Term
| Which organisms are capable of photosynthesis |
|
Definition
|
|
Term
| basic structure of the chloroplast |
|
Definition
is analogous to mitochondria
has a porous outer membrane, innermembrane space, inner membrane and stroma (similar to mitochondrial matrix) |
|
|
Term
| where photosynthesis takes place in chloroplast |
|
Definition
|
|
Term
| relationship between wavelength and energy |
|
Definition
| Shorter wavelengths = higher energy |
|
|
Term
| general types of photoreceptors and how they are able to absorb light at different wavelengths |
|
Definition
chlorophyll
carotenoids
phycocyanin
the different structure of the photoreceptors allows them to absorb different wavelengths |
|
|
Term
| How photon absorption takes place |
|
Definition
Absorption of photon promotes delocalized electron to excited state (higher-energy orbital). This high energy state makes it every unstable and so the electron returns to the ground state by 4 mechanisms:
loss as heat, emitted as light (fluorescence) exciton transfer and photooxidation |
|
|
Term
| 4 mechanisms for returning to the ground state |
|
Definition
energy given off: loss as heat, fluorescence
energy transfer: exciton transfer, energy is directly transferred to another molecule and photooxidation, an alectron from the excited molecule is transferred. Both of these are used during photosynthesis |
|
|
Term
| general arrangement of the light harvesting complexes in association with the reaction center |
|
Definition
| Those that absorb higher energy photons are on the outside and those that absorb lower energy on the inside – so that the energy is passed from the outside to the reaction center on the inside |
|
|
Term
| general structure of these light harvesting complexes |
|
Definition
| proteins carrying photoreceptors |
|
|
Term
| the arrangement of the complexes involved in photosynthesis |
|
Definition
| PSII -> cytochrome b6f -> PSI |
|
|
Term
| Order of electron transfer in photosynthesis |
|
Definition
| PSII -> pheophytin -> plastoquinone -> cytochrome b6f -> PSI -> Ferrodoxin -> NADP+ reductase |
|
|
Term
| what donates the first electron during photosynthesis and why |
|
Definition
| Water donates an electron to the P680 molecule of photosystem II to replace the electron that it lost when a photon of light strikes it. |
|
|
Term
| nature of the chlorophyll centers of PSII and PSI |
|
Definition
Both photosystems have 2 chlorophylls each
PSII: is associated with P680 meaning its absorption max is at wavelength 680
PSI: is associated with P700
Electrons flow spontaneously from low to high reduction potentials |
|
|
Term
| why the absorption of light is essential to electron transfer |
|
Definition
| excitation of the reaction centers by light drives a series of redox reactions |
|
|
Term
| what happens to replace the electrons lost in transfer from PSII and PSI |
|
Definition
| water is split. Uses a manganse catalyst to extract electrons from water to form O2. A tyrosine radical transfers the water-derived electrons to P680+ |
|
|
Term
| flow of electrons through cytochrome b6f – the PQ cycle |
|
Definition
| is similar to the Q cycle. Final acceptor is plastocyanin |
|
|
Term
| understand the differences between cyclic and noncyclic electron flow and the relevance of each |
|
Definition
Noncyclic: Electrons donated by plastocyanin are transferred to ferredoxin and used to reducde NADP+.
Net result: Electrons are transfered from water, through Photosystem II through cytochrome b6f, PS I, and then to NADP+
4 electrons from water are transferred, 8 photons absorbed, 2 NADPH are produced, 8 protons are pumped for each O2 molecule
Cyclic: Electrons from PSI do not reduce NADP+ but return to cytochrome b6f, then transfered to plastocyanin, and back to PSI to reduce P700* which produces a proton gradient. 2 protons are pumped? Requires light energy at PSI not PSII |
|
|
Term
| why noncyclic flow is called the Z scheme |
|
Definition
| Electrons follow zig-zag pattern with regard to reduction potential. Pattern is due to P680 being excited to P680*, P680* donating electron which will eventually get to P700 at a higher reduction potential, which excites up to P700* (at a lower potential) |
|
|
Term
| main differences between photophosphorylation and oxidative phosphorylation |
|
Definition
The production of ATP using the energy of sunlight is called photophosphorylation.
Oxidative phosphorylation: This phosphorylation is powered by redox reactions in which the electrons from food are transferred to oxygen which builds up a proton gradient to make ATP |
|
|
Term
| Principles of ATP synthesis |
|
Definition
o Proton gradient used to phosphorylate ADP
o Photophosphorylation since involves photosynthesis
o CF1CF0 complex
Analogous to F1F0 ATP Synthase (C = chloroplast)
Transfers protons from lumen to stroma side (inside to outside)
o Proton gradient both chemical and electrical
Electrical diminished by flux of magnesium and chloride ions |
|
|
Term
|
Definition
Carbon fixation, Reduction, Regeneration
Products of carbon fixation: ribulose-1,5-bisphosphate is split and 2 molecules of 3-phosphoglycerate result
Net reaction: 3 CO2 + 3 ribulose-1,5-bisphosphate -> 6 (3-phosphoglycerate)
Products of reduction: 1,3bisPG results and Bisphosphoglycerate reduced to Gly-3-P
Net reaction: 3-phosphoglyerate -> Gly-3-P
Products of regeneration: 5 molecules of Gly-3-P are converted into 3 molecules of Ribulose-5-P which will eventually become Ribulose-1,5-bisphosphate
Net reaction: 5 molecules of Gly-3-P used to make 3 molecules of ribulose-5-P and 1 molecule of Gly-3-P can be converted to other metabolites |
|
|
Term
| Why is the calvin cycle called dark reactions? |
|
Definition
| Doesn't directly need light to run, but it indirectly needs light because light creates the ATP and NADPH that the cycle uses to fix carbon |
|
|
Term
| name and catalytic functions of Rubisco |
|
Definition
Ribulose bisphosphate carboxylate/oxygenase
enzyme adds CO2 to a 5C sugar and then cleaves to product to form 3C units
3 CO2 + 3 ribulose-1,5-bisphosphate -> 6 (3-phosphoglycerate) |
|
|
Term
| Net reaction of Calvin cycle |
|
Definition
| 3CO2 + 9 ATP + 6NADPH -> G-3-P + 9 ADP + 8 Pi + 6 NADP+ |
|
|
Term
| Quantum yield for Calvin cycle |
|
Definition
| # photons absorbed vs. amount of C fixed or O2 released |
|
|
Term
| General ways Calvin cycle is regulated |
|
Definition
| Availability of light is key and High pH favors carboxylation of Lys residue on RuBisCO. The high PH is a signal that light reactions are pumping protons out of stroma (high PH in stroma) and that ATP and NADPH are available for Calvin cycle |
|
|
Term
| Photorespiration reaction |
|
Definition
Ribulose bisphosphate + O2 -> 3-phosphoglycerate + 2-phosphoglycolate
Is catalyzed by rubisco and it's similar to carboxylase (attaches O2 instead of CO2)
Carbon is lost as CO2. Reaction is wasteful but its purpose is to dissipate free energy of ATP + NADPH when not enough CO2 available for Calvin cycle. The overproduction of this energy can result in the shutdown of multiple pathways so you need a way to keep their levels down |
|
|
Term
| how is the name photorespiration appropriate? |
|
Definition
Consumes O2 and produces CO2
It uses the products of the light reactions. |
|
|
Term
| Why is the C4 pathway called C4? |
|
Definition
| Because plants fix CO2 into 4C molecules so that photosynthesis can proceed |
|
|
Term
|
Definition
| way of storing CO2 in different forms until the plant can run calvin cycle instead of losing it through photorespiration |
|
|
Term
| What does C4 pathway compete with? |
|
Definition
| Rubisco because they both compete for CO2. This competition is compensated for by both mechanisms taking place in different types of cells at different times of the day |
|
|
Term
| storage form of sugars in plants |
|
Definition
sucrose and starch
3C sugars produced by Calvin cycle converted to sucrose or starch |
|
|
Term
| Process of forming starch |
|
Definition
2 Gly-3-P -> Glc-6-P (similar to gluconeogenesis)
o Glc-6-P -> Glc-1-P
sugar is then activated by AMP transfer to form ADP-glucose. Starch synthase transfers ADP-glucose to end of starch
polymer |
|
|
Term
| Process of forming sucrose |
|
Definition
3C sugars converted to UDP-glucose and fructose-6-phosphate. Fru-6-P reacts with UDP-Glc to form sucrose-6-P
Then converted to sucrose. Preferred transport form of carbon because linkages not subject to amylases and is very stable |
|
|
Term
| the 3 sources of fatty acids |
|
Definition
Dietary triacylglycerols (TAGs)
TAGs synthesized by liver
TAGs stored in adipocytes |
|
|
Term
| general processes which contribute to atherosclerosis |
|
Definition
| Characterized by hardening of the arteries due to lipid accumulation in blood vessel walls. These lipids are deposited by lipoproteins |
|
|
Term
|
Definition
Chylomicrons, VLDL, IDL, LDL, HDL
This is in order from least to most dense |
|
|
Term
|
Definition
| particles consisting of lipids and specialized proteins. Protein component makes them soluble and target particles to cell surfaces |
|
|
Term
| general route of transport of lipoproteins |
|
Definition
| Chylomicrons transport TAGs to adipose tissue and cholesterol to liver, liver ships out VLDL which circulates in blood and donates TAGs to tissues, as they donate TAGs, they become smaller and denser which forms IDLs. As the IDLs give off more TAGs, these form LDL (bad), which is the primary circulating form and transports to the liver as well as to other tissues. Lipoproteins from tissues (HDL) transport back to the liver |
|
|
Term
| fatty acids (FA) in bloodstream is bound to |
|
Definition
|
|
Term
| During beta oxidation, lipases releases FAs from what? |
|
Definition
|
|
Term
| process of fatty acid activation |
|
Definition
First a phosphate group from ATP (AMP) gets attached to it which releases PPi, then the AMP is exchanged for CoA. The goal is to form acyl-CoA with the help of acyl-CoA synthetase.
Cost is 2 ATP equivalents. The hydrolysis of PPi makes this energetically feasible |
|
|
Term
| how FA get transported into mitochondrial matrix and why |
|
Definition
First the acyl group from acyl-CoA is attached to carnitine. This allows it to go through the carnitine transporter. Once it goes through the transporter, it’s on the matrix side where it is attached to CoA to reform acyl-CoA
On the matrix side, the acyl group is removed from carnitine and carnitine goes through the transporter again (into the cytosol) so it can attach to other acyl groups that need to be transported.
Activation occurs in cytosol; oxidation in the mitochondrial matrix. Oxidation occurs in the matrix because you'll end up forming acetyl-CoA which can be used in TCA and the TCA machinery is in the matrix! |
|
|
Term
| net products of each beta oxidation round |
|
Definition
| 1 QH2, 1 NADH, 1 acetyl-CoA, 14 ATP |
|
|
Term
| Process of beta oxidation |
|
Definition
In the general process of the cycle, 2C units are removed one at a time from an acyl-CoA chain.
In the first step, the bond between C2 and C3 is oxidized to form a double bond. In this step, 2 electrons are passed to FAD, and then to Q to form QH2.
In the second step, water is added across the bond.
In the third step, the molecule is oxidized again to form a carbonyl group. This forms NADH
In the final step, the molecule is split leaving a molecule of acetyl-CoA and an acyl-CoA molecule that's 2 carbons shorter |
|
|
Term
| problem that arises from unsaturated bonds and how this problem is addressed in beta oxidation |
|
Definition
Steps proceed normally until you get to that double bond. At this point, you can skip step 1 of the round because the bond is already there. The problem is that the bond is cis and should be trans. Isomerase makes the switch, then back to normal steps. Another problem is having a double bond out of place(such as in round 5 of the beta oxidation of linoleate). You'll have to convert this bond which costs NADPH
Take home note: you'll end up with less NADPH and less ATP |
|
|
Term
| # of beta oxidation rounds for a FA |
|
Definition
number of carbons/2 - 1
ex: 16C molecule = 7 rounds |
|
|
Term
| Odd chain FA in beta oxidation |
|
Definition
| steps proceed normally until the very last step which leaves a 3C fragment (propionyl-CoA). It takes 8 steps just to convert this one 3C fragment into acetyl-CoA. Intermediate steps of this process are a part of TCA (the conversion of succinyl-CoA to malate) |
|
|
Term
| Places where beta oxidation takes place |
|
Definition
| mitochondrial and also peroxisomes |
|
|
Term
| How does beta oxidation differ in peroxisomes vs mitochondria? |
|
Definition
Differs in 1st step!
• Still an oxidation using FAD prosthetic group but electrons passed to O2 directly, rather than to Q (peroxisomes don’t carry Qs) |
|
|
Term
| Where fatty acid synthesis occurs |
|
Definition
|
|
Term
| cofactor used in FA synthesis |
|
Definition
| ACP and it resembles CoA because it has sulfhydryl groups |
|
|
Term
| differences between fatty acid anabolism and catabolism |
|
Definition
cofactor: biotin for oxidation, ACP for synthesis
electron acceptor/donors: NAD+ and Q are acceptors for oxidation, NADPH is donor for synthesis
ATP cost: 2 ATP needed to activate acyl group once for multiple rounds of oxidation, 1 ATP consumed for each acetyl added to synthesize acyl chain |
|
|
Term
| how acetyl-CoA is transported into cytosol during synthesis |
|
Definition
| acetyl group is attached to oxaloacetate to form citrate which is transported through the transporter. Once it's in the cytosol, it is then converted back to acetyl CoA |
|
|
Term
| name of the enzyme that catalyzes the first step in FA synthesis and its product |
|
Definition
| Acetyl-CoA Carboxylase and the product is malonyl-CoA |
|
|
Term
|
Definition
| is 1 protein with 7 catalytic functions. The benefits is that product of one reaction quickly diffuses to next active site |
|
|
Term
| where the first 2 substrates are loaded and the direction of transfer of one substrate onto the second during FA synthesis |
|
Definition
Acetyl group loaded onto Cys residue
Malonyl transferred from CoA to ACP domain of enzyme
Both substrates have thioester link
Direction of transfer: cys site -> ACP site |
|
|
Term
| Final product of FA synthesis |
|
Definition
|
|
Term
| cost of fatty acid synthesis of palmitate |
|
Definition
|
|
Term
| general principles of how FA chains are elongated and desaturated |
|
Definition
Elongase extend chains beyond 16 carbons
Desaturases introduce double bonds in ER |
|
|
Term
| how fatty acid synthesis is regulated |
|
Definition
Rate of synthesis controlled at first step: acetyl-CoA being carboxylated by Acetyl-CoA carboxylase.
This enzyme is inhibited by palmitoyl-CoA which is the end product (feedback inhibition) and activated by citrate which indicates plenty of acetyl-CoA.
Additionally, it is allosterically regulated by +/- phosphoryl group in response to hormone signals |
|
|
Term
| What happens in ketogenesis? |
|
Definition
| 3 acetyl-CoAs are combined to form HMG-CoA. acetone is a non-enzymatic by-product |
|
|
Term
|
Definition
| acetoacetate and 3-hydroxybutyrate |
|
|
Term
| Two key features of TAG synthesis |
|
Definition
FA chains must be activated and attached to CoA. They then are
attached to glycerol-3-phosphate |
|
|
Term
| 2 general mechanisms of phospholipid synthesis |
|
Definition
| the head group could either be activated (head group exchange or the displacement of CMP?) and added to diacylglycerol or the glycerol backbone is activated first and then the head group is added |
|
|
Term
| For cholesterol synthesis, it starts with |
|
Definition
| the first steps of cholesterol synthesis resemble that of ketogenesis, but cholesterol synthesis starts once the ketogenesis intermediate HMG-CoA is formed |
|
|
Term
| Where does cholesterol synthesis take place? |
|
Definition
|
|
Term
| control step of cholesterol synthesis |
|
Definition
|
|
Term
| General steps of cholesterol synthesis from mevalonate |
|
Definition
| Mevalonate -> isoprene derivative -> squalene -> cholesterol |
|
|
Term
| How many steps does it take to make cholesterol? |
|
Definition
|
|
Term
| Cholesterol is a precursor of other hormones, such as testosterone and estrogen |
|
Definition
|
|
Term
| Only route for cholesterol disposal |
|
Definition
| cholesterol is the precursor of bile acids, and the excretion of bile acids is the only route |
|
|
Term
| route of cholesterol transport to and from cells |
|
Definition
Cells can either synthesize cholesterol or take it up from LDL: LDL binds to cell-surface receptor and gets endocytosed, Lipoprotein degraded inside cell and cholesterol released
Excess cholesterol removed from cell by HDL: Cholesterol moved from cytosolic leaflet of bilayer to extracellular side
Diffuses from there to docked HDL particle
Note that cholesterol is never really degraded |
|
|
Term
| two ways the human body has of adapting to changes in input |
|
Definition
| compartmentation and hormonal control |
|
|
Term
| Where each of the metkabolic processes take place in the cell |
|
Definition
matrix: TCA, oxidative phosphorylation, beta oxidation, ketogenesis
cytosol: glycolysis, gluconeogenesis, pentose phosphate pathway, fatty acid synthesis, nucleotide synthesis
Both: amino acid synthesis and degradation, urea cycle
This necessitates metabolite transporters |
|
|
Term
| Liver function (fed state) |
|
Definition
stores glucose as glycogen
Once the stores fill up, excess glucose and amino acids catabolized to acetyl-CoA
Acetyl-CoA used to synthesize fatty acids |
|
|
Term
| Liver function (fast state) |
|
Definition
Breaks down glycogen to glucose -> sent to other tissues
TAGs broken down to acetyl-CoA -> can be used to make ketone bodies
Amino acids can be broken down and converted to glucose or ketone bodies |
|
|
Term
| Muscle function (fed state) |
|
Definition
| Take up glucose and store as glycogen |
|
|
Term
| Muscle function (fast state) |
|
Definition
Protein (its own tissue) broken down to amino acids
Used to generate glucose (by liver) |
|
|
Term
| Muscle function (active state) |
|
Definition
Breaks down glycogen to produce ATP
Lactate and alaline produced and exported
FAs and ketone bodies broken down to acetyl-CoA
Heart muscle uses fatty acids as primary fuel because of the abundance of mitochondria (site of beta oxidation) |
|
|
Term
| Adipocytes function (fed state) |
|
Definition
| Take up glucose (for glycerol bacbone)and FAs to combine them into TAGs |
|
|
Term
|
Definition
eliminate waste; maintain pH balance
Forms alpha-ketoglutarate from glutamine to produce glucoe in gluconeogenesis |
|
|
Term
| Liver function regardless of fed or fast state |
|
Definition
| Processes lactate and disposes of amine group through urea cycle |
|
|
Term
| Adipocytes function (fast state) |
|
Definition
|
|
Term
| why circulatory systems are key to metabolic regulation |
|
Definition
| Circulatory system delivers metabolites from and to organs |
|
|
Term
| how the Cori cycle operates and the energy cost to operate it |
|
Definition
Muscle breaks down glycogen during periods of high activity
Lactate generated to reoxidize NADH
o Lactate travels to liver to participate in gluconeogenesis
o Glucose generated in liver travels back to muscle
Net effect: transfer of energy from liver to muscle
Energy cost: 6 ATP |
|
|
Term
| how the glucose-alanine cycle operates and the net effect of the cycle |
|
Definition
During exercise, muscle protein breaks down and pyruvate (from glucose) is converted to alanine.
Alanine travels to liver and fed into the urea cycle which reforms pyruvate.
Pyruvate is fed into gluconeogenesis to form glucose which is sent back to the muscle.
Net effect: transport of N from muscles to liver |
|
|
Term
| What stimulates insulin release and where it is produced |
|
Definition
Insulin released in response to rise in blood glucose levels
Insulin synthesized in beta cells in pancreatic islets of Langerhans |
|
|
Term
| similarities and differences between glucokinase and hexokinase and where each of these enzymes operate |
|
Definition
Glucokinase: Km 5-10 mM, sigmoidal plot, greatest sensitivity to substrate concentrations, not sensitive to inhibition, is a polypeptide but can be allosteric
Hexokinase: Km < 0.1mM, hyperbolic plot, present in tissues that are less dependent on glucose for energy |
|
|
Term
| effects of elevated insulin levels |
|
Definition
glucose uptake (lowers glucose levels in blood)
GLUT4 glucose transporters localized to membranes of intracellular vesicles
Binding of insulin to receptor stimulates translocation of GLUT4 glucose transporters in muscle and adipose tissue
• Stimulates fusion of vesicles with plasma membrane
Opens the cellular doors to let glucose in (increases uptake) |
|
|
Term
| pathway for stimulating glucose use and storage and for inhibiting breakdown of glycogen as an insulin effect |
|
Definition
| Insulin stimulates glycogen storage (activates glycogen synthase) and inhibits glycogen breakdown (inhibits glycogen phosphorylase). Both is accomplished by dephosphorylation |
|
|
Term
| What else does insulin stimulate? |
|
Definition
|
|
Term
| Conditions for which Glucagon/Epinephrine is released |
|
Definition
|
|
Term
| Processes Glucagon/Epinephrine stimulate and where |
|
Definition
Glucagon Stimulates production of glucose in liver
Glucagon Stimulates lipolysis in adipose tissue (mobilizes stored TAGs)
Epinephrine stimulates muscles to break down glycogen |
|
|
Term
| signaling pathway that leads to protein kinase activation |
|
Definition
| protein kinase A has is a tetramer in its inactive form(2 R subunits and 2 C subunits). When a ligand binds to the G protein receptor, it causes a conformational change to the G protein and causes it to release cAMP. Binding of cAMP to R domains releases active C domains and the kinase is activated. I guess this leads to glycogen breakdown in the response of epinephrine or glucagon |
|
|
Term
| general benefits of signaling cascades |
|
Definition
| Greatly amplifies effects of hormones |
|
|
Term
|
Definition
appetite suppressor
Leptin basically tells the brain that we're full and let’s start storing some of this food we ate |
|
|
Term
| Effect of adiponectin (in adipocytes) |
|
Definition
High levels indicate there’s a need for ATP
Activates AMP-dependent protein kinase which turns on ATP producing pathways and turns off ATP consuming pathways
Increases catabolism of glucose and fatty acids |
|
|
Term
| Effect of resistin (in adipocytes) |
|
Definition
| Blocks activity of insulin |
|
|
Term
| General contributions to obesity |
|
Definition
Lack of leptin or leptin resistance
High set point weight |
|
|
Term
|
Definition
Type I (junior onset) is the lack of production of insulin
Type II (adult onset) is when your cells don't respond to insulin |
|
|
Term
|
Definition
Cells fail to take up glucose
Liver responds by making more – increasing blood glucose levels more |
|
|
Term
|
Definition
Hyperglycemia: high blood glucose
Production of ketone bodies (ketoacidosis) – low blood pH |
|
|
Term
| nitrogen has more oxidation states than any other major element |
|
Definition
|
|
Term
| general process by which nitrogen is fixed |
|
Definition
| process is carried out by diazotrophs (nitrogen fixing organisms). Basically nitrogen gas becomes NH4. catalyzed by nitrogenase which is a metalloprotein: has Fe-S and Fe-Mo cofactors. Process is extremely expensive and snsitive to O2 |
|
|
Term
|
Definition
| the conversion of NH4 to NO2 |
|
|
Term
|
Definition
| the conversion of NO3 to N2 |
|
|
Term
|
Definition
| reduces NO3 to NO2 and NO2 to NH4 |
|
|
Term
|
Definition
| N2 -> NH4 -> NO2 -> NO3 -> N2 |
|
|
Term
|
Definition
|
|
Term
| reaction of glutamine synthetase |
|
Definition
is important in assimilating to nitrogen inside cells
Glutamine is first activated by phosphoryl transfer and then NH2 is exchanged for the Pi
enzyme is present in all cells |
|
|
Term
| Why is nitrogen assimilation necessary |
|
Definition
| NH4+ toxic to cells so you need a way of getting nitrogen inside in a different form |
|
|
Term
|
Definition
| the process of moving amine groups. Involves amino acids and keto acids |
|
|
Term
| General reaction of transamination |
|
Definition
| Amino acid-A + Keto acid-B <-> Keto acid-A + Amino acid-B |
|
|
Term
| Cofactor required for transamination and why |
|
Definition
| PLP. The aldehyde group of PLP forms a Schiff-base linkage |
|
|
Term
| General steps of transaminase reaction |
|
Definition
• Amine donor binds 1st
• Amine group transferred to PLP and keto acid product released
• Keto acid substrate (amine acceptor) binds
• Amine group transferred from PLP to keto acid
• Amino acid product released |
|
|
Term
| Why are some amino acids essential? |
|
Definition
| humans can't make them and must get them from food |
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
Met -> Ser
This one is a little weird because it requires Ser which requires Met |
|
|
Term
| Importance of THF in AA synthesis |
|
Definition
| is important as a carrier of 1C compounds in amino acid and nucleotide metabolism |
|
|
Term
|
Definition
|
|
Term
| Why is the synthesis of histidine unusual? |
|
Definition
| all the other AAs are synthesized by carbohydrate metabolism but histidine is synthesized from ATP + Gln + Glu + PRPP |
|
|
Term
| Many neurotransmitters are amino acid derivatives |
|
Definition
|
|
Term
| What is the precursor for catecholamines |
|
Definition
|
|
Term
| What is the precursor of serotonin and melatonin |
|
Definition
|
|
Term
| What is the precursor for nitric oxide radical? •NO |
|
Definition
|
|
Term
| Why is •NO an unusual signaling molecule? |
|
Definition
| it can't be stored, it doesn't need cell surface receptors because it can easily diffuse into cells, and it doesn't require an enzyme to break it down because it can do it own its own |
|
|
Term
| What is the organ where most amino acid catabolism takes place? |
|
Definition
|
|
Term
| Glucogenic vs ketogenic AAs |
|
Definition
glucogenic AAs are ones where once broken down, they give rise to TCA intermediates
ketogenic AAs give rise to acetyl-CoA |
|
|
Term
| What are the two ketogenic AAs |
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
PRPP is made 1st unlike in pyrimidine synthesis where the base is first build and then attached to PRPP
Common product is IMP
To make adenine, you need an amine group from Asp
To make guanine, you need an amine group from Gln
So the whole process requires Gln, Gly, Asp, HCO3, and THF |
|
|
Term
| How is purine synthesis regulated |
|
Definition
Both A & G need to be at similar levels so:
High [GTP], increased AMP
High [ATP], increased GMP
Also, PRPP (the first step) is inhibited by ADP/GDP |
|
|
Term
|
Definition
base is first build and then attached to PRPP. Product is UMP
Requires, Gln, Asp |
|
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Term
| In pyrimidine synthesis. how is UMP converted to UTP and CTP? |
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Definition
| Kinases convert UMP to UDP, and then UDP to UTP. CTP synthetase then makes CTP from UTP |
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Term
| How pyrimidine synthesis is regulated? |
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Definition
feedback inhibited by UMP, UDP, and UTP
ATP activates 1st step in synthesis which balances the levels of purines and pyrimidines |
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Term
| general process by which dNTPs are made |
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Definition
The NTP is first converted to NDP (so they are dephosphorylated)
The 2'OH group on the NDP is then converted to -H by rebonucleotide reductase (dNDP)
dNDP is then converted to dNTP |
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Term
| how dUTP is converted to dTTP |
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Definition
dUTP is hydrolyzed to dUMP
a methyl group is added and then it's converted to dTTP. uses THF as a cofactor |
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Term
| During nucleotide catabolism, bases can be detached from sugars |
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Definition
| and salvage pathways can reattach them |
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Term
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Definition
| waste product is uric acid which can't be broken down further due to its solubility? But it can deposit in joints to cause gout and excess can cause kidney stones |
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Term
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Definition
doesn't result into waste products!
C & U are broken down into beta-alanine and T is broken down into beta aminoisobutyrate. These products are then fed into other metabolic pathways |
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Term
| Two ways to feed into the urea cycle |
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Definition
Through glutamate!
1) Glutamate dehydrogenase reaction...as glutamate --> alpha ketoglutarate, NH4 is released and is free. This NH4 combines with CO2 to form carbamoyl phosphate and enters the urea cycle this way.
2) Transamination reaction. Glutamate gives NH4 to oxaloacetate, forming aspartate. Then aspartate enters the urea cycle.
Both ways make a-ketoglutarate which is used for TCA or gluconeogenesis. |
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Term
| reaction of carbamoyl phosphate synthetase |
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Definition
1. Phosphate group gets added to bicarbonate
2. Ammonia attacks the resulting molecule and displaces the phosphate group
3. Another phosphate group gets added which forms carbamoyl phosphate which is activated and the starting molecule for the urea cycle |
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Term
| Intermediates of the urea cycle feed into other pathways |
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Definition
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Term
| Energy cost to make 1 urea molecule |
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Definition
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Term
| Control point of urea cycle |
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Definition
| carbamoyl phosphate synthetase. If concentration of glutmate is high, this enzyme is activated and signals that we have plenty of -NH2 donors to feed into cycle |
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Term
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Definition
Urea transported through bloodstream to kidneys for excretion as urine
some organisms can use urease to convert urea to ammonia |
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