Biochem Final Flashcards

Why is apoptosis a more beneficial mode of cell death compared to necrosis?

necrosis causes the cell to swell and lyse, leaking its contents and
causing an inflammatory response
apoptosis causes the cell to fragment into pieces that can be phagocytosed

The steps of apoptosis include:

Normal cell > nuclear condensation > membrane
_________ > cell shrinkage > fragmenting > apoptotic bodies
> ___________

blebbing, phagocytosis

How do statins play a role in apoptosis? Is this process caspase dependent?

They cause a reduction in the mitochondrial membrane potential which
increases leakiness and allowing release of SMAC leading to apoptosis, yes

Following DNA damage, p53 is ___________


What role does p53 (tumor suppressor gene) play in apoptosis?

prevents the cell from replicating by stopping the cell cycle at G1

An active ___/_____ complex drives the cell cycle. How does p53
affect this complex?

CDK/Cyclin, inactivates it when damage is detected

What happens in cancer that apoptosis is unregulated and mainly absent?

mutations in "tumor suppressing" genes

In normal GF binding, the site is inactive when empty. Binding of the
EGF activates the tyrosine kinase receptor. Mutations and cancer cause
tyrosine kinase to be constantly _______ which leads to:

active, constant cell growth

SMACs located inside ___________ are released into the cytosol
following an increase in permeability and bind to ____

mitochondria, IAPs (inhibitor of apoptosis protein)

IAPs normally __________ apoptosis and __________ caspases

inhibit, inhibit

When IAPs are deactivated, apoptosis can _________


Protein that "pokes holes" in the mitochondrial membrane,
increasing it's permeability (or "leakiness")


Cytochrome C and SMAC are different proteins that perform
_____________, which is:

the same function: initiate apoptosis via caspases

There are two main caspases:

initiators and executioners

The death receptor pathway is an example of a(n) ___________ pathway


When extracellular and intracellular (or intrinsic) apoptosis
pathways overlap, it is called


Ras and RhoA lead to cell ___________


What drugs target RhoA and therefore cell proliferation and migration?


What is a virus that contains two single-stranded linear RNA
molecules and carries its genetic blue print in the form of RNA
instead of DNA?


Retrovirus contain viral RNA and several copies of ______________ for
rapid replication

reverse transcriptase

Is the incorporation of the virus genome into the host temporary or permanent?


Host-cell _____________ makes virus-related RNA

RNA polymerase

What is the permanent step in the life cycle of a retrovirus that is
disrupted can prevent proliferation?

integration into the host chromosome

Reverse transcriptase is highly error prone and has a fast
replication cycle. Why does this matter to HIV positive patients?

every HIV virus is unique which makes it more difficult to treat.
drug therapy must be targeted to individuals and modified over time to
prevent resistance as mutation occurs

What is the name of the initial docking protein used by HIV to infect
host cells?


What is the name of the secondary docking protein that serves to
stabilize the fusing of the virus with the host cell?


HIV belongs to a subset of retrovirus called


HIV infects the _______ T cells and begins to replicate


The number of CD4 and viral load of a patient is __________ correlated


After the infection, there is an initial drop in CD4 count followed
by ____________ during latency

an increase

What are 3 enzymes that can be targeted in HIV therapy?

reverse transcriptase, integrase, and protease

Antiretroviral therapy is always a combination of two Nucleoside
Reverse Transcriptase Inhibitors (NRTIs) and a:

NNRTI, Protease Inhibitor, Integrase I, or Entry I

Taking multiple HIV meds serves to protect the _________ and prevent
drug __________

immune system, resistance

How does the drug AZT differ from the nucleoside thymidine?

it has a 3' N group instead of an OH

What is the target of NRTIs?

reverse transcriptase

NRTI is a ____ dependent DNA polymerase


NRTI must enter the cell and be ______________


These drugs competitively inhibit incorporation of normal nucleotides
and terminate chain elongation due to lack of 3' OH group


These drugs act as non-competitive inhibitors in HIV therapy


Do NNRTIs require phosphorylation for activity?


NNRTIs bind to a hydrophobic pocket in the p66 subunit of

reverse transcriptase

Protease inhibitors prevent infected T-cells from producing:

new copies of the virus

Once HIV's genetic material is inside DNA, the cell produces genetic
material that must be cut up and put together correctly to form new
copies of the virus. What completes this function?


These drugs are designed to prevent cleavage, meaning a virus cannot
mature and infect a new cell (immature viruses)

protease inhibitors

Do protease inhibitors target and inhibit ALL proteases?

no, drugs are specific for HIV proteases

Protease inhibitors end in ____ except 3 that are actually integrase
inhibitors (Raltegravir, Dolutegravir, Elvitegravir)


What are some problems with protease inhibitors?

require STRICT patient adherence, GI side effects can affect compliance

_______ inhibitors target the permanent incorporation step


Newest form of HIV therapy are ___________ inhibitors


Entry Inhibitors are (sometimes/always) used in combination with
other therapies


Fuzeon is an entry inhibitor that targets the gp___ protein


gp120 anchors HIV to target cell binding to CD4. CCR5 chemokine
receptor binding stabilizes complex and allows gp41-mediated fusion of
virus membrane with target cell membrane. How does the drug Miraviroc
disrupt this process?

it's a CCR5 antagonist. the drug binds to CCR5 preventig gp120
binding, fusion, and entry

LDLRs are up-regulated by statins through _______


What are the ligands for LDLR?

ApoB-100 and ApoE

PCSK9 promotes the degradation of _________


Is PCSK9 upregulated by statins? What effect could this have on LDLR?

yes, it could reduce statin's LDLR-raising ability

An adaptor protein facilitating the endocytic internalization of LDLR
in the liver, a process that is required for receptor-mediated uptake
of LDL


There are two types of familial hypercholesterolemia, one is
autosomal dominant and one is autosomal recessive. Which results from
a PCSK9 gain of function mutation?

autosomal dominant FH

Autosomal recessive FH affects what proteins/receptors?

ARH affects LDLRAP1 while phytosterolemia affects ABCA5 or ABCA8

What are the first line of treatment for hypercholesterolemia patients?


What are some of the moderate intensity statins used?

Sim, Prav, Lov

What are two examples of high intensity statins?

Ator, Rosu

If a patient does not achieve the anticipated response from
moderate/high intensity statins, What are 4 additional therapies that
can be added?

Ezetimibe (Zetia), PCSK9 inhibitors, and both BAS and Niacin have
been assessed as monotherapies but do not show evidence of benefit as
co-treatments to statins

Fatty deposits around joints are known as


In genomic DNA sequencing, polymorphisms indicate duplications which
make one residue too long. Is this typically a disease-causing mutation?


Do mutations in exons typically results in disease?


What is another name for mutations in non-coding areas of the genome
such as exons?


When reading genomic DNA sequencing, what does a * represent?

stop codon

A premature stop codon is what type of mutation?


This type of mutation occurs when the addition or loss of DNA bases
changes a gene's reading frame (3 bases that each code for one amino
acid); this mutation shifts the grouping of these bases and changes
the code for amino acids. The resulting protein is usually
nonfunctional. Insertions, deletions, and duplications can all be this
type of mutation


This type of mutation is a change in one DNA base pair that results
in the substitution of one amino acid for another in the protein made
by a gene.


As part of DNA genome sequencing you see that L21dup indicates an
upregulation in PCSK9. What impact will this have on statin treatment?

it will increase effectiveness so a smaller dose will be needed

NPC1L1 aids in the _______________ from the GI tract. The drug
Ezetimibe targets this protein channel.

absorption of cholesterol

Polymorphic variations in NPC1L1 gene could be associated with
non-response to

ezetimibe treatment

In protein homeostasis, protein __________ provides an important
mechiams for regulating biological activities


The secretory exocytic pathway of proteins consists of what two organelles?

ER and Golgi

Which organelle serves as the major quality control site for proteins?


In the ER, improperly folding proteins are subject to degradation
through the ______ pathway via autophagy


Impaired ability of the ER to handle misfolded proteins leads to
stress and _______ response

unfolded protein response (UPR)

Efficient degradation of misfolded proteins is critical as they can
cause many disease states including

prion disease, alzheimers, parkinsons, type II diabetes

In the cytosol, protein degradation is largely mediated through the
action of

ubiquitin-proteasome system (UPS)

What are considered the recycling centers of the cell because they
degrade virtually all biomolecules?


Proteins are folded in the ____ and sent to the _____ for further
modifications. If a misfolded protein is detected, quality control
will send it to lysosomes for degradation through ___________.

ER, Golgi, autophagy

___________ is a highly conserved, small protein in ALL eukaryotic
cells that contains 7 lysine residues


In the process of ________________, the carboxylic acid of the
C-terminal glycine of ubiquitin forms an isopeptide bond with the
epsilon group of a lysine (side chain) residue of a target protein


During ______________, the carboxylic acid of the C-terminal glycine
of a fresh ubiquitin molecule forms an isopeptid bond with the epsilon
amino group of one of the 7 lysine residues OR the N-terminal amino
group of the bound ubiquitin. The chain is usually 4+ in lenth


There are 3 main ubiquitination enzymes: E1, E2, and E3. Which
conveys specificity?


Of this 3 ubiquitination enzymes, which has only 2? Which has 35
different enzymes? Which has hundreds?

E1, E2, E3

The existence of multiple E1, E2, and E3 enzymes in hierarchical
order allows for _____________ of the process and high substrate specificity

tight regulation

Lysine 48-linked polyubiquitin chain targets protein for
_____________ degradation and can be targeted for drug therapy


Multi-monoubuquitination targets ______________ proteins for
internalization and lysosomal degradation. What does this process determine?

turnover rate

Does the 26S proteasome require ATP for proteolysis?


What is the 26S proteasome?

machine" that degrades protein

The 26S proteosome is comprised of a 20S proteasome with alpha and
beta subunits and a 19S _________ particle. Where does the 19S
particle attach?

regulatory, at the alpha ring of the 20S

In proteasome degradation, a target protein needs to be
polyubiquitinated by at least ____ ubiquitins in order to be recognized


The recognition of the target protein by the 19S regulatory particle
depends on


What is required of the target protein in order for it to fit into
the small barrel of the 26S proteasome for degradation? What else is
needed to make this happen?

partial unfolding, ATP hydrolysis

In protein degradation, what occurs just prior to the passage of the
unfolded substrate protein into the core of the 26S proteasome?


The alpha ring allows a peptide with no more than 4 residues to enter the

20S core particle

Proteolysis by _________ of the 20S particle creates short peptides

beta subunits

Proteasome inhibitors have anti-_______ effects. What are they used
to treat?

tumor, multiple myeloma

Proteasome inhibitors disrupt regulated degradation of pro-apoptotic
factors, causing an accumulation of polyubiquitinated proteins which
leads to ______________. These drugs are recognizable by the suffix
-____ . What is the name of the first oral form of these drugs?

cell toxicity, -mib, Ixazomib

UPR is a cellular stress response associated with what organelle?


A key player in UPR response is GPR78, aka ___) which is a molecular chaperone


What are the 3 intracellular receptors that are activated upon GRP78
(BiP) dissociation?


When PERK is activated, it leads to ___________ arrest


When ATF6 is activated it leads to an increase in transcription of ER
stress response genes. This increase is known as


Activation of IRE1 encourages


The translational arrest by PERK, ATF6, and IRE1 is mediated through
phosphorylation of of


The _____ pathway utilizes the UPS to eliminate misfolded proteins in
the ER


During _________, misfolded proteins are retrograde transported
across the ER membrane into the cytosol through the Sec61 peptide channel


In addition to being the building blocks for DNA/RNA, nucleotides
serve as energy carriers for the cell via ___/___, components of NAD
and ___, and signal transducers such as cAMP and _____


What are the two pathways for nucleotide synthesis?

de novo, salvage

What function is dependent on the de novo synthesis of nucleotides?


The de novo nucleotide synthesis pathway occurs in 3 stages:
synthesis of ___________
reduction of ribonucleotides to _____________
conversion of dUMP to ____


Bases and nucleosides released during degradation of nucleic acids
are recycled to regenerate nucleotides in:

salvage pathway

What is the key to both de novo and salvage nucleotide synthesis?


What is PRPP synthesized from?

ribose 5-phosphate

What enzyme converts ribose 5-phosphate into PRPP? What is required?

PRPP synthetase, ATP

De novo nucleotide synthesis occurs in most cells EXCEPT


In de novo nucleotide synthesis, which aa residue should you follow?


What is the key regulatory enzyme and committed step in de novo synthesis?

PRPP amidotransferase

What are the feed-forward activators of the rate-limiting step in de
novo NT synthesis?

PRPP and glutamine

What are the feedback inhibitors of the rate-limiting step in de novo
NT synthesis?


The amide nitrogen of glutamine is transferred to PRPP at C1 to form:


Antifolate drugs target what two enzymes in de novo NT synthesis?

GAR and AICAR transformylases

Folate once taken into the body is converted to its active form THF
by what enzyme?

DHFR, dihydrofolate reductase

Micronutrient required for TMP and IMP synthesis


Inosine monophosphate or ___ regulates PRPP amidotranferase. Do high
levels inhibit or activate?

IMP, inhibit

AMP and GMP are made from


What is the energy source for AMP synthesis?


AMP and GMP also regulate the formation of IMP by inhibiting which enzyme?
GAR transformylase AICAR transformylase
PRPP amidotransferase Adenylosuccinate lyase

3. PRPP amidotransferase

Synthetases require ____


What is the rate-limiting step in AMP Synthesis?

adenylosuccinate synthetase

What is the rate-limiting step in IMP Synthesis?

IMP dehydrogenase

Is diphosphate to triphosphate kinase specific?


___ is the energy for AMP, while ___ is the energy for GMP


Is there more or less regulation/steps in the de novo synthesis of
pyrimidine ribonucleotides compared to that of purines?


What is the precursor to cytidine and thymidine nucleotides?


What are the two activators of CPS II (carbomyl phosphate synthetase II)


What are the feedback inhibitors of CPS II


What is the feedback inhibitor of OMP decarboxylase?


Disease state caused by orotate phosphoribosyl transferase and OMP
decarboxylase deficiencies. Characterized by developmental delay,
megaloblastic anemia and elevated levels of orotic acid (orotate) in
urine. How is it treated and why?

Orotic aciduria, treated with uridine because UTP shuts down oratate production

Precursor to cytidine and thymidine nucleotides


Carbamoyl phosphate synthetase II (CPS-II) is:
a. Activated by PRPP b. Inhibited by UMP c. Activated
by ATP d. The key committed step in the formation of carbamoyl phosphate

All but B

ATP, Bicarbonate, glutamine and CPS II react together to form
________ which then becomes ______.

Carbomoyl phosphate, OMP

OMP becomes UMP via ____________. UMP becomes UTP which then become
CTP via _____________.

OMP decarboxylase, CTP synthetase

IMP is capable of becoming both ATP or GTP. What determines its final form?

the enzyme that acts on it, adenylylsuccinate synthetase or IMP dehydrogenase

Synthesis of deoxynucleotides from their corresponding
ribonucleotides is catalyzed by what highly regulated enzyme (is also
a drug target)? What does this enzyme do? This enzyme only works on:

ribonucletide reductase, replaces the OH at the 2'C with a H,
ribonucleoside diphosphates

UMP is the precursor for dTMP but not the IMMEDIATE precursor. What is?


dUMP is converted to dTMP by _________, a drug target

thymidylate synthase

What does thymidylate synthase do to dUMP?

adds a methyl group

Initial activation of RR (ribonucleotide reductase) occurs via ___
and leads to the formation of dCTP and ___


High [TTP] lead to the inhibition of CDP, why? This also leads to the
activation of GDP to dGTP. High [dGTP] leads to the inhibition of UDP
and the activation of ADP leading to dADP and finally dATP. High
[dATP] levels lead to the shutdown of ___________, making it the
master regulator of this entire pathway

allosterically blocks, RR (ribonucleotide reductase)

What gets cleaved off during nucleotide breakdown? What do you end up with?

phosphates get cleaved off, free bases and ribose-1-phosphate

Some nitrogenous bases are reused to re-form nucleotides in the
salvage pathway. What happens to the rest?

degraded and excreted

Adenine and Guanine get broken down into __________ which is then
oxidized to uric acid


What is the correct sequence of appearance of intermediates in the
degradation of adenosine?
a. Adenosine --> hypoxanthine -->xanthine --> inosine
--> uric acid
b. Adenosine --> inosine --> hypoxanthine --> xanthine
--> uric acid
c. Adenosine --> xanthine --> hypoxanthine --> inosine
--> uric acid


Disease state caused by the overproduction of purine nucleotides
followed by excess breakdown and elimination


Disease state caused by an HGPRT deficiency, leads to severe
neurologic disease characterized by self-mutilating behavior,
spasticity, writhing of arms and legs, and cognaive deficits. Causes
excess uric acid production

Lesch-Nyhan syndrome

Tamoxifen is an example of a drug that targets
A. Receptor tyrosine kinases
B. Nuclear receptors
C. G protein coupled receptors
D. Adhesion receptors


Cetuximab specifically prevents
A. EGF from binding to its receptor
B. The EGFR from undergoing autophosphorylation
C. Intracellular domain binding of the EGFR


Terminally differentiated cells can withdraw from the cell cycle at
A. S phase
B. G0 phase
C. G1 phase
D. G2 phase


In HIV therapy, the earliest possible target to prevent replication
of the retrovirus is
A. Reverse transcriptase
B. Integrase
C. Protease
D. Reconstruction enzyme


Put the following steps of retroviral replication in the correct order:
1. cDNA strand is inserted into host chromosome
2. Reverse transcriptase is used to make viral DNA from viral RNA
3. Translated into viral proteins that are used to make the virus envelope
4. Host-cell RNA polymerase makes virus-related RNA
5. Assembly, budding and release
A. 1, 2, 3, 4, 5
B. 2, 1, 4, 3, 5
C. 3, 1, 2, 4, 5
D. 1, 3, 2, 4, 5


Transcriptionally active chromatin is
A. Acetylated, methylated, heterochromatin
B. Deacetylated, methylated, euchromatin
C. Acetylated, undermethylated, euchromatin
D. Deacetylated, undermethylated, heterochromatin


IAPs normally apoptosis and caspases.
A. Suppress, activate
B. Suppress, inactivate
C. Promote, activate
D. Promote, inactivate


The rate limiting step of the Michaelis Menten equation is
A. E + S ES
B. ES E + P C.
A and B occur at the same rate, so both are rate limiting


Niacin can _________ glycogen stores and _________blood glucose levels.
A. Deplete, lower
B. Increase, elevate
C. Deplete, elevate
D. Increase, lower


An enzyme acting on S at a low concentration has a Km.
A. Low
B. High


In glycolysis, hexokinase is
A. Inhibited by glucose 6 phosphate
B. Inhibited by Mg2+
C. Inhibited by ATP
D. Inhibited by glucose


In cancer cells, GLUT 1, GLUT 4, and hexokinase are
A. Upregulated
B. Downregulated
C. Unaffected


In the PDH complex, E2 is responsible for
A. Regeneration of the oxidized form of lipoamide
B. Transfer of the acetyl group to CoA
C. The oxidative decarboxylation of pyruvate


NADH is an of the citric acid cycle
A. Activator
B. Inhibitor


Following a carb-rich meal, how would the body respond?
A. By activating gluconeogenesis.
B. By activating the citric acid cycle.
C. By activating glycolysis.
D. None of the above.


In the pentose phosphate pathway there is generation of
A. 2 NADPH, 2 fructose 6 phosphates, 2 glyceraldehyde 3 phosphates
B. 6 NADPH, 3 fructose 6 phosphates, 1 glyceraldehyde 3 phosphate
C. 2 NADPH, 6 fructose 6 phosphates, 2 glyceraldehyde 3 phosphates
D. 6 NADPH, 2 fructose 6 phosphates, 1 glyceraldehyde 3 phosphate


_________ can lead to the production of oxaloacetate which feeds into gluconeogenesis
A. Glycerol
B. Phosphoenolpyruvate
C. Alanine
D. Glycerol 3 phosphate


Gluconeogenesis is positively regulated by
A. ATP, insulin
B. AMP, Fructose 2,6 bisphosphate
C. Acetyl CoA
D. Fructose 1,6 bisphosphatase


The RNA primer in DNA replication provides the
A. free 3' OH to which nucleotides are added
B. free 5' OH to which nucleotides are added
C. free 3' PO4 to which nucleotides are added
D. free 5' PO4 to which nucleotides are added


In the methylation of DNA, what molecule is always the donor of the
methyl group?
B. SAM-e


Which of the following groups making up the core structure of an
amino acid will affect the chemical behavior of a peptide?
A. The carboxyl group
B. The amino group
C. The R group
D. The hydrogen


The amino acid sequence determines ___________ of a protein A. structure
B. location
C. function
D. A and C
E. All of the above


In deoxyhemoglobin, the LYS residue on the alpha subunit interacts
with the C-terminal of the beta subunit. Which of the following
statements BEST describes the type of bond formed? A. Covalent bond
B. Hydrogen bond
C. Ionic bond
D. Peptide bond


Which statement BEST describes the effect of epinephrine on
mobilization of fats?
A. stimulates activation of lipoprotein lipase which converts
triglycerides to fatty acid that then enter fat cells to be stored
B. stimulates activation of gastric lipase which converts
triglycerides to fatty acid that are then absorbed by the intestines
and packaged into chylomicrons
C. stimulates activation of hormone sensitive lipase which converts
triglycerides to fatty acid that then enter muscle cells to be used
for energy
D. stimulates activation of carnitine acytransferase which converts
triglycerides to fatty acid that then enter mitochondria to be oxidized


During ketosis,
A. oxaloacetate levels are low, limiting the activity of the citric
acid cycle and the use of acetyl-COA in the citric acid cycle; this
leads to the conversion of acetyl-CoA into ketone bodies.
B. oxaloacetate levels are low, limiting the activity of the citric
acid cycle and increasing the use of acetyl-COA for the synthesis of
fatty acids.
C. oxaloacetate levels are high, increasing the activity of the
citric acid cycle and production of acetyl-COA which is stored in the
liver as ketone bodies.
D. oxaloacetate levels are low, limiting the activity of the citric
acid cycle and the use of ketone bodies in the citric acid cycle; this
leads to the conversion of ketone bodies into acetyl-CoA


Which of the following statements is/are TRUE regarding the
biological role of lipids?
1. structural component of membranes
2. major energy source during the fed state
3. transmit biological information
4. aid in the emulsification of fats
A. 1 only
B. 1 and 3 only
C. 1, 2 and 4 only
D. 1, 3 and 4 only
E. all statements are true


The three most nutritionally important omega 3 fatty acids are
alpha-linolenic acid, eicosapentaenoic acid (EPA) and docosahexaenoic
acid (DHA). Which statement BEST explains why these fatty acids are essential.
A. the body is unable to make long chain fatty acids
B. the body is unable to make polyunsaturated fatty acids
C. the body is unable to make monosaturated fatty acids
D. the Surgeon General wants Americans to eat more fish


Flash forward to the fall semester of your P3 year. You find yourself
in pharmacology class where Dr. Riggs is going over the mechanism of
action of a cancer drug, Ara-A. This drug is an antimetabolite of
deoxyadenosine. In addition to being a competitive inhibitor of DNA
polymerase, Dr. Riggs also says that Ara-A reduces cellular levels of
deoxyadenosine triphopshate but does not affect de novo synthesis of
ribonucelotides. Dr. Riggs asks: ?based on what you learned in
biochemistry, how do you think Ara-A is doing this?
A. Ara-A nucleotide(s) inhibits ribonucleotide reductase, blocking
formation of deoxyadenosine triphosphate
B. Ara-A nucleotide(s) inhibits PRPP synthetase, blocking formation
of deoxyadenosine triphosphate
C. Ara-A nucleotide(s) inhibits PRPP amidotransferase, blocking
formation of deoxyadenosine triphosphate
D. Ara-A nucleotide(s) inhibits adenylosuccinate synthetase,
blocking formation of deoxyadenosine triphosphate


Dephosphorylation of a nucleotide is the process by which the
A. the amino group is removed
B. the glycosidic bond is cleaved
C. the phosphate group is removed
D. ribose is converted to deoxyribose


OMP decarboxylase is a key enzyme in the de novo synthesis of
pyrimidine nucleotides. A deficiency in this enzyme will cause
1. Reduced UMP levels
2. Reduced TTP levels
3. Orotic aciduria
4. Reduced CTP levels
A. 1 only
B. 1 and 3 only
C. 1, 3 and 4 only
D. all are correct


Leucovorin is a folate analog that can be used in cancer patients to
prevent harmful effects of methotrexate WITHOUT affecting the
anticancer effect of methotrexate (MTX). Based on what you know about
the mechanism of MTX, which statement BEST explains how leucovorin may work.
A. Leucovorin is converted to tetrahydrofolate reductase (THF)
without using dihydrofolate reductase (DHFR), supplying THF for the
formation of THF-derivatives needed for nucleotide synthesis
B. Leucovorin blocks methotrexate from binding to thymidylate
synthetase, thus allowing TMP formation to resume
C. Leucovorin competes with methotrexate for binding to DHFR,
resuming THF synthesis and formation of THF-derivatives needed for
nucleotide synthesis


What is the mechanism of action of lovastatin?
A. Lowers the blood pressure by inhibiting protein kinase ATK.
B. Lowers cholesterol by inhibiting HMG CoA reductase.
C. Lowers the blood pressure by inhibiting HMG CoA reductase.�
D. Increases good cholesterol by inhibiting protein kinase ATK.


In the purine salvage pathway, the formation of guanosine
monophosphate (GMP) from guanine is catalyzed by:
A. hypoxanthine-guanine phosphoribosyl transferase (HGPRT)
B. adenine phosphoribosyl transferase (APRT)
C. uracil phosphoribosyltransferase (UPRTase)
D. purine nucleoside phosphorylase (PNP)


Inhibition of PRPP synthetase will
A. decrease purine de novo nucleotide synthesis
B. increase purine de novo nucleotide synthesis
C. decrease pyrimidine de novo nucleotide synthesis
D. increase pyrimidine de novo nucleotide synthesis
E. A and C


Inhibition of xanthine oxidase by allopurinol blocks formation of _____________:
A. adenine
B. uric acid
C. guanine
D. inosine


In purine de novo synthesis, formation of guanosine monophosphate
(GMP) is activated by ________________.
A. uridine triphosphate (UTP)
B. inosine triphosphate (ITP)
C. guanosine triphosphate (GTP)
D. adenosine triphosphate (ATP)


ribonucleotide reductase (RR) converts _____________ to ______________
A. ribonucleoside monophosphate (NMP) to deoxyribonucleoside
monophosphate (dNMP)
B. ribonucleoside diphosphate (NDP) to deoxyribonucleoside
diphosphate (dNDP)
C. deoxyribonucleoside diphosphate (dNDP) to ribonucleoside
diphosphate (NDP)
D. deoxyribonucleoside diphosphate (dNDP) to deoxynucleoside


SCID (or bubble boy disease) is associated with a deficiency in
adenosine deaminase (ADA), causing levels of deoxyadenosine
triphosphate (dATP) to increase. High dATP inhibits DNA synthesis by:
A. inhibiting DNA polymerase
B. inhibiting thymidine monophosphate (TMP) synthesis
C. inhibiting PRPP synthesis
D. inhibiting ribonucleotide reductase (RR)


True or False: in the pyrimidine de novo pathway, thymidine
monophosphate (TMP) originates form uridine monophosphate (UMP)
A. True
B. False


thymidine is a ____________
A. ribonucleotide
B. ribonucleoside
C. deoxynucleotide
D. deoxynucleoside


Phosphoribosyl pyrophosphate (PRPP) is a key precursor in the
formation of
A. Pyrimidine nucleotides
B. Purine nucleotides
D. A and B only
E. A, B and C


Thymidylate synthase converts ___________ to _____________
A. deoxyuridine monophopshate (dUMP); thymidine monophosphate (TMP)
B. uridine monophosphate (UMP); thymidine monophosphate (TMP)
C. deoxycytidine monophosphate (dCMP); thymidine monophosphate (TMP)
D. thymidine; thymidine monophosphate (TMP)