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135 Cards in this Set

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Lipid Metabolism:
What are the three stages of the synthetic mechanism of Cholesterol?
1.synthesis of five carbon intermediates from acetyl-CoA
2.Construction of 10, 15, and 30 carbon intermediates from 5 carbon intermediates
3.CYCLIZATION and formation of cholesterol
Lipid Metabolism:
compounds that are synthesized from five carbon precursors (isopentenyl pyrophosphate and dimethylallyl pyrophosphate) are known as...
Lipid Metabolism:
Categories of isoprenoids (6)
*bile acids
*coenzyme Q
*fat-soluble vitamins
Lipid Metabolism:
a six carbon intermediate that is a precursor of the five carbon molecule known as isopentenyl pyrophosphate, and is synthesized from acetoacetyl-CoA and acetyl-CoA through HMG-CoA as an intermediate
Lipid Metabolism:
What is the product of the reaction catalyzed by HMG-CoA reductase
Lipid Metabolism:
what is the name of the enzyme that is the major regulation point of cholestrol synthesis?

How is it regulated (5)?
HMG-CoA reductase

1.allosterically inhibited by cholesterol
3.Translation of mRNA that codes for the enzyme.
4.Translation of mRNA into enzyme
5.Degradation of HMG-CoA reducatase

this is an exapmle of feedback inhibition
Lipid Metabolism:
What is the name of a drug that inhibits cholesterol production by acting on HMG-CoA reductase?
Lipid Metabolism:
What is the allosterically regulator of HMG-CoA reductase?
The end product of the pathway, Cholesterol inhibits HMG-CoA reductase
Lipid Metabolism:
The major regulation point in cholesterol production is early in the pathway. Why would this be the case?
*Melvalonate is the product of the second rxn, and is the first comitted step in the synthesis of Cholesterol.
*Cholesterol is an energetically costly process that requires ATP, NADPH, and the protein synthesis of many enzymes responsible for catalyzing the many reactions in the porcess(19 enzymatic reactions for cyclization alone)
*Thus to stop the whole process it must occur early
Lipid Metabolism:
What controls the phosphorylation of HMG-CoA
Ultimately cholesterol synthesis is turned OFF via phosphorylation when ATP levels are low;
*A protein kinase is activated by AMP
*AMP levels increase as ATP levels rise
Lipid Metabolism:
What is the cause of transcriptional regulation of HMG-CoA reductase?
*WHEN CHOLESTEROL LEVELS ARE LOW the transcription factor SREBP is released from the ER or Nuclear envelope.
*SREBP (sterol regulatory binding protein) activates transcription of the gene that encodes for HGM-CoA reductase
Lipid Metabolism:
Translational regualtion of HGM-CoA reductase is effected by what?
Translation of HMG-CoA is inhibited by MEVALONATE, and by DIETARY CHOLESTEROL
Lipid Metabolism:
What causes degradation of HMG-CoA ?
Degradation of HGM-CoA reductase is modulated through the portion of it located in the membrane.
As Cholesterol (and other sterols)concentrations INCREASE the enzyme forms oligomers that are susceptible to degradation
Lipid Metabolism:
What is the name of the four carbon precursor that when combined with Acetyl-CoA (+ H2O) forms HMG-CoA
Lipid Metabolism:

HMG-CoA + 2 (H+) + NADPH --> ?
What general catergory does this reaction belong to ?
Mevalonate + CoA + 2(NADP+)
HGM-CoA reductase
Cholesterol metabolism
oxidation/reduction rxn
Lipid Metabolism:

What is the precursor of 3-isopentyl- pyrophosphate?
mevalonate (C6 but has 0 Phosphates) via four intermediates and requiring three ATP and the release of one Pi and CO2 (last step)
Lipid Metabolism:
*Molecule that is used to form isoprenoids
*and can be produced via an isomerization of isopentyl-pyrophosphate
Lipid Metabolism:
Addition of dimethylallyl-pyrophosphate and isopentyl- pyrophosphate form a C(#?) molecule?
Both dimethylallyl-pyrophosphate and isopentyl- pyrophosphate are five carbon molecules thus
a TEN CARBON MOLECULE is the product
*one pyrophosphate is lost
Lipid Metabolism:
additon of isopentyl-pyrophosphate to Geranyl pyrophosphate yields?
farnesyl pyrophosphate a 15 carbon isoprenoid.
this reaction loses (i.e. uses) one pyrophosphate
Lipid Metabolism:
This 30 carbon molecule is formed by the recation of 2 farnesyl pyrophosphate molecules

what kind of reaction is this and what is a good indication of it?
a reduction has occrued
one would know this if they were aware that NADPH is required
*two pyrophosphate are split
Lipid Metabolism:
in reactions that cleave a pyrophospahte from a molecule, what helps "pull" the reaction in addition to the energy provided by the pyrophosphate
Pyrophosphates are easily split into two orthophosphates thus are removed from the right side of the equation and thus pull the reaction forward
Lipid Metabolism:
Besides Cholesterol, what are some other products that can be formed from Squalene?
Vitamins A E and K
Lipid Metabolism:
What is the last linear precursors of cholesterol (how many carbons?) and what is the first cyclized product?
SQUALENE is the last linear precursor of cholesterol and has 30 carbons.
the first cyclized product is LANOSTEROL.
Lipid Metabolism:
How many reactions are there between LANOSTEROL and CHOLESTEROL?
There are 19 enzymatic reactions, including two decarboxylations
rearrangement/reduction of double bonds
release of formic acid
Lipid Metabolism:
where is HMG-CoA reductase found?
HMG-CoA reductase is bound in the membrane of the endoplasmic reticulum
_________ form miclelles with lipids as a mechanism of transporting them in the aqueous environment of the blood
Trigycerides arising form the digestive systme are packaged into _________ in the blood stream called __________, which travel into the blood stream via the ________ system
Lymph system
Triacylglycerols are also synthesized by the liver where they are packaged as ____ _____ _____ _____ (_____s) and released into the blood.
Very Low Density Lipoproteins
A Chylomicron remnant is.....
The remains of a Chylomicron that is returned to the liver
An LDL is a
Low Density Lipoprotein that transport endogenous fats and cholesterol from the liver to the tissues
__________ _____ in the shell of a LDL is regongnized by target cell receptors for________.
Apoprotein B-100
What are HDLs and why are they said to be "good cholesterol"
High Density Lipoproteins

HDLs scavenges cholesterol and facilitates its transport to VLDLs, HDL, or the liver. Thus is helps to clean up the blood stream of excess cholesterol
This is a hereditary disease that results in cholesterol levels 3-5 times normal. It is associated with a defective receptor in liver tissue.

without functional LDL receptors LDLs are unable to reenter the liver and accumulate in the blood.

high concentrations of LDLs result in oxidation of the LDL and then become the target of Macrophage cells of the immune system. These aggregates form FOAM CELLS. Foam cells become trapped in the walls of blood vessels and contribute to the formation of atherosclerotic plaques.
What are the five major classes of steroid hormones?
Name a Progestagen and its function
*Progesterone is a class of steroid hormone and
*is essential for maintenance of pregnancy
What is the function of Glucocorticoids?
Glucocorticoids are a class of steroid hormones that enhance the degradation of fat and proteins
and also inhibit the inflammatory response
What is the function of mineralocorticoids?
Mineralocorticoids are a class of steroid hormones
*that act on the kidney to increase reabsorption of Na+ and excretion of K+ and H+
*leading to increase in blood volume and pressure
What is the function of Androgens?
Androgens are a class of steroid hormones that are responsible for development of male secondary sex characteristics.
What is the function of estrogens?
Estrogens are a class of steroid hormones that are required for female secondary sex characteristics and also participate (along with progesterone) in the ovarian cycle.
*have aromatic ring
What is the relationship in terms of synthesis between androgen and estrogens
Estrogen (C18) is synthesized from Androgen (C19) a by an enzyme:
*Estrogens have a benzene ring thus are aromatic compounds
* Estrogen is associated with some cancers and AROMATASE INHIBITORS are used as a treatment to slow growth of the cancer cells.
How many Carbons does Cholesterol have?
Cholesterol has 27 carbons
Cholesterol is a precursor of the bile acids. Name 4 bile acids that are syntheiszed form cholestreol.
*cholate (cholic acid) *chenodeoxycholate
What is the function of bile acids?
And what is their potential role in lowering over all cholesterol levels?
*Bile acids act like detergents in the digestion of lipids by solubilizing lipids (lipids are insoluble in aqueous media)
*bile acids are excreted in the feces most however is recycled.
*Thus drugs that inhibit recycling of bile acids can lower overall cholesterol levels because bile acids lost to excretion will be replenished de novo.
What is the only way sex hormones are removed from the body?
Via the urine
Complexes I, II , III, IV are what?
*are multiprotien complexs that carry electrons
Complexes I and II use _____-_____ porteins with _______ to carry electrons.
IRON-SULFUR proteins

what is so special about flavins?
Flavin mononucleotides have ring structures and on carry one or two electrons at a time by being reduced.
This structure is an iron-sulfur cluster that would be found in complexes I and II of the ETS.
The sulfur is from Cysteine residues.
the iron can exisit in two reduced states 2+ and 3+ the difference being the addition or subtraction of one electron.
What does this structure represent and why is it important?
Which complexes would one find this structure?
Can CoQ accept protons?
YES. CoQ has a quininoe that can accept protons from the mitochondria matrix when it accepts electrons from Complexes I and II.
*CoQ has three oxidative states:
CoQ-, COQ, CoQH2
*CoQ can release electrons ONE AT A TIME
What is the sequence of electron transfer in the ETS?
*NADH --> Complex I --> CoQ --> Complex III-->**

*FADH2 --> Complex II --> CoQ -->
Complex III-->**

**(Complex III)--> cytochrome C-->
Complex IV --> 1/2 O2 + 2(H+)--> H2O

*** Thus electrons entering the ETS from FADH2 by passes Complex I (a proton pump)
Which steps in the ETS pump protons?
*COMPLEX III --> cytochrome C
Where are the components of the ETS located?
The complexes of the ETS are embedded in the inner mitochondrial membrane where they move indepentent of each other.
What kind of proteins are in Complex III that allow it to carry/transfer electrons.
What is the functional group of this protein?
Cytochrome proteins have a HEME GROUP.
Hemes have iron that is held in place by nitrogens from PORPHYRIN rings.
What does Complex IV have in common with Complex III?
What is different?
*in relation to their structure and ability to hold e-
Both Complexes (III and IV ) have CYTOCHROME PROTEINS.
Complex IV has a cytochrome protein that uses both COPPER (Cu+/Cu++) and IRON(Fe++/Fe+++) to transfer e- and H+ to O2 to form H2O.
What is the sequence of steps in Complex IV that result in the reduction of O2 to 2 H2O.
1.cytochrome C tranfers one electron at a time to Complex IV
a)1st e- goes to Cu (Cu++-->Cu+)
b)2nd e- goes to Fe (Fe+++-->Fe++)
2. O2 binds Fe++
3. Formation of PEROXIDE BRIDGE (Fe-O2-Cu)
4.H+ binds to an O, thus BREAKS O-O (Fe=O, Cu-OH)
5. H+ binds to ferryl group
(O=Fe + (H+) -->Fe-OH)
6. 2 more H+ bind to both -OH thus releasing 2 H2O
7. cytochrome C ready to begin again
What is the Q cycle?
*The Q cycle describes the transfer of electrons from CoQ through Complex III to cytochrome C.
what is the sequence of events in the Q-cycle?
*Complex III where the Q-cycle takes place. There are Two binding sites for CoQ; CoQ0 and CoQi.
*CoQ can only give up electrons (e-) and protons(H+) from one of the two sites, CoQ0.
* CoQ can exist in three oxidative states; CoQ-, CoQ, CoQH2. (CoQH2 is fully reduced)
1. CoQH2 is bound at site CoQ0. CoQ is bound to the other site CoQi.
2. CoQH2 releases 2 (e-); one goes to cytochrome C (-->Complex IV) the other (e-) goes to CoQ at site CoQi.
Thus @ site CoQi
(CoQ + (e-) --> CoQ-)
3. CoQ @ site CoQ0 leaves and is replace by a new CoQH2
4. new CoQH2 releases 2 (e-); one goes to cytochrome C (-->Complex IV) the other (e-) goes to CoQ- at site CoQi and this draws 2(H+) from the matrix.
Thus @ site CoQi
(CoQ- + (e-) + 2(H+)--> CoQH2)
5. at this point two things happen CoQ @ site CoQ0 leaves and is replaced by a CoQH2 or CoQH2 @site CoQi leaves. In short the cycle starts again.
Where is Cytochrome C (Cyt C)?
Cytochrome C is a peripheral membrane protein. It alternately binds cyt c1 of Complex III and cyt c oxidase in Complex IV.
What are reactive oxygen species and where are they most likely to be formed in the ETC?
How are they removed?
*Reactive oxygen species are free radicals of oxegen such as superoxide (O2-) and peroxide (H2O2).
*interruption of e- flow at COMPLEX IV can leave O2- without adding 2(H+) to form H2O.
*the cell has an enzyme Superoxide Dismutase (SOD) to deactvate superoxides and along with another enzyme reduces superoxides to H2O.
How does Superoxide Dismutase (SOD) work?
1.SOD accepts an e- from superoxide (O2-)
2.reduced SOD (from 1st step) combines its extra e- with that of another superoxide (O2-) and 2(H+) to make peroxide (H2O2)
3.another enzyme, CATALASE, converts H2O2 to H2O.
*In addition vitamins E and C protect the cell form free radicals
What is the net difference of protons are removed form the mitochondrial matrix by Complex IV and the reduction of O2 to H2O
*the net difference protons between the inside and outside of the inner membrane of the mitochondrial matrix is 12.
*FOUR PROTONS are taken from the matrix and combined with oxygen to form two water molecules.
*FOUR PROTONS are taken from the matrix and pumped outside the matrix.
*THUS the number of protons in the matrix DECREASE by 8 and the number of protons outside the matrix INCREASE by 4.
How is ATP created by oxidative phosphorylation?
ATP is produced from ADP and Pi in Complex V.
Complex V(ATP Synthase)changes conformation as protons from the outside of the mitochondrial inner membrane reenter the matrix through it (Complex V)
What are the two essential functions of electron transport?
1.Pump protons out of mitochondrial matrix (establish a proton gradient)
2. Reoxidize NADH and FADH2 to NAD+ and FAD.
What is the chemiosmotic hypothesis? And what are 3 important aspects of it?
*Bonus who originally proposed it?
*Chemiosmotic hypothesis explains how mitochondria make ATP. NOT by substrate level phosphorylation, BUT by OXIDATIVE PHOSPORYLATION.
*1.Intact inner mitochondrial membrane
2.Electron transport creates proton gradient
3. ATP is made by movement of protons back into the mitochondria
At a practical level, what does it mean to say that electron transport and oxidative phosphorylation are COUPLED?
The mitochondrial inner membrane must remain impermeable to protons except those that enter via the ATP synthase (Complex V) and result in ATP production
Beyond the most practical level what does COUPLING mean (ETS, OXI-PHOSPHOR)
If either of them stops they both stop. In addition the Citric acid cycle also relies on the ETS and Oxidative Phosphorylation.
Describe the structure of Complex V (ATP Synthase)
*The complex has two main subunits(F1 and F0) that each contain separate polypeptide chains (e.g. F1 has 5 type of chains)
*Subunit F0 spans the mitochondrial inner membrane and acts as a pore/pump for H+ to reenter the matrix.
*As H+ reenter matrix through the F0 subunit, ATP synthase spins like a turbine forcing the catalytic sites on F1 to cycle through 3 conformational states
*ATP Synthase (F1 subunit) has three catalytic sites that alternate between three different states.(L,O,T)
-L state new ADP and Pi are brought in close proximity
-T state ADP and Pi are brought close enough for a reaction to occur(low transition state energy)thus forming ATP
-O state new ATP is released and ADP and Pi enter.
*** Three ATP are produced per 360 degree revolution of the complex
The ETS is in the inner membrane of the mitochondrial matrix.
How does NADH produced in Glycolysis transported into the mitochondrial matrix?
*NADH cannot cross the mitochondrial inner membrane and there are not transporters for the molecule itself.
*NADH outside the matrix must donate its electrons to the ETS via a shuttle.
*In mammals this involves the MALATE-ASPARTATE SHUTTLE
What are the steps in the MALATE-ASPARTATE SHUTTLE?
1. Oxaloacetate is reduced to malate by accepting electrons from NADH
(NADH + Oxaloacetate --> NAD+ + Malate)
2. Malate is transported into the matrix
3. Malate (inside the matrix) is converted back to Oxaloacetate after "donating" its electrons to NAD+
(NADH + Oxaloacetate <-- NAD+ + Malate)
*Oxaloacetate cannot be transported across the inner membrane.
4. In a Transamination reaction an amine group is removed from Oxaloacetate and given to Glutamate forming alpha-ketoglutarate and Asparate (the result of the deanimation of oxaloacetate)
5. Aspartate is transported across the inner membrane and converted back to oxaloacetate and then Malate to continue the cycle
Name 7 inhibitors of electron transport and the complexes they effect.
1.AMYTAL -Complex I
2.ROTENONE -Complex I
4.CYANIDE- Complex IV
5.AZIDE (N3)-Complex IV
7.DCCD-Complex V
*Note AMYTAL and ROTENONE are not as lethal as those inhibitors that effect Complex III and IV.
Name a Chemical that is known to UNCOUPLE the ETS and how it works.
DNP or 2,4 dinitorphenol
*DNP is a lipid soluble substance that can carry protons across the mitochondrial inner membrane thus decoupling the ETS
What is the name of the protein that moves ADP and ATP across the mitochondrial inner membrane?
What are the structures of acetyl-CoA, Oxaloacetate and Citrate?
What enzyme catalyzes the formation of Citrate?
Draw the structures of citrate and isocitrate.
What enzyme catalyzes the formation of isocitrate?
Draw the structures of succinyl-CoA and alpha-ketoglutarate.

What enzyme catalyzes the formation of succinyl-CoA?
alpha-ketoglutarate dehydrogenase complex
Draw the structure of alpha-ketoglutarate and isocitrate.

What enzyme catalyzes the formation of alpha-ketoglutarate?
isocitrate dehydrogenase
Draw the structures of succinyl-CoA and succinate.
What enzme catalyzes the formation of succinate?
Succinyl CoA snythetase
Draw the structures of succinate and fumarate.
What is the name of the enzyme that catayzes the formation of fumarate?
succinate dehydrogenase
Draw the structures of fumarate and malate.
What enzyme catayzes the formation of malate?
Draw the structures of oxaloacetate and malate.
What enzyme catalyzes the formatin of oxaloacetate?
malate dehydrogenase
Draw the structures of pyrivate and acetyl-CoA.
What is the enzyme that catalyzes the formation of acetyl-CoA?
Pyruvate Dehydrogenase complex
How many enzymatic subunits does pyruvate dehydrogenase complex have?
How are they labeled?
Coenzyme of each?
What enzymatic function does each serve?
*three enzymatic subunits in pyruvate dehydrogenase complex.
*E1, E2, E3
coenzyme; TTP (Thiamine pyrophosphate) decarboxylates pyruvate (release of CO2) then oxidizes acid aldehyde (removes e- into THIAZOLE RING.(act as an e- sink)
coenzyme; lipoamide
The disulfide group is in the fully oxidized form (S-S)--> (S-H,S-Acetyl group).
Then transfers acetyl group to CoA.
coenzyme; FAD
FAD accepts e- and H from reduced lipoamide (S-H, S-H of disulfide group)
thus S-H S-H + FAD --> S-S +FADH2.
What is the coenzyme of E1?
TTP Thiamine pyrophosphate
THIAZOLE Ring acts as an electron sink
Five member ring
What is the coenzyme of E2?

has a disulfide group that completes a five membered ring. Two sulfurs are in adjacent positions on the ring.
alternate between (S-S and S-H, S-H)
What is the coenzyme of E3?
Functions to oxidize lipoamide back to S-S state after CoA is transfered to acetyl group by accepting tow e- and 2 H
In Acetyl-CoA what kind of bond connects the two groups?
A THIOESTER bond helps drive the formation of citrate from acetyl-CoA and oxaloacetate.
What are the folds of the inner mitochondrial matrix called?
What reaction in the citric acid cycle forms a Nucleotide-triphosphate?
What type of reaction is this?
This rxn has a negative delta G (sub-zero prime), where does the energy come from?
*A high energy GTP molecule is formed in the reaction that is catalyzed by Succinyl-CoA synthetase.
(Succinly-COA +GDP+Pi-->Succinate + GTP + CoA)
*The energy for this reaction comes from the high energy THIOESTER bond of CoA
What steps are involved in the conversion of pyruvate to acetyl-CoA?
1. decarboxylation of pyruvate by E1 to form an "activated" form of acetaldehyde bound to TPP.
2. Transfer of the activated acetaldehyde to LIPOAMIDE (oxidation occurs in the transfer accompanied by reduction of the disulfide bond of lipoamide)
3.Transfer of acetyl group to coenzyme A (CoA)
4. transfer of electrons from lipoamide to FAD (forming FADH2, and regenerating disulfide on lipoamide)
5. Transfer of electrons form FADH2 to NAD+ to form FAD and NADH
what is a coenzyme?
Coenzyme is a prosthetic group of an enzyme complex that enhances the enzymatic activity of the enzyme.
If a person had the disease BERIBERI what would be found in the blood stream in higher than normal concentrations? WHY?
*There would be elevated levels of pyruvate and alpha-ketoglutarate.
*Beriberi is a disease associated with diets lacking in vitamin B (Thiamine).
*Enzymes that convert pyruvate to acetyl-CoA and Alpha-ketoglutarate to succinyl-CoA rely on TTP to transfer an "activated" aldehyde unit.
* Without Thiamine cells are not able to carry out the reactions.
C.A.C., regulation:
If NADH levels are high what enzymes are effected?
And how +or-?
*Pyruvate Dehydrogenase -
*P. Dehydrogenase specific kinase +
(thus phosporylation of P. Dehdro. is inhibitory)
*Isocitrate Dehydrogenase -
*Alpha-ketoglutarate dehydrogenase -
Thus overall C.A.C is inhibited
What is th most important control on C.A.C.?
What are reactions that "fill up" intermediates of metabolism called?
Anaplerotic reactions;
aspartate--> other aminoacids, purines, pyrimidines
Anaplerotic reactions;
Fatty acids and sterols
Anaplerotic reactions;
Alpha-ketoglutarate -->?
Glutamate --> other aminoacids--> purines
Anaplerotic reactions;
Succinyl-CoA -->
Porphyrins, hemes chlorophyll
Anaplerotic reactions;
Acetyl-CoA -->Citrate --> sterols, fatty acids
Oxaloacetate --> aspartate--> other aminoacids, purines, pyrimidines
What is compound that binds with dihydroLIPOAMIDE causing it to lose function?
What is the antidote?
* (BAL) 2,3, dimercaptopropanol
What are the two enzymes of the GLYOXYLATE CYCLE that differ form the CITRIC ACID CYCLE?
ISOCITRATE LYASE (catalyzes the cleavage of isocitrate to glyoxylate and succinate)
MALATE SYNTHASE (catalyzes the lingage of Acetyl-CoA to GLYOXYLATE to form MALATE)
How is the glyoxylate cycle able to form net amounts of glucose from acetyl-CoA?
The cycle avoids two decarboxylation reactions of the C.A.C. that would normally remove two carbon atoms in the form of CO2.
Which reaction in the Citric Acid cycle adds water across a double bond?
Fumarate + H2O --> L-Malate
(enzyme fumarase)
What are the two decarboxylation reactions within the citric acid cycle?
*ISocitrate + NAD+ --> Alpha-ketoglutarate + NADH + CO2 + H+
*Alpha-Ketoglutarate + CoA + NAD+
--> Succinyl-CoA + CO2 + NADH + H+
Note: Pyruvate to Acetyl CoA also releases CO2 but in not WITHIN C.A.C.
What are the four redox reactions of the C.A.C.?
*ISocitrate + NAD+ --> Alpha-ketoglutarate + NADH + CO2 + H+
*Alpha-Ketoglutarate + CoA + NAD+
--> Succinyl-CoA + CO2 + NADH + H+
*Succinate + FAD --> Fumarate + FADH2
*Malate + NAD+ --> Oxaloacetate + NADH + H+
Lipid Metabolism:
two important five carbon precursors of isoprnoids
*isopentenyl pyrophosphate *dimethylallyl pyrophosphate
What activates Pyruvate dehydrogenase phosphatase?
Ca++ and Mg++
*Ca++ is released for muscle contration and when epinephrine G-protein receptors are activated
*Mg++ binds strongly with ATP
thus low [Mg++] is an indiaction of high levels of ATP OR in other words
high [Mg++] indicates low levels of ATP
What is the name for a transporteer that transports molecules in oposite directions. e.g. the Na/K ATPase
Form of transport that uses energy in the form of ATP or an electrochemical gradient to move at least one molecule AGAINST its concentration gradient
Form of transport that moves molecules with their concentration gradient, and thus does not require energy.
Transport that results in no net change in charge
Type of transport that ends in a net change in charge
Electrogenic transport
An example of an electrogenic transporter
Na/Glucose pump
uses Na gradient to pump glucose against its concentration gradient by using the energy of Na gradient
An Na+/Ca++ exchange pump is what kind(s) of transporter?
The Na+/Ca++ exchange pump uses the energy of Na+ moving into the cell to pump Ca++ out
*The net difference in charge between the ions make this an ELECTROGENIC PUMP.
*The use of a concentration gradient is an example of SECONDARY ACTIVE TRANSPORT.
*The fact that the ions are moving in opposite directions make this a ANTIPORT.
How does DIGITOXIGENIN stimulate the heart to pump?
*Digitoxigenin binds Na+/K+ ATPase and prevents its operation.
*If Na+/K+ ATPase does not work the Na+ gradient is lost.
*The Na+ gradient is used to run the
Na+/Ca++ exchange pump
*Thus [Ca++] rises causing muscular contraction
What are a few properties of Passive transport/
They are usually Pore Channels
Driven by diffusion
Faster than active transport
e.g. Voltage gated Na channels of nerves
Name the experimental technique used to study channel responses to various cellular conditions i.e. the electro-chemical milieu.
placing a small pipette on cell membrane and measuring voltage and chemical concentrations within the pipette
The CFTR and MDR transporters are both this type of ATP transporter
ABC-Domain transporter
Na/K ATPase is this type of transporter (all have common AT binding site that transiently binds to phosphate)
Specific amino acid sequences that target proteins to specific organelles
Address Labels
Mitochondrial "targeting sequence"
Some transporters move molecules form one side of a membrane to another by _________. e.g. Lactose permease
Lactose premease bind H+ and lactate and then changes conformation to switch which direction the openings are facing i.e. the transporter everts
Gap Junctions are composed of________ proteins.
The Acetylcholine receptor is an example of a ________-_____ ion channel.
The name of a toxin that binds to Acetylcholine receptors. (hint; snake venom)
4 key features of ion channels
*High SELECTIVITY for specific ions
*Can be in OPEN AND CLOSED states
*Transition between open and closed states is REGULATED
*Open states often spontaneously convert to closed state
Two types of Facilitated transport
Pore-facilitated transport
e.g. glucose transporter ?where
Carrier facilitated transport
moves molecules across lipid bilayer by shielding the molecule from the hydrophobic environment of the inner bilayer
Describe the structure of Glycerophospholipids
*glycerol backbone
*phosphate at #3 position
*fatty acids at #1 and #2 positions
C1 usu. saturated 16-18 C long
C2 usu. unsaturated 16-20 C long
Naming phosphglycerides
X= compound attached to phosphate
e.g. Phosphatidylserine
or phosphatidylinositol
What are ether lipids
*Variants of phospholipids with ether linkages instead of ester linkages
*They are much more resostant to hydrolysis

R-C-O-C =ether
Uses light c, chemistry and mechanics to pump protons in a halobacter
Are deviatives of
amino-alcohol that contains a long (18C)unstaurated hydrocarbon chain
Lipids that contain a sugar moiety...
Sphingolipids containig a sugar moiety
A glycosphingolipid found it the gray matter of the brain
CFTR is a
*Cystic Fibrosis transmembrane conductance regulator
*AN ATP-regulated chloride ion channel
*ABC-domain (two ATP binding sites)
*Cystic fibrosis is due to a defect in this chloride pump