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BIOL 3421 - molecular biochem > lipid biochemistry: active lipids > Flashcards

lipid biochemistry: active lipids Flashcards

1
Q

what is the basic role of phosphoinositides

A

cell signaling and differentiating

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2
Q

what is the head group of phosphoinositides

A

inositol

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3
Q

at which positions can inositol be phosphorylated

A

3, 4, 5

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4
Q

how many phosphates total can there be on a molecule of phosphatidylinositol

A

4 (PI already has a phosphate, and then 3 more can be added to the inositol head group)

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5
Q

give the abbreviations for all the phosphorylated forms of phosphatidylinositol

A

PI, PIP, PIP2, PIP3

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6
Q

what is the full name of PIP2

A

phosphatidylinositol 4,5-bisphosphate

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7
Q

where is PIP2 found + in what orientation

A

clustered on the inner leaflet of plasma membranes

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8
Q

what cleaves PIP2

A

phospholipase

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9
Q

what activates the phospholipase that cleaves PIP2

A

extracellular signals

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10
Q

give the full names + abbreviated names of the products of PIP2 cleavage

A

inositol 1,4,5-triphosphate (IP3)
diacylglycerol (DAG)

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11
Q

once IP3 and DAG are made via PIP2 cleavage, where do they go

A

IP3: travels into the cytosol
DAG: stays embedded in the membrane

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12
Q

why does IP3 travel to the cytosol but DAG stays embedded in the membrane once PIP2 is cleaved?

A

IP3 is water soluble while DAG is not water soluble

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13
Q

which type of pathway is PIP2 cleavage involved in?

A

GPCRs and trimeric G proteins

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14
Q

describe how PIP2 cleavage is involved in GPCR/trimeric G protein pathways

A

IP3 causes Ca2+ to exit the ER
DAG and Ca2+ activates protein kinase C

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15
Q

what is the full name of PIP3

A

phosphatidylinositol-3,4,5-triphosphate

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16
Q

how is PIP3 formed

A

phosphorylation of PIP2

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17
Q

what phosphorylated PIP2 to create PIP3

A

phosphoinositide 3-kinase (PI3K)

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18
Q

which carbon of PIP2 is phosphorylated to get PIP3

A

C3

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19
Q

what is the charge of PIP3? which part of the molecule carries the charge?

A

negatively charged, inositol head carries the charge

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20
Q

what is the outcome of the PIP3 signaling pathway

A

growth, proliferation, survival

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21
Q

why is PIP3 a target for cancer treatment

A

PIP3 signaling pathways are related to growth, meaning it correlates with tumor progression

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22
Q

what is the PIP3 signalling pathway initiated by

A

receptor tyrosine kinases (RTKs)

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23
Q

describe how PIP3 is part of the cellular response to insulin

A

it activates glycogen synthesis (lowers blood glucose), brings GLUT4 to the PM so glucose can leave the bloodstream, and the insulin receptor is an RTK

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24
Q

what can PIP3 do with adaptor or scaffold proteins?

A

it uses those proteins to help cluster together proteins that are involved in the same signaling pathway

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25
Q

give an example of an adaptor protein that PIP3 uses

A

AKAP5

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26
Q

using AKAP5 as an example, describe how PIP3 interacts with adaptor proteins

A

AKAP5 has binding sites for PIP3, which localizes the adaptor and its associated proteins into lipid rafts

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27
Q

what is a conjugated lipid

A

one with alternating double and single bonds

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28
Q

describe how conjugated dienes produce specific colors

A

the delocalized electrons (due to conjugation) can be excited by certain wavelengths of visible light, and so they will reflect a different wavelength = color

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29
Q

how do birds acquire different colors

A

by ingesting conjugated dienes via their diet

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30
Q

how do birds acquire sex-specific feather colors?

A

either by different diets between males and females, or by different metabolic processing of the conjugated dienes

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31
Q

what is the general function of eicosanoids

A

they are signalling hormones

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32
Q

what type of signalling do eicosanoids do

A

paracrine signalling

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33
Q

what is paracrine signalling

A

signalling over short distances

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34
Q

how many carbons are eicosanoids composed of

A

20

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35
Q

which fatty acid are all the eicosanoids derived from? give the shorthand name and the common name

A

20:4Δ(5,8,11,14)
arachidonate

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36
Q

list the 3 eicosanoids we cover in this course

A

prostaglandin, thromboxane, leukotriene

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37
Q

what structural characteristic defines a prostaglandin

A

5C ring

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38
Q

where were prostaglandins originally discovered

A

prostate gland

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39
Q

T or F: prostaglandins can be released by most tissues

A

true

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40
Q

when are prostaglandins released

A

when there is a site of injury or inflammation

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41
Q

list the roles of prostaglandin at a site of injury/inflammation

A

promote either vasodilation or vasoconstriction, promote tissue inflammation and pain, promote fever

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42
Q

describe how prostaglandins regulate the female reproduction system

A

they’re required for ovarian follicle to rupture and release eggs during ovulation. They stimulate smooth muscle contraction in uterus during menstruation and childbirth

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43
Q

when are synthetic prostaglandins used

A

can be used to induce labour

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44
Q

what structural characteristic defines thromboxanes

A

a 6C ring

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45
Q

what produces thromboxanes

A

platelets (thrombocytes)

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46
Q

where in the body are thromboxanes released

A

released near damaged blood vessels

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47
Q

describe the roles of thromboxanes at damaged blood vessles

A

they promote local platelet aggregation to help form blood clots, promote formation of new platelets, vasoconstriction, and increases in blood pressure

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48
Q

what structural characteristics define leukotrienes

A

they have 3 conjugated double bonds in a row. They do not have any rings like the other eicosanoids do

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49
Q

which of the eicosanoids have rings in their structure? which doesn’t?

A

prostaglandins and thromboxanes have rings, leukotrienes do not

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50
Q

what produces leukotrienes

A

leukocytes

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51
Q

when do leukocytes release leukotrienes

A

during allergies or asthma attacks

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52
Q

describe the roles of leukotrienes during allergies or asthma attacks

A

they promote inflammation, increase mucus production, and they can cause contraction of smooth muscle in bronchioles

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53
Q

how do some anti-asthma medications work? what do they target?

A

they target leukotriene synthesis

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54
Q

other than allergies and asthma, what else do leukotrienes play a role in

A

arthritis and inflammatory bowel disease

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55
Q

what is the full name for NSAIDs

A

nonsteroidal anti-inflammatory drugs

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56
Q

what do NSAIDs do

A

inhibit the enzymes that help from prostaglandins and thromboxanes from their precursor molecule (arachindonate)

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57
Q

give 3 examples of nonsteroidal anti-inflammatory drugs

A

aspirin, ibuprofen, motrin

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58
Q

how many rings do sterols have

A

4

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59
Q

describe the structure of the 4 sterol rings

A

three 6C rings and one 5C ring

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60
Q

are sterols rigid or fluid

A

rigid

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61
Q

are sterols planar or not planar

A

planar

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62
Q

describe C-C rotation in sterols

A

there is little rotation around C-C bonds in sterols, as they’re rigid and planar

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63
Q

what are bile acids formed from

A

polar derivatives of cholesterol

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64
Q

where are bile acids secreted from

A

liver

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65
Q

where are bile acids stored

A

gall bladder

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66
Q

where are bile acids moved to from the gall bladder

A

moved into the small intestine

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67
Q

role of bile acids in the small intestine?

A

helps emulsify fats to allow digestion of fats by lipases

68
Q

what are steroid hormones formed from

A

oxidized derivatives of cholesterol

69
Q

describe the basic structure of steroid hormones

A

they have the sterol nucleus but lack the alkyl chain

70
Q

where are sex (steroid) hormones synthesized

A

testes and ovaries

71
Q

where are adrenocortical (steroid) hormones synthesized

A

in the adrenal gland

72
Q

where do steroid hormones go once they’re synthesized

A

they travel to target tissues in the blood bound by hydrophilic carriers

73
Q

where do steroid hormones go once they’re synthesized

A

they travel to target tissues in the blood bound by hydrophilic carriers

74
Q

what do steroid hormones do once they reach their target tissue

A

they can trigger changes in gene expression

75
Q

why might lipid signalling molecules in plants be fragranced

A

to attract pollinators or to repel herbivores

76
Q

list 3 functions of lipid signalling molecules in plants (other than fragrance), and give examples

A

bending a shoot towards light (auxin), repairing insect damage (jasmonate), or ripening fruit (ethylene)

77
Q

which plant lipid is responsible for bending shoots towards light

A

auxin

78
Q

which plant lipid is responsible for repairing insect damage

A

jasmonate

79
Q

which plant lipid is responsible for ripening fruit

A

ethylene

80
Q

what are plant lipids often made from

A

fatty acids or sterol derivatives

81
Q

most fragrant plant signalling molecules are generated from ____ units

A

isoprene

82
Q

what are isoprenes? what is their basic structure?

A

isoprenes are lipids. 5C molecules joined via condensation reactions to build 10-40C molecules

83
Q

isoprene units contribute to many other active lipids too, such as _________________

A

fat soluble vitamins

84
Q

which isoprene-unit molecule produces geranium smell

A

geraniol

85
Q

which isoprene-unit molecule produces pine smell

A

b-pinene

86
Q

which isoprene-unit molecule produces lime smell

A

limonene

87
Q

which isoprene-unit molecule produces mint smell

A

menthol

88
Q

which isoprene-unit molecule produces spearmint smell

A

carvone

89
Q

are vitamins essential?

A

yes

90
Q

can vitamins be synthesized by the body?

A

no

91
Q

describe the origins of the word “vitamin”

A

originally every vitamin was believed to have amine in it
vital + amine = vitamin

92
Q

what are the two categories of vitamins?

A

water soluble and fat soluble

93
Q

list the fat soluble vitamins

A

A, D, E, K

94
Q

how are the fat soluble vitamins synthesized?

A

by isoprene condensation

95
Q

what is the name of vitamin A1

A

retinol

96
Q

list the main structural characteristics of vitamin A1

A

lipid with trans double bonds and a hydroxyl group

97
Q

from which foods do we acquire vitamin A1

A

fish oils or dairy, or it can be formed from B-carotene precursor that’s prevalent in carrots/sweet potatoes

98
Q

what characteristics does vit A have due to the conjugated double bonds

A

it can absorb light

99
Q

what two things are formed from retinol when it’s oxidized

A

retinal or retinoic acid

100
Q

by which process are retinal and retinoic acid formed from retinol

A

oxidation

101
Q

T or F: B-carotene is comprised of isoprene units

A

true

102
Q

what functional group does retinal have

A

aldehyde

103
Q

what is the initial structure of retinal after the oxidation of retinol

A

a cis double bond on carbon 11

104
Q

T or F: 11-cis-retinal is the final form of retinal

A

false; it undergoes a change

105
Q

what happens to 11-cis-retinal (because this isn’t its final form)

A

it binds to a protein (opsin) in rod cells of the retina to form rhodopsin pigment. Rhodopsin is excited by visible light and changes 11-cis-retinal to all-trans-retinal

106
Q

what is the result of 11-cis-retinal changing to all-trans-retinal

A

a signal cascade that results in vision

107
Q

what protein does 11-cis-retinal bind to on the way to converting to its new form

A

opsin

108
Q

where do 11-cis-retinal and opsin bind

A

in rod cells of the retina

109
Q

11-cis-retinal + opsin = ?

A

rhodopsin pigment

110
Q

how does rhodopsin convert 11-cis-retinal to all-trans-retinal

A

it’s excited by visible light

111
Q

what are rods and cones

A

photoreceptors

112
Q

where are rods and cones located

A

in the inner layer of the eyeball (retina)

113
Q

what is the retina

A

the inner layer of the eyeball where rod and cone cell photoreceptors are located

114
Q

what is a photoreceptor

A

a modified neuron

115
Q

visual information captured by ____ is relayed by ____ to the ____ towards the brain

A

photoreceptors, neurons, optic nerve

116
Q

in order for vision to occur, what must rods release

A

neurotransmitters

117
Q

what do rods release neurotransmitters to

A

neurons

118
Q

rods –> release NTs to neurons –> ? –> ?

A

optic nerve, brain

119
Q

what type of vision do we get from rods

A

light (greyscale)

120
Q

what type of vision do we get from cones

A

colors

121
Q

describe the structures of rod and cone photoreceptors

A

the outer segment has many membranous disks filled with visual pigments

122
Q

what is the visual pigment of rods

A

rhodopsin

123
Q

retinal lipid + opsin protein = ?

A

rhodopsin pigment

124
Q

? + ? = rhodopsin pigment

A

retinal lipid + opsin protein

125
Q

what type of protein is opsin

A

a GPCR

126
Q

how do the conformational changes of retinal affect vision

A

conformational changes of cis retinal to trans retinal = conformational changes in the opsin protein (a GPCR)

127
Q

T or F: the trans state of retinal is permanent

A

false; it is not permanent and will eventually convert back to its cis form

128
Q

what gets activated once light (photons) activate the visual pigment

A

transducin

129
Q

what is transducin (what type of protein)

A

a G protein

130
Q

once activated, what does transducin do

A

it activates phosphodiesterase (PDE)

131
Q

what does PDE stand for

A

phosphodiesterase

132
Q

what does PDE do once it’s activated by transducin

A

it converts cGMP –> GMP (causing cGMP levels to fall)

133
Q

as PDE forms GMP, what is the effect of cGMP levels falling

A

cGMP-gated cation channels close = hyperpolarization

134
Q

how do Na+ channels close during the visual cascade

A

closed via light-induced signal transduction

135
Q

what happens to the rod’s membrane potential when a Na+ channel closes

A

Na is no longer coming in = membrane potential gets more negative = hyperpolarization

136
Q

describe the behavior of hyperpolarized neurons

A

they’re less likely to release neurotransmitters, so they’re turned “off” when hyperpolarized

137
Q

T or F: a rod is “off” in the presence of light

A

TRUE

138
Q

when will rod cells be depolarized

A

in the DARK

139
Q

T or F: the absence of a neurotransmitter release from the rod is what triggers vision

A

TRUE!!!

140
Q

which neurotransmitter do rods release

A

glutamate

141
Q

describe how the visual signal is ceased

A

when light isomerizes cis retinal to trans retinal, it causes opsin to expose its C-terminal. Because of this, rhodopsin kinase will phosphorylate residues on the C-term of opsin. Arrestin then binds to phosphorylated opsin and stops the GPCR from activating its G protein

142
Q

during the cease of the visual signal, which enzyme phosphorylated opsin

A

rhodopsin kinase

143
Q

during the cease of the visual signal, which part of opsin gets phosphorylated

A

C-terminal

144
Q

during the cease of the visual signal, which protein binds to phosphorylated opsin to prevent it from activating its G protein

A

Arrestin

145
Q

how is retinoic acid formed

A

via the oxidation of retinal

146
Q

what functional group does retinoic acid have

A

carboxylic acid

147
Q

what type of molecule is retinoic acid

A

a hormone

148
Q

which form of retinoic acid is a hormone

A

all-trans

149
Q

role of retinoic acid? (3)

A

it regulates gene activity in the early embryo to determine anterior/posterior axis patterning, cell differentiation, and organogenesis

150
Q

T or F: excess or deficiency in vitamin A during pregnancy has no negative effects

A

false; it’s correlated with increased risks of birth defects in many mammals

151
Q

vitamin A deficiency is the leading cause of ___ ___ in children

A

preventable blindness

152
Q

what is golden rice and why is it beneficial

A

rice that’s enriched with beta carotene. Useful because it decreases the risk of childhood blindness (B-carotene is a precursor of retinol, which is involved with the visual signal)

153
Q

exposure to __ __ causes a compound in the skin to be converted to vitamin D3

A

UV light

154
Q

what disease does vit D prevent

A

rickets

155
Q

what is rickets

A

a disease where bones soften in children

156
Q

where is/was rickets common

A

in cold climates where heavy clothing blocked UV light

157
Q

which form of vit D is produced in yeast and added to our milk and butter

A

D2

158
Q

why is vit D2 added to our milk and butter

A

to mimic vit D3

159
Q

T or F: vit D3 is biologically active

A

false; it needs to be converted to an active form

160
Q

what is D3 converted to to become active? where does this take place?

A

D3 is converted to calcitriol (a hormone) via reactions in the kidney and liver

161
Q

what type of molecule is calcitriol

A

a hormone

162
Q

what does calcitriol do

A

it increases absorption of calcium from foods and deposits it into bones

163
Q

describe the basic structure of vit E and K

A

aromatic rings with a long side chain formed from isoprenoids

164
Q

T or F: humans are rarely deficient in vit E and vit K

A

true

165
Q

what does vit E do

A

helps prevent oxidative damage to membranes

166
Q

what does vit K do

A

assists with blood clotting

167
Q

what does the drug Warfarin do? what vitamin does it mimic, but what sets it apart from this vitamin

A

Warfarin is a blood thinner that mimics vitamin K, but it actually prevents excess blood clotting (unlike K)

BIOL 3421 - molecular biochem (20 decks)

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