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51 Cards in this Set
- Front
- Back
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Explain the steps of Fatty Acid synthesis... What is the total equation (reactions-->product)
Name the enzymes involved with FA synthesis... (5) |
1. Acetyl CoA synthesis
2. Conversion of Acetyl CoA from Malonyl CoA 3. Elongation of FA 8 Acetyl CoA + 7 ATP + 14 NADPH --> 1 Palmitic acid a. (PC) Pyruvate Carboxylase b. (PDH) Pyruvate dehydrogenase c. Citrate ligase d. (ACC) Acetyl CoA Carboxylase e. FA (fatty acid) synthase complex |
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Details about Acetyle CoA synthesis (enzymes, location)
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1. after pyruvate is made from glycolysis it is taken into Mitochondria and either reacts with PDH (pyruvate dehydrogenase) or PC (Pyruvate carboxylase)
2. Reaction with PDH makes Acetyl CoA and with PC makes OAA 3. OAA and Acetyl CoA combine to make citrate, which then leaves mitochondria 4. Citrate reacts with citrate ligase to make OAA and Acetyl CoA |
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How is malonyl CoA made from acetyl CoA what process is it used in?
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Second step (and rate limiting step of Fatty acid synthesis)
1. Acetyl CoA Carboxylase (ACC) enzyme is added and it takes away a carbon and makes Malonyl CoA |
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How does elongation of Fatty acid occur after Malonyl CoA was converted from Acetyl CoA? Is there an instance that elongation might continue? (where?)
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each Malonyl CoA (2 carbons) are added on to the Fatty acid chain at the Fatty Acid synthase complex until Palmitic Acid (c16) is made initiates negative feedback on Acetyl CoA
-- elongation might continue if it were in the brain (catalyzed by FA elongase) |
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What regulatory roles does acetyl CoA have in FA synthesis? (stimulation, inhibition)... What does insulin in the body have to do with FA synthesis?
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1. Self regulated controls total amount if citrate formed.
Stimulates- PC Inhibits- PDH... (since PDH makes acetyl CoA you can see the self inhibitory status of Acetyl CoA) 2. Insulin Stimulate- PDH to create more Acetyl CoA Upregulates- synthesis of citric ligase and malic enzyme (creates pyruvate) |
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Describe the regulation of Acetyl CoA's conversio to malonyl CoA...
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Allosterically regulated--
1. Citrate- promotes activity 2 Palmitoyl CoA inhibits activity 3. Must be dephosphorylated (take away ATP) (insulin dephosphorylates) 4. Glucagon and Epi phosphorylate Induction/Repression A high carb/low fat diet up regulates ACC |
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Describe the regulation factors involved with FA elongation...
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Allosterically regulated
1. Phosporylated sugars activate (G6P, F6P) 2. FA synthesis occurs during fed state 3. Induction and depression during famine state |
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What is the fate of Fatty Acids after they are synthesized?
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converted into TAGs (triacylglycerol)
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Explain the process of desaturation of palimitic Acid... and what are the parts necessary?
What does "essential fatty acid" mean and what are two? |
Process of making double bonds onto fatty acid to be used else where in the body. Most fatty acids double bond at either 4,5,6, or 9 C's and can not go passed 9. Done in the ER using
1. Fatty acyl CoA desaturases 2. NADH 3. Cytochrome B5 Used to make PUFAs (polyunsaturated fatty acids) Essential fatty acids are the fatty acids that are essential that are not made in our body... 1. Linoleic acid 2. Linolenic acid |
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Describe the way in which TAGs are made from fatty acids...
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Two routes that this could go down....
1. Glycolysis creates DHAP during process in cytoplasm.... DHAP is converted to G3P from enzyme (glycerol phosphate dehydrogenase). --- Second route is more common simply taking the glycerol made in the liver and with enzyme (glycerol kinase) making G3P. Now, we add two fatty acetyl CoA's and that gives us Phosphatidic acid, and then the Phosphate leaves we have diacylglycerol. From there we add yet another acetyl CoA fatty acid and BAM!! TAG! |
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What happens after TAGs are made?
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TAGs are packaged with apoproteins and creates VLDL (very low density lipoproteins) which are secreted into the blood and help with cell membranes/cholesterol in membranes
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Depending on Fasting or Fed (after meal immediately) what is role of LPLs (lipoprotein ligases)?
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Regardless of stage LPLs will have the same role it is simply a matter of how much the adipose cells secrete..
Higher insulin/glucose ratio the more LPLs are secreted... LPLs 1) break down TAGs and VLDLs into FAs and glycerol |
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What are the two major regulatory factors of adipose tissue?
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1. Leptin
2. Adiponectin- most abundantly secreted |
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What is roles of adiponectin in FA synthesis?
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inhibits FA synthesis (during fasting state) increases FA degredation and glucose uptake by binding to
1. AdipoR1,R2 which stimulates a. AMPK/PPAR-a both degredate FA and only AMPK also does glucose uptake |
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What is the regulatory role of Leptin?
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Leptin is released from adipocytes and goes to brain sending "I'm full signals" to your hypothalamus... if controlled we will be able to allow better dieting
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What is the metabolically committed step in glycolysis? (enzymes/products)
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2nd of 3 irreversible steps
1. F6P --> F1,6BP (Fructo 1,6, bisphosphate Uses phosphofructokinase (PFK) (key in regulation of metabolism... i.e. commited step catalyzer) |
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Why does the brain, muscles, and red blood cells use glucose but the liver doesnt (as a primary energy source)?
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Liver stores glucose and release it when levels are down
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What enzymes catalyze the 3 irreversible reactions in glycolysis?
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1. Hexokinase
2. Phosphofructokinase 3. Pyruvate Kinase |
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What reaction in glycolysis produces NADH?
What are the monosaccharide units of Lactose and Sucrose and how do they enter glycolytic pathway? |
G3P--> 1,3BPG using G3PD (glyceraldehyde 3 phosphate dehydrogenase)
Lactose- Galactose is converted to G6P Sucrose- Fructose (from adipose) is converted to F6P Fructose (from liver) is converted to G3P |
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Explain the PPP (pentose phosphate pathway), what are its products and phases...
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Process that produces
a. NADPH- to be used in FA synthesis b. pentoses (5-carbon sugars)- to be used in building blocks for RNA/DNA In 2 phases: 1. Oxidative- Ribose and NADPH 2. Nonoxidative- synthesis of 5-carbon pentose |
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How is PPP and glycolysis regulated?
What occurs is there is a G6P dehydrogenase deficiency? |
PPP- controlled by amount of NADPH...(if high then G6P channeled into glycolysis after G6P dehydrogenase is inhibited)
Deficiency- causes hemolytic anemia due to low level of NADPH in RBCs |
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What is the point of gluconeogenesis and glycogen metabolism?
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To keep serum glucose levels normal
If low- glucose from liver glycogen is released If high- glucose is made into glycogen in the liver |
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If we think of gluconeogenesis as glycolysis backwards... what are the 4 enzymes needed to avoid the irreversible ones from glycolysis?
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1. pyruvate carboxylase
2. PEP carboxylase 3. Fructose 1,6 bisphosphate 4. Glucose 6-phosphate |
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What is the role of pruvate carboxylase both during gluconeogenesis and citric acid cycle?
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During
1. Gluconeo- pyruvate to OAA to be transported to cytoplasm via Malate Shuttle 2. Citric Acid Cycle- precursor to OAA |
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What is the role of skeletal muscle/lactate in gluconeogenesis?
What is process called? |
Lactate produced from muscle is converted to pyruvate and transferred as an AA (analine) to the liver... and then converted back to pyruvate where it can be used to make sugars
Called Cori cycle |
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What is unique about the liver that allows it to release glucose and not most other tissues?
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Has enzyme G6P which allows the release of 6P (also located in kidney, intestines.)
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Describe the structure of glycogen and its function...
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highly branched polymer which is the stored form of glucose...
Function is to maintain blood glucose level needed by the brain and other tissues, it provides glucose for muscle activities |
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What 4 enzymes are involved in glycogen degredation (glcygenolysis)?
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1. Glycogen phoporylase
2. Transferase and debranching enzyme (alpha-1,6 glucosidase) 3. Phosphoglucomutase 4. Glucose-6 phosphatase |
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What is the reactions and final products of glycogen degredation?
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There are basically 4 steps
1. Glycogen is phosphorylized glycogen--> Glucose 1 - phosphate + (Glycogen n-1 residue) 2. Transferase and debranching enzyme (a 1,6 glucosidase) Glycogen (n-1 residue) --> Glucose-1-phosphate + Glycogen residule 3. Phosphoglucomutase enzyme Glucose-1-phosphate --> glucose-6-phosphate 4. Glucose- 6 phosphatase G6P-> glucose |
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What enzymes are used to make glycogen (glycogen synthesis) from Glucose -1phosphate?
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1. UDP-1 pyrophosphorylase
2. Glycogen synthase 3. Branching enzyme |
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Describe the steps (reactions + enzymes) for glycogen synthesis...
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1. UTP + glucose-1-phosphate--> UDP-glucose + PPi (UDP-1pyrophosphorylase)
2. UDP-glucose + glycogen --> Glycogen + UDP (glycogen synthase) 3. Glycogen --> Glycogen more branched Branching enzyme takes away 1,4 and makes 1,6 |
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In general explain Insulin, Epi, and Glucagon's roles in reguatlion of blood glucose levels...
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1. Insulin- dephosphorylation and stimulates glycogen synthesis and FA synthesis
2. Epi- Phosphorylation and stimulates glycogen breakdown in skeletal muscle and liver 3. Gluc- phosphorylation and strongly stimulates glycogen breakdown in liver |
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What Glycogen Storage Disease and name has the following deficiency:
a. Glucose-6- phosphatase or Glucose 6- phosphate in liver only b. a(1,4) glycosidase in lysosomes |
a. I Von Gierke's-
Inceases: liver size, lipids in blood, glycogen in liver, lactic acid Decreases: blood glucose, pH, b. II Pompe's- lysosomal (only one), leads to cardiac failure, nerve and muscle damage |
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Describe the following terms...
a. snRNA b. miRNA c. siRNA |
a. (small nuclear RNA)- combine with proteins to make spliceosomes-- which are proteins involved in the editing process of mRNA to make mature mRNA
b. microRNA- naturally occuring RNA that inhibits translation of mRNA or initiates degredation c. small interfering RNA- Same is (b) but not natural |
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Describe the following terms...
a. promoter b. TATA box c. cistron |
a. a sequence of nucleotides that direct the polymerase to initiation site so transcription can occur
b. are of repeats of Thymin and adenine that also serves as recognition site for polymerases (inside promoter region) c. the sequence being translated of mRNA... (Eurkaryotic cells are monocystric) |
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Describe the following terms...
1. snRNP 2. What disease is caused by a mutated B-globin mRNA splice site, meaning certain spliceosomes can not recogonize what to splice and what not to splice? 3. What disease or cause of disease inhibits mRNA polymerase II? |
1. recognize splice sites of introns and assemble into splicesomes which remove introns and ligase exons together
2. B-Thallasemia 3. Anita phalloides- "Death cap" poisoning |
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If your body had an antibody that recognized snRPS as foreign what would happen... and name of disease?
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interfere with the processing of snRPS and therefore cause problems in mRNA processing... called Systemic Lupus Erythematosis (SLE or Lupus)
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Describe the classes of Eukaryotic RNA polymerases and roles...
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1. RNA polymerase I- makes rRNA [5.8S, 18S, 28S]
2. RNA polymerase II- makes mRNA 3. RNA polymerase III- makes tRNA and 5s rRNA |
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Describe the prokaryotic RNA polymerase...
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has a core enzyme 4 subunits (2a, B, B')
Also has 2 dissociable subunits a. sigma- initiation of transcription b. rho- termination of transcription |
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Describe in detail the three types of point mutations...
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1. silent mutations- codon changes but amino acid does not
2. Missense mutation- change in codon codes for a different amino acid 3. Non-sense mutation- when codon is changed to a stop codon which causes a premature stop |
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Describe in detail three types of mutations other than point mutations...
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1. Insertion- involves the addition of one or more codons inserted
2. Deletion- loss of one or more bases in code for a gene 3. Frameshift mutation- causes a complete change in the code due to change not occuring in multiple of three |
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1. How is protein synthesis activated?
2. How are the amino acids of this process activated? (2 steps) |
1. tRNA attaches to AA to activate a complex called aminoacyl-tRNA
2. 2 steps both catalyzed by aminoacyl tRNA synthetase-- (Activation and Transfer steps) a. AA + ATP <-> Aminoacyl-AMP + PPi t. Aminoacyl-AMP + tRNA <-> Aminoacyl-tRNA + AMP |
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What is the significance of peptidyl transferase site on ribosomes?
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site for peptide bond formation on the larger ribosomal subunit
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What are the basic steps of initiation in translation?
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1. Initiating codon in mRNA is usually AUG, indented from the 5' side
2. AUG codes for methionine (met) 3. Initiation begins at P site and A is free |
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Describe briefly the process of elongation in translation...
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Very tedious one codon at a time till stop codon coded. Uses GTP for each peptidyl transferase used to make peptide bonds, and GTP for translocation and EF's
1. empty A site is aligned with a triplet codon on mRNA 2. proper aa-tRNA occupies the A site by binding to mRNA codon 3. After use of GTP and Elongation factors, peptide bond forms betwen the C end of the peptide at P site and a-amino group of the new AA at the A site. 4. Formation of bond catalyzed by petidyl transferase (RNA enzyme) 5. Translocated from A site to P site |
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Briefly describe Termination...
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1. PRF's (protein release factors) recognize stop codon and bind to it at A site.
2. Alters peptidyl transferase's confirmation which causes peptide chain to be released from tRNA at P site |
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Describe the processing events involving folding and chaperones
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1. folding- occurs immediately after proteins leave ribosomes on N-terminal end... process is mediated by chaperone proteins
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Explain how post translation modifications occur in peptides... (specific examples)
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Long chains can be excised from end or middle of polypeptide that end up converting previous form from inactive to active... 1) proinsulin-- insulin
2) Pepsinogen to pepsin |
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Where do proteins go after they are made?
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1. made in polysomes of cytosol often stay there
2. Some of those go to specific organelles 3. Some are made on ribosomes in RER and go into subcellular organelles 4. Some from RER are exocized through Golgi and secretory vessel |
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What are the roles of the glucose transporters... (i.e. GLUT 1 and 3), GLUT 2, and GLUT4
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1. GLUT 1,3- most cells (continuous), and has high affinity
2. GLUT 2- a. pancreas and liver b. low affinity (uptake only during high serum level of glucose) c. Uptake of glucose in Pancreas release insulin 3. GLUT 4- a. Muscle and fat b. intermediate affinity c. Insulin mobilizes receptor to surface, increasing glucose uptake |
