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201 Cards in this Set
- Front
- Back
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What is palmitate?
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The basic fatty acid w/ structure (16:0)
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Where does B-oxidation take place? FA synthesis?
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matrix
Cytoplasm |
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What do you remove during Beta oxidation? What do you add during FA synthesis?
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C2 unit- acetyl-CoA
C3 unit-malonyl-CoA |
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Draw the structure of malynyl-CoA
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1
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what is the purpose of malynyl-CoA in FA syntheisis? How does this happen
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provides an enolate, a reactive intermediate by losing a CO2
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What do you need to make palmitate?
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8 Acetyl-CoA
14 NADPH atleats 7 ATP |
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How do you get Acetyl-CoA from the mitochondria to the cytoplasm for FA synthesis?
Steps |
citrate transporter
1. add acetyl-CoA + OAA to make citrate 2. Tranport citrate 3. Disassemble citrate using ATP-citrate lysase to phosporylate the citrat then cleave it (requires energy) |
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what is the precursor for the components of the citrate transporter
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Acetyl-CoA and OAA are from pyruvate
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Why is citrate synthesis favorable?
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thioester cleavage in the last step is favorable
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What are the fates of malate?
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1. Reimport it w/ aspartate or OAA to make NADH
2. oxidatively decarboxylate it to pyruvate -this makes the CO2 for malonyl CoA and the NADH into NADPH (low E=FA synthesis) |
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What is Acetyl-CoA carboxylase?
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The biotin-dependent enzyme (similar to pyruvate carboxylase)that turns Acetyl-CoA to Malonyl CoA by adding a CO2 to it.
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Mechanism of Aceyl-CoA?
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2
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What activates acetyl-coA carboxylase?
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citrate
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What inhibits acetyl-coA carboxylase?
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palmityl-CoA and being phosphorylated (depolymerazes it)
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Systemically what stimulates the phosphorylation (inactivation) of ACC?
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low E compounds like glucagon and epinephrine via CAMP
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Signal integration/Hormones that affect ACC?
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Glucagon-hormone that causes glycogen to be degraded b/c there is low energy-inactivates ACC
Insulin-hormone that increases glycogen synthesis b/c of high energy- activates ACC Signal integration-Insulin gets rid of cAMP so that ACC can't be phosphorylated (inactivated) during high energy state. This stops fat making and breaking from occuring at the same time |
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What are the components of fatty acid synthase?
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flexible phosphopantetheline arm
8 enzymes (1 ACC and 2-8 on FAS dimer) |
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In fatty acin synthesis waht is the acceptor and what is the nucelophile?
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Acceptor: acetyl-coA
Nucleophile: malonyl-Coa |
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Steps of fatty acid syntehsis
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2 & 3: Turn acetyl-CoA and malonyl-CoA into Acetyl ACP and malonyl ACP w/ transferase
4: Condense acetyl coA and malonyl-CoA w/ Condensing enzyme to make acetoacyl-ACP 5: reduce the carbonyl furthest from the thiol to OH w/ ketoreductase 6: dedydrate so that OH falls of and double bond is formed 7: reduce so that double bond goes away Rpeat those steps until at C16 8: Thioesterlase (TE) hydrolysezes so that the palmitoyl ACP is released and then goes to palmitate |
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What makes palmitate into longer things (c18, c20, c22, ect..)
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ER- redident elongases
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How does ER (resident elongase)work?
What does this make |
Delta 9 desaturase introduces a cis- double bond
allows for 4e- reduction of H20 Makes essential fatty acids like: arachadonic acid (20:4) linoleic acid (18:2) -omega 6- only from diet -omega 3 |
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What is the amino acid catabolism cofactor?
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PLP (pyridoxial phosphate
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What do you have to get rid of to make glucose from amino acids?
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1 g nitrogen/ 3 Glc synthesized
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What are 2 ways to get rid of nitrogen on an amino acid?
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1. oxidative deamination
2. transamination |
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Why is transamination the better wayof getting rid of a nitrogen on an amino acid?
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there is no redox
no free ammonium (no pH change) consolidation of nitrogen- no variety |
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What is the oxidative deamination reaction?
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3
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What are the trasnamination half reactions?
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4
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What is the dunatahn hypothesis?
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says that the aa-PLP is the one perpendicular to the pi funcion which expalins the diversity of the system. B/c it is flat you can rotate it so the bond you want to break is in the back
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Draw the transamination mechanism?
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5
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Why is PMP wo stable when bound to enzyme?
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The H from the amino acid and the O from the PLP will always H bond, making it flat
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What is the purpose of transamination?
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to collect nitrogen into a small number of compounds
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What are the sources of ammonia (NH3)?
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1. oxidative deamination
2. amino acid oxidase 3. nitrogenase (from N2 fixing bacteria) |
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How is oxidative deamination (as a source of ammonia reculated?
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Enzyme (GluDH) is Active at low energy: ADP, NAD+, Leu
Inactive at high energy: GTP, NADH |
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What performs amino aid oxidases to make ammonia?
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kidney peroxisomes (trashcans)
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Why does nitrogenase require ATP
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to overcome the kinetic (not the thermodynamic) barrier
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What are the 2 tissue that are involved in the urea cycle?
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liver- turns ammonia (NH3) into urea
kidney- excretes urea |
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What is the role of carbamomyl phosphate?
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reactant in the urea cycle that reacts w/ ornithine to make citruline.
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What makes up carbamoyl phosphate?
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2ATP, HCO3, and NH3
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What are the two types of CP (carbamoyl phosphate) synthase?
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CPI: in mito chonrdria, NH3 donor for urea synthesis
CPII: in cytoplasm, Gln donor, for pyrimidine biosynthesis |
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what is the structure of carmoyl phosphate?
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6
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What are the 2 ways of using amino acids?
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1. Use the carbon skeleton to make alpha-keto acids that participate in the CAC
2. Use the ammonium to make carbamoyl phosphate to participate in the urea cycle |
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Why is energetically feasible to have the urea cycle and the CAC from amino acids?
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the 2 processes are linked by the arpartate agino succinate shunt of the CAC, where OAA is regenerated
Oaa made into fumarate in urea cycle Fumurate made into OAA in the CAC |
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What is the glucose alanine cycle?
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When pyruvate aculumlate in muscle, alanine is made. This alanine goes to the liver, loses and NH3, and glucose is made.
Just like the cori cycle (lactic acid) This is a methos of transporting Nh4 to the liver where it is made into urea |
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What did Garrod discover?
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one gene, one enzyme
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What is maple syrup urine diesase
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A dease that shows up postnatal (when babies loose acces to moms detox system).
Defect in alpha-ketoacid dehydrogenase complex: don't break down branched chain aa right. Therefore there is a build up of isoluecine, leucine, and valine. Treatment: vegetarian diet which is low in Ile and Leu |
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With PKU, how do we know that problem is not due to a deficiency?
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Different outcomes w/ different blocking at different stages shows that it is due to an accumulation
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What iss PKU?
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When you can't convert Phe into tyrosine so you make alpha-keto acids instead. Phe is oxidatively deaminated, making phenyl pyruvate, instead of oxidative deamination of tyrosine to make 4-hydroxylphenylpyruvate. Phenyl pyruvate causes myelin damage and gives mousy smell.
Treatment: avoid Phe in diet |
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Glucogenic amino acids?
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go thru pyruvate before being degraded
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ketogenic amino acids?
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go thru acetyl-Co A before being degraded
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What are anaplerotic reactions?
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reactions that make a citric acid cycle intermediate
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What is the most important metabolic decision a cell makes?
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converting pyruvate to acetyl-CoA
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What is the monomer of glycogen? How do you break it down? build it up? Hormone effects?
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G6P
phosphorylase glycogen syntase glucagon and epinephrine inhibit cAMP so that it is not made during low energy |
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What is the monomer of fat? How do you break it down? build it up? Hormone effects?
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acetyl-CoA
hormone synsetive lipase acetyl-CoA glucagon and epinephrine inhibit cAMP so that it can't be made during low E states |
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What is the monomer of Protein? How do you break it down? build it up? Hormone effects?
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amino acid
hormone sensitive lipase acetyl-CoA starvation and skeletal muscle protein affect it |
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Which processes take place only in the mitochondria?
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CAC and Ox phos
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Which processes take place only in the cytopasm?
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glycolysis, glycogen, PPP, FA synthesis
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Which processes take place in both the cyto plasm and the mitochondria?
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Gluconeogenesis, urea cycle (both more in cytoplasm), and aa catabolism
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What is the power source for making glucose?
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B-oxidation of fats in the liver, b/c it makes acetyl-CoA
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Describe the patway of using your energy during starvation
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glucose
glycogen fat: ketone bodies (b-hydroxy butarate_ |
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What is acyl-coA dehydrogenase?
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the enzyme used in the first step of B-oxidation of fatty acids
-there are 4 types: short chain, medium chain, long chain, and very long chain |
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What are the 3 ways of getting an MCAD deficiency?
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1.genetic (10% of SIDs)
2. Inducible: Jamaicain vomiting sickness when you ingest hypogluin A 4: Lacking L-carnantine the b vitamin |
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What is the role of L-carnatine?
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it is used to shuttle fats and help break it down. W/ out it there can be an acetyl co A defiriency
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symptoms of MCAD deficiency
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muscle weakness
abnormal liver fxn hypoglycemia organic acidura not enough energy b/ not enough free CoA: not enough acetyl CoA -no OAA -no FADH2/NADH acyl-carn in urine floppy/lethargic impaired ketogenesis (acetyl-coA generation) ONLY SEEN WHEN FASTING |
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What do CAT, canitine acyl transferase do?
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they take short chain FA that aren't being metabolized and release the CoA
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Treatment for MCAD deficiency?
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high carb/ low fat diet
L-carintine supplement |
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What is the basic structure of a purine?
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7
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What is X on a purine with adenine?
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NH2
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What is the X on purines for guanine?
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dbl bonded O
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where are purines made?
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cytoplasm
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what are the 2 distinct routes for making purines?
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salvage (start w/ a base unit)
Denovo (star w/ random pieces) |
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What are purines used for?
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nucleotides
making NAD and FAD |
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What is PRPP? configuration?
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a precursor of purines and pyrimidines
-it is in alpha configuration so the things made from it w/ SN2 reactions have beta conficuration (base up) |
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Basic steps for the purine de novo pathway?
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R5P + PRP make IMP
IMP make AMP or GMP |
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basic steps for purine salvage pathway
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Base + PRP makes product and PPi
uses HGPRT |
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what is HGPRT? what disease is associated w/ its deficicency?
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used in salvage rxns of bases
Lesch-nyhan diseases -increase uric acid -lack of soluble bases: gpit -self mutalating |
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what is the first regulated step of de novo purine (IMP) synthesis?
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PRPP to PRA
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know where each part of the purine ring comes from
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see slide 31-3
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What are antimetabolites?
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they stop DNA from being made b/c they act like purines or pyrimidines and don't allow DNA replication
(affect DNA more than RNA) |
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what is a metabolite?
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an intermediate in a miosynthetic pathway
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What is necessary for an anti metabolite to work?
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recognition by salvage, kiase, RNR, and DNA polymerase
It then provides negative feedback even tho none of the real base ahs been made |
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what are nucleosides?
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nucleotides w/ the R5P analogs (modified)
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What regulates purine synthesis
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-amount of purine you need
-neg. feed back that controls the composition, post IMP. Need a balanced ppol to avoid mutagenesis |
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What are two things that use the salvage pathway a lot (not purines)?
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parasites (exclusive)
cancer cells ( try to take preformed purines from environment) |
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which purine synthesis pathway requires more energy?
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de novo pathway
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what does the pase of a pyrimidine look like?
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8
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What is X on a pyrimidine w/ cytosine?
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NH2
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what is X on a pyrimidine w/ uracil?
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dbl bond O
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What is the purpose of glutamine in UMP (pyrimidine) synthesis?
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provides an amonia source
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What is the role of CPS II in pyrimidine biosynthesis?
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it does the 1st step (regulated) making carbamoyl phosphate
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Why are there different enzymes in pyrimidine synthesis?
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prevents metabolite loss- different active sites w/ out diffusint into solution
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How is pyridine synthesis regulated?
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CTP inhibits step 2,, but only in bacteria b/c animals need to do step 2 to make urea
-CUDO and CUTP inhibit step 1 in animals |
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What is the role of RNR?
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Last step in making bases ready for DNA.
Reduces the DNP to DNA w/ its disulfide bone chemistry providing the electrons to pull off the 2' OH (reduce) |
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What is the RLS in DNA replication?
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RNR
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What regulates RNR?
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the cell cycle
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What is responsible for having a balanced DNA pool size to avoid mutagenesis and allow repair?
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RNR
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what "type of chemistry does RNR do?
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radical chemistry
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What activates RNR at the activity site? at the spefificity site?
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1. ATP
2. ATP, dATP, dGTP, dTTP, other nucleotides |
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What inactivates RNR?
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dATP at the activity site
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Know how RNR works
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slide 31-7
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What type of mutation at the active site damages RNR?
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any mutation
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how do you keep RNR from reducing anything around?
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the radical is store off site. R1 is active site and R2 is storage site
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How can you inhibit RNR
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put in things that react w/ radicals and will penetrate to protiens
-Hydroxy urea: gets rid or radical storage and makes NO, sensitizes cancer cells to radiation/drugs b/c it can't replicate or repair DNA |
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What is the magic bullet?
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a compound screened for that can kill the desired microbe
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what is salvarsan?
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a arenical magic bullet
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what is melarsoprol? What do they treat? How do they work?
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a more modern aresnical
-used against late (CNS) stage sleeping sickness, which is caused by tyranosames/trapanosomes -looks like purines so they are uptaken by trapansomes b/c trapansomes are dependent on purine salvage |
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What are trapanosomes?
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protist that look likethey are closely related to algae
-have many plant like genes, but no plastids - they have modified peroxisomes called glycosomes |
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What do trapanasomes do with glycolysis?
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they compartementalize it so it is not so risky, but it leads to glycosomes enzymes being unregulated
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What is the net consumption of ATP and NADH by glycosome w/ trypanasome metabolism?
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0 for both
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How does melarsamine work?
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it binds to the 1 cistine near the active site of GAPDH, replacing the thiols and blocing the fxn
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What do glycosomes contain that make it have the metanolism of a plant?
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-soluble NADH dependent fumarate reductase
-pentophosphate enzymes -sedoheplalose biphosphate(calvin cycle) |
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Why is glycolysis of trypanasomes supercharged?
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if there is enough E, then it expoerts 13BPG provinding 2ATPs to cytoplasm and imports the PEP needed to pay form the investment
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Why is melarsamine toxic for people?
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it blocks thiol entermediates, and we have some too
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What is eflouritine?
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blocks the gumbiense form of sleeping sickness
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What is protosil (basic)?
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the first antimetabolite prodrug
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what is an antimetabolite?
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it fools a pathway into doing a random/wrong step, potentiating the toxicity of a drug
-it has to be recognized by the pathway and the target |
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what are prodrugs?
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they are metabolically activated to reveal the reall drug
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How does prontosil work?
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it inhibites folate synthesis, making it selective for backteria.
Does this by reducing across the azo bond to a sulfanilamide, so that PABA is no longer attached and it can't extend |
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What does prontosil work against?
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pieperal fever (pregnant women)
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what is cytochrome p450
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a liver enzyme that inactivates a lot of drugs
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what is the main reaction of cytochrome p450
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9
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What activates cytochrome p450
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steroid hormones
xenobiotics some drugs (phenobarbitol-has an effect on many drugs) |
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what makes drugs have a longer 1/2 life, making p450 harder to work on them?
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putting a flourine on it, which raises the oxidation potential
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what is hiphenzime?
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a drug for psychotic conditions, w/ its metabolism controlled by P450
-In order to make it stay around longer, an OH is added to it raising its oxidation potential |
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How is combination chemotherapy used to block folate biosynthesis?
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use the synergy of sulfur blocking step 1 and hinetheprim blocing step 3
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What is the function of thymidylate synthase?
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It takes dUMP and N, N methylene THF and makes THF and folate for DNA synthesis and repair
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how is thymidylate synthase targeted?
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5FU antimatabolite is activated by PRP to make FdUMP instad of dUMP. FdUMP is a suicide substrate for TS, but the toxic effects are getting rid of folate which is neceesary to make DNA
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Mechanism of thymidate synthesis
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32-7
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Which 2 enzymes are in charge of recycling folate
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-DHFR (dihydrofolate reductase): reduces DHF to THf
-SHMT (serine hydroxylmethyl transferase): PLP enzyme thad uses formaldehyde |
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What is MAT?
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an enzyme that blooks DHFR by looking like DHF but binding tighter, blocking folate synthesis
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what is the order for giving 5Fu and MTX?
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give 5Fu 1st, works better b/c there is more PRP being made into FdUMP, so TS is even more inhibited
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What does MTX do?
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it inhibites purine biosynthesis so there is a rise in PRPP
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What are the functions of F in drugs?
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1. block p450 action: longer 1/2 life
2. Block H+ elimination (FdUMP) 3. Good LG 4. Hydroxyl mimic ( very small) |
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What is triflouridine?
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herpes topical drug
WHAT ELSE SHOULD I KNOW ABOUT IT? |
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What is cytarabine?
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a nucleoside analog that is a DNA chain terminator. Leads ot DNA damage and can be used to target cancer
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What is leukemia?
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a blood disease where very immature cells proliferate in the marrow
There kill normal RBC They enter the circulation and destroy the organs |
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What is the role of adenosine deaminase? What happens when there is a deficiency?
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It turns adenosine into inosine
-deficiency causes to few WBC b/c it maked dATP which inhibits RNR so that WBC die |
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Which is more toxic 2-F0adenosine or clofarabine?
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2-F-adenosine b/c the 2' OH is harder to cleave
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What are the steps/mechanism of action of clofarabine?
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1. enter cells
2.gets phosphorylated by DCK so that it is trapted in the cell 3. Inhibits RNR -binds to allosteric site lowering dCTP and dATP unballencing the nucleotide pull -depresses the inhibition dCK b/c synthesis of compounds that inhibited it are inhibited: potentiates its own phosphorylation 4. Inhibit DNA repair by being incorporated (less than dATP 5. Inbibit DNA replication as an elongation terminator ( more than dATP) 6. relases cytchrome from mtio, telling cell that something is very wrong |
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What drugs do cannabouds come from? what are they good for? what are their main problems?
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Marijauna
chronic pain intoxication and hypomotility |
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What was the process of identifiying THC, the agonist for cannaboids?
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againoist (THC) to
receptor (CB-cannaboid)to licand (-natural ligand-endocanaboid) |
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what is different about nonpsychotic analogs of cannaboids?
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they don't bind to the ceceptor
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how can you ffind out the natural ligand (AEA) of a canaboid?
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radio label the ligand and see if it is displaced
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which, antagonist or aganoist, always have to look like the ligand?
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agonist
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How is AEA made?
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phospholipase D cuts the longer product at the phosphate bond and releases AEA
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What is the parter of AEA?
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AG
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Where is AEA/EAG broken down? How?
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it is taken up bly glial cells then degraded by glial cells
-part of the functionality is removed, turning it into AA then FAAH 9ser protease) cleaves AA and AEA |
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How can you keep CBs around longer?
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block the FAAH protease so it isn't degreade
Block the inhibitor that transports it to glial cells so it can't be degraded |
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what is rimonabant
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A drug that inhibits CB2, which makes one not want to eat (discovered by doing the opposite of marijuana/CBs)
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What are the 2 CB recptor subtypes?
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CB1- brain, testis
CB@- peripheral (many immune cells) |
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What are eicasanoids?
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signaling molecues derived from fatty acids.
they give local effects b/c they are chemicaly unstable |
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Describe the derivation of fatty acids?
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1. Fatty acid (ie linolate) has an Arachnoic Acid in it
2. The AA is cleaved from the center of the glycerol 3. The free AA is metabolized by COX or LOX |
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What to eicosanoids PGE/PGE2 do?
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joint inflammation in arthritis
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What eicosanoids are COX products? What do they effect?
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Prostacyclins- vascular endothelium
Prostaglandins- all tissue ( alter [cAMP] Thromboxames- platelet aggreagation (clotting) |
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What are eicoasanoid LOX products? what do they effect?
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Leukotraines- muscle contriction (asthma)
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what is the intermediate inbetween AA and making COX products?
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PGH2
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What is PGHS? What inhibits it? What is the effect
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Enzyme that converts AA to PGH2
-Asprin -Stops all Cox products and more LOX products are made. This can cause aprin induced asthma |
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How are all effects of eicosanoids mediated?
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-G protein coupled receptors
membrane-mediated effects |
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What does PGI2 do? What is the problem w/ PGI2? How has it been solved?
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-Blocks platelet aggregatio
-short half-life b/c supsceptible to acid catalyzed hyrdolysis -make analogs w/ longer half lifes, by making dbl bonds to triple bonds, lowering the e- density |
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What is a contractile bioassay?
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-drip blood/product over a muscle and see if it contrsits or relaxes
-see what happens on next muscle to see if product is made -good for looking at short 1/2 life compounds |
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What are the 2 forms of PGHS, the membrane associated enzyme? What does each form do?
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COXI form:
-constitutive expression -makes prostagalndids that block stomach lining (need this!) COX 2: -Inducible expression -Responds to inflammatory stimuli ( want to stop this) |
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When when are using a COX 2 selective inhibitor, do we want the (COX2/COX1) ration to be large or small?
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small
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What are the stages in Drug Discovery?
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1. Lead Discovery- often natural product
2.Lead Modification 3. Target Validation 4.Drug-Receptor Interaction 5. Drug metabolism studies (increase potency) |
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When modifying the lead in drug discovery (step 2) what should one do?
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1. identify parmacophore/active part
2.structure-activity studies 3. increase potency |
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When one is validating the target (step 3) in drug discovery, what should one use as help?
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1. hints from deficiencies
2. genome sequencing 3. processes that are missing in humans |
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When one is studying drug recceptor interaction (step 4) in drug discovery, what should one consider?
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1. complex of drug bound to receptor (XRAY)
2. antagonist or agonist? 3. irreversible or reversible |
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What is an agonist?
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increase the activity of something
looks like the ligand |
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What does an antagnoist do?
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Prevents binding/receptor activation
-doesnt have to look different -does not change the % activity |
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What does an inverse agonist do?
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Decreases % activity
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What are antacids?
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stomach acid neutralizes
they are neutransmitters from amino acids that are all precursors from one another |
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What is histamine
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a neurotransmiter that regulates some stomach activity
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What is H. pylori infection?
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it causes peptic uclers
acid secretion increases ulceration |
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What are the 2 sub types of histamine receptors?
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H1: hyprsensitivity to immune insult (give you allergies)
H2 receptors: secretes gastric acid (bad when you have ulcers) which each have an agonist and an agtagonist |
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What is cimetidine?
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An H2 antagonist of histamine, ulcer medication
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How was the lead compound of cimetidine (H2 antagonist) made more potent?
What problem did this cause? How was it solved |
-add a dbl bonded S near end
-put an H on one of the nitrogens -The pKA was increased :{ -Add a CH3 to solve the pKA problem |
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What does cimetidine do? What is it working agains?
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-it regulates (lowers) gastric secretion of the parietal stomach cells
-H/K ATPase, Cl- transporter, and HCl secreted into lumen all activate stomach acid |
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What kind of side effects does Omeprazole/cimetidine have? Why
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none b/c it only effects the parietal cells
-It is trapped in the cell due to the permanent positive charge |
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What would you do to the dosage of a omeprazole if they have less cyt P450?
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decrease the dosage b/c cyt p450 is in charge of degrading omeprazole, so the omeprazole in these people have a longer half life
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which form of omeprazole is better for people?
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the S form
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Which drug is a self trapping agent?
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omeprazole
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What are the steps of sending cholestero throught the body?
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1.In small intestines and chylimicrons carry it to the liver
2. Liver cleaves it into esters 3. enters blood as VLDL 4. Changes to LDL (bad form) 5. Passes thru LDL receptor to peripheral tissue 6. Extra LDL is exported as HDL 7. back to liver |
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What are bile salts and what do they do?
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They are degraded cholesterol from liver that are passed to gall bladder then to small intestine to emulsify food
They are ether excreted or reuptaken |
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What makes cholestor not from diet? by what pathway?
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Acetyl-CoA by the de novo pathway
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what do we need cholesterol for? where is it made?
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making membranes
In the ER |
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What controls the concentration of blood cholesterol?
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LDL receptors. More are displayed when peripheray needs cholesterol more
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What is the role of ion exchangers?
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they soak up bile salts and get rid of them, decreasing LDL by only 15%
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What type of genetif disorder is Familia Hypercholesterolemia? What is the result? What causes it? Treatment?
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autosomal dominant
High blood cholesterol, always making it LDLR mutations -Liver transport (statins only work w/ a functional LDLR) |
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What is HMG-CoA reductase?
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the enzyme for the RLS in the synthesis of cholesterol
it is derived from acetyl-CoA |
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What are statins?
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They inhibit HMG-CoA reductase, which makes cholesterol
-also increases the activity of LDLR receptors so that blood level cholesterol is decreased |
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What does the use of antibiotic invariabily lead to?
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resistance
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What 2 types of ammunity are there?
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natural
acquired -point variants -mobile genetic elements |
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What helps to beat resistance to antibiotics?
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combination therapies
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What are the validatide targets of antibiotics (5)
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1. cell wall biosynthesis
2. protein biosynthesis (macrolides) 3. DNA/RNA replication 4. Golate metabolism 5. isoprenoid biosynthesis |
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What is the main intermediate in the HMG-CoA reductase pathway?
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mevalonate
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How is IPP formed?
What is it sued for? |
From acetyl-CoA w/ melvanoic acid
-to make terpenes (whcih make steroids |
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What is DMAPP formed from?
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melvonic acid pathway and DXP oathway, link btween plants and animals
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What causes malaria?
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plasimodium palciparum a protozoan that is a primitive eukaryote
-hase an organelle called an aplicoplast that is derived from plastid |
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What is aplicoplast?
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genome essential for parasitiv survivval
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What pathway does malaria use?
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DXP pathway
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What prevents malaria?
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Chloroquine: resistance is spreading
Fosmidomycin: not on the market yet, inhibits the DXP pathway |
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What does the DXP pathway lead to the formation of? Where does it take place? Who uses it?
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DMAPP and IPP
Plastids Plants and bacteria |
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What does the melvonate pathway produce?
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DMAPP and IPP
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