synaptic membrane
neurotransmitter deactivation via enzyme metabolism or reuptake

81
Q

what is depression believed to be caused by

A

functional deficit of monaminergic transmission eg NA, dopamine, serotonin

82
Q

what are the 5 ways depression is treated

A

monoamine reuptake inhibitors such as TCA’s, SSRI’s, SNRI’s
monamine oxidase inhibitors (stop the breakdown of monoamines in the presynaptic knob so more is available)
atypical antidepressants
electroconclusive therapy
mood stabilising drugs such as lithium

83
Q

give three examples of gastrotrasnmitters and what they are

A

they are gaseous molecules synthesised in the body which act as signalling molecules such as NO, CO and H2S

84
Q

what is the problem with gastrotransmitters

A

they are environmental pollutants which can readily cross the cell membrane and induce paracrine signalling

85
Q

what are the effects of CO and high vs low conc

A

high conc leads to neurological and cardiovascular disorder

in low conc can stimulate vasodilation and be cardio/neuro protective

86
Q

what effect does NO have

A

causes relaxation of smooth muscle and therefore vasodilation

87
Q

what is signal transduction

A

converts extracellular 1st signal from messenger into a change in cellular function

88
Q

what are the three main stages of signal transduction

A

reception
transduction (hierarchy, amplification, specificity, complexity)
response

89
Q

describe with an example what hierarchy is in signal transduction

A

components of a pathway arranged in a particular way to transmit a signal from the outside to change something on the inside of the cell

90
Q

what is amplification

A

from a single molecule of the primary messenger which could induce many downstream molecules leading to many changes inside the cell from secondary messengers affecting kinases which affect protein activity

91
Q

how are signal transduction pathway specific and give an example

A

one messenger molecule may bind to the same receptor but on different cells and elicit a very different response between them
adrenaline can binds to different tissues and caused a different response depending on the cell type

92
Q

why is signal transduction complex

A

many different types of receptors, G proteins, enzymes, 2nd messengers - lots of cross talk and cell type specificity

93
Q

what do GTPases do?

A

hydrolyse GTP to GDP

94
Q

how are G proteins secured to the cell

A

anchored to internal surface of cell membrane via lipid tails ie prenylation

95
Q

what are the two major groups of G proteins and give examples

A

g protein - receptor associated - heterotrimeric such as A, B, Y subunits (Gas, Gai, Gaq)
small GTPases - monomeric such as RAS and RHO

96
Q

how are G proteins activated and stopped

A

switch on by ligand binding then switched off by GTPase activity - inactive when GDP (no Pi) bound but active when GTP bound

97
Q

describe how the Gs pathway works

A

stimulatory pathway - alpha subunit of Gs bound to GDP and in inactive state. binding of ligand to receptor causes G protein to release GDP and attach GTP. the a unit bound to GTP dissociates from the g protein and binds to adenylate cyclase which converts ATP into cAMP (secondary messenger). GTPases convert GTP back to GDP releasing inorganic phosphate and a unit rebinds with b and Y

98
Q

what affect does Gs have vs Gi on cAMP

A

Gs increases

Gi decreases

99
Q

after inactivation of Gs what breaks down cAMP

A

phosphodiesterase breaks it down into water and H2O

100
Q

what is the role and mechanism of the Gq pathway

A

Gq stimulates phospholipase which increases DAG and IP3. Phospholipase C turns PIP two into DAG and IP3

101
Q

what is the role of DAG

A

it stays in the membrane where it activates protein kinase C (which can also be activated by Ca)

102
Q

what is the role of IP3

A

released into the cytosol where it triggers Ca release

103
Q

which g proteins do cholera and pertussis toxin affect

A 
cholera = Gs
pertussis = Gi
104
Q

what are the symptoms and mechanism behind cholera toxin and treatment

A

bacterial infection through dirty water or food causes diarrhoea and vomiting (severe dehydration) - treated with ORT
toxin stimulates Gs pathway and inhibits GTPases so remains in an active state - in intestinal epithelial cells high cAMP results in excess loss of Cl- so water moves with it from cells into the lumen

105
Q

what are the symptoms behind whooping cough (pertussis toxin) and the mechanism of action

A

airborne through droplets which can be treated by antibiotics and prevented with vaccination this pathway inhibits Gi therefore an overall stimulatory effect on cAMP leading to increased insulin secretion and sensitivity to histamine

106
Q

what are some examples of PDEs inhibitors

A

caffeine and viagra (stop breakdown of cAMP)

107
Q

name 5 secondary messengers

A 
cAMP
cGMP
DAG
IP3
Ca
108
Q

where does Ca come from to take effect on a cell

A

can come from extracellular routes or from stores within the ER - also founding the mitochondria

109
Q

how is cGMP produced

A

from GTP via enzyme guanylyl cyclase or by NO

110
Q

what are the three main groups of protein kinases

A

serine/threonine kinases
tyrosine kinases
dual specificity kinases

111
Q

where is phosphate added to on an amino acid

A

to the OH group

112
Q

what are protein kinase inhibitors used for

A

therapeutic agents fro cancer, HIV, RA, cardiovascular disease

113
Q

what is gleevec (imatinib)

A

used to treat myelogenous kinases inhibits receptors kinase tyrosine

114
Q

what are the functions of lipids

A 
energy store 
component of cell membrane 
soluble fat soluble vitamins 
biosynthetic precursors 
signalling molecules
115
Q

where does cholesterol come from and why does it need a carrier

A

25% from diet and the rest made from the liver (also intestine but small)
it is insoluble so is attached to a lipoprotein

116
Q

what are the four types of lipoprotein classification

A

chylomicrons (largest)
VLDL
LDL
HDL (smallest)

117
Q

what is the role of VLDL

A

transport lipids made in the liver to peripheral tissues

118
Q

what is the role of LDL’s and why can they be bad

A

provide cholesterol for peripheral tissues - it is the main cholesterol carrier.
can be damaging - has single layer of ApoB on outside - can be oxidised leading to pro inflammatory response and protherogenic leadings to CVD

119
Q

what is the role of HDL and why are they good

A

tranport cholesterol to liver from peripheral tissues - contains mainly apoA which is protected against oxidation and has anti-inflammatory properties

120
Q

what is the general structure of a lipoprotein

A

The external monolayer contains phospholipids, cholesterol and apolipoproteins. Cholesterol esters and triacylglycerols are located in the particle core.

121
Q

what are the four classes of apolipoproetins

A

ApoA - present in HDL mediates taking away of cholesterol from peripheral cells and influx to the liver
ApoB - recognises ApoB/E receptors - facilitates LDL uptake
ApoC - activator of lipoprotein lipase - transferred between lipoproteins
ApoE - stabilises VLDL for cellular uptake

122
Q

what does lipoprotein lipase do

A

hydrolyses triglycerides to fatty acids that can be taken up by target tissues and used fro energy production

123
Q

describe the life cycle of VLDL

A

made by liver - transport lipids to tissues broken down by LPL and become LDL which causes release of cholesterol

124
Q

why is HDL good

A

takes up cholesterol from the blood and transports back to the liver

125
Q

how does the liver remove cholesterol

A

in the form of bile slats

126
Q

what does a scavenger receptor do

A

recognises mature HDL and takes in liver to secrete bile

127
Q

what is the role of cholesterol in atherosclerosis

A

major constituent of atheromatous plaques in cholesterol enriched LDL as excess is deposited in arteries

128
Q

describe the development of atherosclerosis over many decades

A

fatty streak
fibrous plaque
advanced plaque
myocardial infarction

129
Q

how do statins work as a treatment for lowering cholesterol

A

cholesterol is made by HMG-CoA reductase (from mevalonate) - statins inhibit this enzyme
this increases expression of LDL receptor which means more cholesterol is taken up from the blood

130
Q

how do statins have a pleiotropic effect

A

they have mulitbenefical effect - improve endothelial function
antioxidant properties , inhibition of inflammation and stabilise atherosclerotic plaques to reduce risk of rupture

IMS (20 decks)

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