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66 Cards in this Set
- Front
- Back
Hydrophobic |
non-polar. found inside protein molecule. |
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Hydrophillic |
polar. found outside protein molecule. |
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Glycine |
small...fits into small spaces. flexible. not chiral! |
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Cysteine |
can form cross-links. |
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Proline |
is kinky. introduces kinks and rigidity. |
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a- helix |
stiff, strong, H-bonding + disulfide bonds coils in right-hand direction. |
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B- sheets |
soft, flexible H-bonding + disulfide bonds parallel/anti-parallel |
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proline |
disrupts helices = no H bonds |
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Uses for GFP |
pigs- proved concept zebra fish- pollution, heart contracting rats- cancer, blood vessels of tumour glow |
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Domain structure |
efficient folding clefts created between domains dif. functions flexibility |
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Antibody antigen binding site formed by |
6 hypervariable loops |
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Recognise antigens by |
shape size charge polar/non-polar |
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Influenza virus enters by |
endocytosis. |
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Influenze virus exits via |
budding. |
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Surface proteins of influenze virus |
- Haemagglutin- binds to sialic acid in host. gives entry into cells - Neuraminidase- removes sialic acid, stops new virus particles sticking together. |
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Target of influenza drugs |
block active site of neuraminidase. |
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Assumptions of Michaelis-menten model |
catalysis is slowest step more substrate than enzyme conc. of enzyme/substrate is constant reverse rxn is negligible. |
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Steady state assumption |
rate of formation of ES is equal to its breakdown. |
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apo enzymes |
protein + associated non-protein component. |
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holo enzymes |
completely protein, fully active. |
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Competitive inhibition |
inhibitor competes for active site. rate catalysis decreases overcome by increasing substrate conc. |
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Non competitive inhibition |
inhibitor can bind simultaneously with substrate binds at another active site. reduces catalysis (less efficient) |
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Uncompetitive inhibition |
binds to enzyme-substrate complex. can't be overcome by increasing substrate conc. |
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Vmax |
maximum velocity of an enzyme-substrate catalysed rxn. |
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Km |
enzymes attraction to substrate... high Km= low affinity (not very attracted) |
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X and Y axis of enzyme vs substrate |
Y= 1/v X= 1[s] |
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Lineweaver-burk plot Y and X intercepts |
Y intercept= 1/vmax X intercept= 1/-Km |
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Homotropic effect |
binding of substrate to one active site influences binding of substrate to another active site. |
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Allostery |
more than one active site. |
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Heterotropic effect |
effectors either inhibit or activate. |
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Other part of enzyme (not active site) is for... |
correct spatial orientation micro-environment recognition + control. |
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Co-factors |
other compounds necessary for enzyme to function. |
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Prosthetic groups |
co-factors tightly bound to enzyme (don't let go) |
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Saturated |
only contains single bonds. |
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Unsaturated |
double bonds, lower melting point. |
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Hydrogenation |
increase fats melting point (spreadable) add H's to polyunsat vege oils creates trans fats! |
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Free fatty acids |
from breakdown of fats (triglycerides) not water soluble- transported by serum albumin. |
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Essential fatty acids |
mammals can't introduce DB beyond C9. diet= linoleic acid (seeds, nuts) precursor of other lipids. |
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Roles of fatty acids |
building blocks of phospholipids modify proteins (covalent attachment) fuel molecules derivatives= hormone/intercellular messengers |
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Phospholipids |
platform= glycerol, 3C alcohol or sphingosine disease where accumulates= Niemann pick. |
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Glycolipids |
asymmetrical orientation. sugar group on outside |
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Cholesterol |
nearly all animal cell membranes. steriod backbone. OH group. |
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Fatty acid degradtion occurs in the... |
mitochondrial matrix |
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Fatty acid synthesis occurs in the... |
cytosol. |
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3 stages of FA degradation |
1. Lipolysis 2. Activation 3. Broken down...acteyl coA...CAC cycle. |
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What molecule carries activated FA into mitochondrial matrix? |
carnitine. |
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Antiport |
transport simultaneously in opposite directions. |
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Ketone bodies |
major fuel source eg. heart, kidneys. water soluble/ transportable acetyl CoA. |
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Entry of acetyl CoA in CAC depends on... |
oxaloacetate. |
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Times of low OA (oxaloacetate) |
1. Fasting 2. Insulin-dependent diabetes. |
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Priorities of metabolism in starvation |
1. provide glucose to dependent tissues eg. brain, RBC. 2. preserve protein |
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Fatty acid synthesis |
acetyl CoA ---> malonyl CoA irreversible rxn, catalysed by acetyl CoA carboxylase. Ends with C16-acyl ACP. |
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Acetyl CoA carried across inner mitochondrial membrane by... |
citrate.
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FA synthesis optimum conditions |
lots of carbohydrate not a lot of FA |
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Global regulation of ACC |
Glucagon + epinephrine- inhibit ACC, stimulate phosphorylation. Insulin stimulates, removes phosphate. |
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Local regulation of ACC |
allosteric stimulation by citrate allosteric stimulation by palmitoyl CoA. |
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FAS (fatty acid synthase) |
inhibitors= useful drugs eg. cancer (decrease signalling) increase immune system (interleukin makes memory T cells store fat) |
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Cholesterol |
Creates membrane fluidity Precursor for signal molecules eg. hormones + vitamin D. |
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3 steps to cholesterol synthesis |
1. synthesis of isopentenyl pyrophosphate. 2. condensation of 6 isopentenyl p. to squalene. 3. cyclization of squalene to tetracyclic product to cholesterol. |
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Initial step of cholesterol synthesis catalyzed by... |
HMG- CoA reductase. |
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Control of HMG- CoA reductase |
1. rate of reductase mRNA synthesis 2. rate of reductase mRNA translation 3. degradtion of reductase 4. phosphorylation of reductase |
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LDL |
low density, bad cholesterol B100 cholesterol transport |
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HDL |
high density, A good cholesterol reverse cholesterol transport (excreted by liver) |
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Cholesterol transported by... |
lipoproteins. |
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Familial hypercholesterolaemia (FH) |
failure to release LDL + loss of receptor. |
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Site of LDL binding |
LA domain |