1. Describe how you would measure glycogen phosphorylase activity?
Draw a graph that shows glycogen phosphorylase activity before and after
phosphorylation of this enzyme. Also show on the graph how activity
will change upon glycogen depletion.
2. How would you make 250 milliliters of 1.4M NaCl? What
percent solution is this? Hint: the molecular weight of NaCl is 58.5.
Answer 5 of the following 7 questions
3. Glycogen and cellulose are both polymers of glucose.
Most animals, however, cannot utilize cellulose as an energy source.
4. Typically, the following concentrations of ions are found inside and outside mammalian cells:
Inside: Na+ = 15mM
K+ = 150mM Cl- =
Outside: Na+ = 150mM K+ = 5mM Cl- = 120mM
Gamma-aminobutyric acid (GABA) is a neurotransmitter that, upon binding
to its receptor, results in the opening of ligand-gated Cl- channels.
What effects would GABA have on a muscle cell?
5. Recently, an experimental drug, LY354740, has been shown to
alleviate some of the signs of schizophrenia in rats. Also recently,
an FDA advisory committee recommended approval of Herceptin as a breast
cancer therapy. Compare and contrast the modes of action of these
6. The binding of a sperm to an egg and the binding of epinephrine
to its receptor on a myocardial cell both result in increased intracellular
Ca2+ levels. Compare and contrast these two systems.
7. You discover a new hormone, Wildcatine, and hypothesize that
it binds to a receptor on pancreatic cells, thereby triggering a signal
transduction pathway utilizing Ca2+ as a second messenger. How would
you test this hypothesis?
8. A recent report showed that the hormone estrogen can bind to
two different receptors, ERa and ERb. Furthermore, the researchers
demonstrated that binding of estrogen to ERa results in increased production
of certain proteins, but binding of estrogen to ERb results in decreased
production of these proteins. How can estrogen bind to two different
receptors and cause such different outcomes?
9. Clostridium botulinum, the bacteria that causes botulism, produces
a neurotoxin that inhibits the release of acetylcholine from pre-synaptic
cells at neuromuscular junctions. Clostridium tetani, the bacteria
that causes tetanus, produces a neurotoxin that causes the increased activity
of acetylcholine at neuromuscular junctions. What effects would these
two neurotoxins have on a muscle cell and why?