Bb 451 Exam Ii

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DNA polymerase I enzymatic activities

Back 1

5' to 3' DNA polymerase activity, a 3' to 5' exonuclease activity (also called proofreading), and a 5' to 3' exonuclease activity.

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primase

Back 2

catalyzes the synthesis of a short RNA segment (called a primer) complementary to a ssDNA template

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DNA ligase

Back 3

an enzyme that creates phosphodiester bonds between adjacent nucleotides between Okazaki fragments. Biotechnologists use this enzyme to join DNA fragments together to create recombinant molecules.

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Topoisomerase II (gyrase)

Back 4

relieves the tension created by the helicase and is essential for replication to proceed efficiently.

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progressive

Back 5

hopping on and off the DNA. DNA Polymerase I

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processive

Back 6

meaning that once it gets onto a DNA molecule, it stays on it for a long time replicating it. DNA Polymerase III

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DNA Polymerase I

Back 7

removes RNA primers; at/near replication fork.

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sliding clamp (Beta clamp)

Back 8

makes DNA Polymerase III processive

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OriC

Back 9

Where initiation of replication in E. coli occurs at a specific site; contains three repeats of an AT rich sequence near some sequences bound by the DNA A protein.

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E. coli mismatch repair

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occurs as a result of action of the proteins MutS (recognizes mismatch), MutL (recruits MutH), and MutH (nicks newly synthesized strand of DNA to allow exonucleolytic removal of nucleotides around the mismatch).

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uvrABC excinuclease

Back 11

removes DNA damage

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Ames test

Back 12

The likehood a compound will make a mutation.

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Ribonucleotide reductase (RNR)

Back 13

catalyzes the formation of deoxyribonucleotides from ribonucleotides. The substrates are ribonucleoside diphosphates (ADP, GDP, CDP, or UDP) and the products are deoxyribonucleoside diphosphates (dADP, dGDP, dCDP, or dUDP).

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lipoprotein lipase

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in the capillaries removes some of the fat from the chylomicrons and they shrink in size and exit the capillaries and move to the liver.

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lipases

Back 15

In the intestines, these use hydrolysis of fatty acids from fats to help emulsify lipids for transport across the intestinal wall.

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chylomicrons

Back 16

where lipids are packaged; They move through the lymph system into the capillaries where they get stuck. The only lipoprotein complex to travel in the lymph system

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hypercholesterolemia

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leading cause of high blood cholesterol due to defect in LDL receptor. Genetic

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Statins

Back 18

inhibit HMG-CoA Reductase and reduce cholesterol by inhibiting its synthesis.

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Ezetemibe

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availble to block reabsorption of cholesterol in recycling

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atherosclerotic plaques

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These may form as a result of free radical (reactive oxygen) species which oxidize unsaturated fatty acids in LDLs. The immune system may attack these.

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Molecules cholesterol can synthesize

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bile salts (glycocholate and taurocholate, among others), which are useful in solubilizing fat in the diet. also leads to synthesis of the steroid hormones. These are derived from pregnenolone and include the glucocorticoids, mineralocorticoids, androgens, and estrogens.

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aromatase

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Derive estrogen from androgens This enzyme makes aromatic rings and is a target of chemotherapy

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Enoyl-CoA-isomerase (also known as Cletus)

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converts cis or trans bonds between carbons 3 and 4 to trans bonds between carbons 2 and 3.

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2,4-dienoyl-CoA reductase (also known as Wallace)

Back 24

reduces two double bonds (2-3 and 4-5) to 3-4.

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Oxidation of an odd number of carbons

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Forms propionyl-CoA; needs to be converted into succinyl-CoA

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Convertion of propionyl CoA to succinyl CoA

Back 26

1. Add a carboxyl group to the middle carbon on the molecule.
2. Two isomerizations
3. Movement of a methyl group that utilizes the cobalt ion in Vit B12.
4. Bam mother fucker- Succinyl CoA. It's magic, that's what's up.

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Ketone bodies

Back 27

ex. acetoacetate and hydroxybutyrate. They provide energy to keep the brain alive. The thiolase reaction in ketone body formation is the reversal of the same reaction that occurs in fatty acid beta oxidation.

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serum albumin

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Carry fatty acids in the bloodstream

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Glycerol

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is the only part of a fat that can be made into glucose (via gluconeogenesis)

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carnitine

Back 30

carry fatty acids into the mitochondria from the cytosol.

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Steps in fatty acid oxidation

Back 31

dehydrogenation, hydration, oxidation, and thiolytic cleavage

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dehydrogenation and oxidation reactions yield

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reduced electron carriers (FADH2 and NADH).

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hydration yields

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hydroxyl group on the third carbon from CoA end in the "L" configuration

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thiolase

Back 34

Catalyzes thiolytic cleavage

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acyl-CoA dehydrogenase

Back 35

come in three forms (specialized for long, medium, and short chain fatty acyl-CoAs)

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sudden infant death syndrome

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medium chain acyl dehydrogenase has been implicated in some instances

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long chain acyl dehydrogenases

Back 37

found in peroxisomes and this is where oxidation of long chain fatty acids (longer than 16 carbons) begins (not in the mitochondrial matrix) Oxidation in the peroxisomes involves transfer of electrons to oxygen to make hydrogen peroxide, instead of FADH2. Peroxisomal fatty acid oxidation is therefore LESS efficient than mitochondrial beta oxidation.

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Oxidation Steps

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1. generates a trans-intermediate plus FADH2
2.s addition of water across the trans double bond to create an intermediate in with an OH on carbon 3 in the L configuration
3.oxidation of the hydroxyl intermediate to a ketone on carbon 3
4.cleaving off of an acetyl-CoA and production of a fatty acyl-CoA with two fewer carbons. The last step is catalyzed by the enzyme thiolase.

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Trans fat

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arises from partial hydrogenation of unsaturated fats, not from regular metabolism of fatty acids.

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Acetyl-CoA carboxylase

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catalyzes the addition of a carboxyl group to acetyl-CoA to form malonyl-CoA

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citrate shuttle

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Acetyl-CoA gets into the cytoplasm from the mitochondrion by

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Malonyl-ACP

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"adding block" for fatty acid biosynthesis.

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Acetyl-ACP

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he starting block for fatty acid biosynthesis.

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elongases

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Synthesis of fatty acids longer than 16 occurs in the endoplasmic reticulum (or mitochondrion) catalyzed by

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desaturases

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Desaturation of fatty acids occurs in the endoplasmic reticulum and is catalyzed by this. Desaturases in mammalian cells cannot work further than 9 carbons from the carboxyl.

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linolenic acid (double bonds at 9, 12, and 15) and linoleic acid (double bonds at 9 and 12)

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must be obtained in the diet of mammals and are called essential.

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Prostaglandins

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made by arachidonic acid by prostaglandin synthase

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COX inhibitors

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Aspirin and ibuprofen are non-steroidal drugs (called NSAIDs) that inhibit COX-1 and COX-2

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COX-2 enzymes

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appear to have no role in stomach maintenance, so inhibitors specific to them were sought. Examples include Celebrex and Vioxx, but they also appear to have negative side effects on the heart.

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To make prostoglandins

Back 50

glycerophospholipids release linoleic acid in a reaction catalyzed by PLA2. Arachidonic acid is made from linoleic acid. prostaglandin synthase makes prostogladins from arachidonic acid.

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cyclooxygenases (COX)

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COX-1 and COX-2; both inhibited by aspirin and ib profin. Celebrex and Vioxx inhibit COX-2 but cause heart problems.

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PLA2

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catalyzes release of linoleic acid from glycerophospholipids. Inhibited by Corticosteroids

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Leukotrienes

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Produced from arachidonic acids; involved in mucus production and bronchial constriction and play important roles in causing asthma attacks; produced by the linear pathway.

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thromboxanes

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These molecules (like prostaglandins) help to make platelets "sticky", favoring aggregation. Thus, taking aspirin reduces synthesis of prostaglandins, which in turn reduces amounts of thromboxanes, which reduces stickiness of platelets, which makes it harder for blood to clot. It is for this reason that people prone to clotting problems are advised to take aspirin daily.

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Ribonucleotide reductase

Back 55

catalyzes the formation of deoxyribonucleotides from ribonucleotides. The substrates are ribonucleoside diphosphates (ADP, GDP, CDP, or UDP) and the products are deoxyribonucleoside diphosphates (dADP, dGDP, dCDP, or dUDP)