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74 Cards in this Set

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  • Back
What is Vmax and what is it determined by?
Vmax is the maximum velocity at which an enzyme can chew up substrate. This value is determined by the number of the specific enzyme in solution
What is Km and what does it tell you?
it is the substrate concentration that gives us half of Vmax. Km tells you have much the enzyme likes the substrate. A very low Km means that the enzyme really likes the substrate
What protein is required for control of gene expression by a water soluble hormone?
CREB protein (cAMP response element binding) will bind to enhancer regions of DNA
What are good examples of water soluble hormones?(6)
insulin, glucagon, catecholamines, PTH, ADH, TSH
How does a lipid hormone have it’s effect on a cell?
It binds it’s receptor inside the cell and the hormone-receptor complex binds to an enhancer region on the DNA. The receptor for the lipid soluble hormone is a DNA binding receptor
What are some examples of lipid soluble hormones?(4)
steroids……………calcitriol……... Thyroxines………………retinoic Acid
What is retinion acid? (derivative of what)
derivative of vitamin A
What are the 4 signal transduction pathways by water-soluble hormones?
cAMP, PIP2, cGMP, and the pathways for insulin and growth factors
Which pathways involve a G protein?
cAMP and PIP2
What is the protein kinase for the cAMP pathway?
Protein kinase A
What is the protein kinase for the PIP2 pathway?
protein kinase C
What is the protein kinase for the cGMP pathway?
Protein kinase G
What is the protein kinase for the insulin and growth factor pathways?
Tyrosine kinase activity of receptor
Which main hormones use the cAMP system? (5)
glucagone, epinephrine Beta (Gs), Epinephrine Alpha 2 (Gi), dopamine, serotonin, and many others
Which main hormones use the PIP2 system? (2)
vasopressin…..epinephrine alpha 1
What is the structure for all receptors associated with the cAMP system?
The fully span the membrane 7 times
Which end of the receptor is extracellular?
amino terminus
Which end of the receptor is intracellular?
carboxylic acid terminus
What is the structure of G proteins?
They are composed of alpha, beta, and gamma subunits
Which G proteins are associated with the cAMP system?
Gs or Gi proteins
What is the second messenger in the cAMP system and what does it do??
cAMP, it activates protein kinase A to phosphorylate enzymes and the CREB protein
What are enhancer regions?
regions to which proteins bind on DNA in order to regulate gene expression
In summary, what was the process of the cAMP system?
hormone binds to 7 transmembrane receptor, which stimulates a trimeric Gs protein which stimulates adenyl cyclase (or Gi would inhibit adenyl cyclase), the adenyl cyclase increases the cAMP which will activate protein kinase A which will phosphorylate proteins and activate CREB
Are epinephrine Beta receptors stimulatory or inhibitory?
Beta receptors are bound to the Gs protein and thus are stimulatory?
Where are Beta 1 receptors mainly found?
What is one key protein activated by epinephrine binding to the Beta 1 receptor?
ligand gated calcium channels
How does calcium influx in cardiac tissue increase contractility?
it will remove the troponin tropomyocin complex and allow myosin to bind to actin.
Where is the Alpha 2 receptor found?
it is mainly a presynaptic receptor which regulates the synthesis and release of neurotransmitter
What is the mechanism for the alpha 2 receptor?
when epinephrine or norepinephrine bind to the alpha 2 receptor, it stimulates the Gi protein which inhibits adenyl cyclase, thus decreasing cAMP and thus decrease protein kinase A activity
What is the key enzyme inhibited by the decreased protein kinase A associated with alpha 2 receptors?
tyrosine hydroxylase... other proteins associated with releaseing the transmitter will also be inhibited
What is the significance of tyrosine hydroxylase?
it is the rate limiting step in the synthesis of catacholamines
What is the pathway for the PIP2 system?
hormone binds to receptor with 7 membrane spanning domains….this activates the Gq protein which activates phospholipase C….which, like it’s name implies, degrades the membrane to release IP3 (one half of phospholipid) into the cytoplasm and DAG (other half of phospholipid) which will remain in the membrane….the released IP3 then goes to the ER and has it release Ca++, which coupled with the DAG will activate Protein kinase C, which will phosphorylate proteins or regulate gene expression
What is one main difference between protein kinase A and C?
protein kinase A is in the cytoplasm while protein kinase C is in the membrane
Where are alpha 1 receptors mainly found?
smooth muscle cells of blood vessels
What is the mechanism of action of the alpha 1 receptor?
hormone to receptor to Gq to phospholipase C to DAG and calcium to protein kinase C to phosphorylation of myosin light chain……if myosin light chain is activated, in smooth muscle the myosin and actin can then interact which causes contraction
Where are receptors for ADH found?
V1 receptors = blood vessels………V2 receptors = renal tubules
What does each receptor for ADH cause?
V1 = vasopressin causes contraction of the smooth vascular muscle... V2 = promotes water reabsorption
What is the structure of an ANF receptor?
the completely spans the membrane, but does so only 1 time as compared the the 7 times for the cAMP and PIP2 system receptors
How is the second messenger produced in the cGMP system?
The ANF receptor will directly comvert the GTP to cGMP, the bypassing the G protein and second enzyme of the cAMP and PIP2 systems
What is the mechanism of action for the cGMP pathway?
ANF binds the single transmembrane domain receptor which directsly converts GTP to cGMP, which activates protein kinase G….which phosphorylates phosphatase which dephosphorylates other proteins….especially myosin light chain…the deactivation of myosin light chain inhibits the myosin actin interaction….thus relaxing muscle
Other than ANF, which other substances stimulate the cGMP system?
NO directly enters the cytoplasm and produces guanylcyclase which converts GTP to cGMP…which then stimulates protein kinase G and relaxes smooth muscle
How is nitric oxide produced?
it is produced in endothelial cells by the breakdown of arginine
What enzyme produces nitric oxide?
nitric oxide synthase
Why can NO difuse through our cell membrane?
it is a gas produced by nitric oxide synthase
How does No activate guanylcyclase?
binds to the HEME group on the guanylcyclase protein
What are the three main drugs which use the NO pathway?
nitroprusside, notroglycerine, and hydralazine
What is a major side effect of nitroprusside?
it breaks down to cyanide, thus cyanide poisoning is the side effect
Why is nitroglycerine not used in hypertensive emergencies while nitropruside is used?
nitroglycerine mainly dialate the veins and not the arteries
When is nitroglycerine used?
in acute anginal attack because it decreases preload and thus decreases oxygen demand by the heart
What is the structure of the insulin receptor?
it is actually two separate transmembrane receptors that are connected by the insulin molecule that they bath attach to. The insulin molecule binds to the N terminus, just like the previous pathways... whereas kinase activity is activated through second messengers in the cAMP, cGMP, an PIP2 pathway, how is the kinase activity activated in the insulin / growth factor system?
What type of kinase is protein kinase A, C, and G?
serine, threonine kinases
What type of kinase if tyrosine kinase?
tyrosine kinase
What happens when the insulin receptor in phosphorylated by the tyrosine kinase?
the triggers the binding of a major protein which will cover the entire bottom protion of the receptor.
What is the name of the protein which binds to the Insulin receptor after the receptor has been phorphorylasted by tyrosine kinase?
IRS-1... (insulin receptor substrate)
After IRS-1 is bound to the insulin receptor, what will it cause?... What is special about these proteins?
binding of several types of proteins with an SH2 domain.
What is the function of three of the SH2 domain proteins bound to the IRS on the insulin receptor?
(several of them are related to oncogenes) 1. one is p21 ras G protein related.... 2. one is related to PI kinase... 3. one simply actives protein phosphatases (remove phosphates from proteins)
What will the SH2 protein related to PI kinase cause?
-translocation of GLUT-4 to membrane in Adipose and muscle cell... -Pi kinase also changes gene expression in the nucleus
What are the unique feature of the p21 ras G protein?
it is monomeric, as opposed to trimeric, it is cytoplasmic, as opposed to membrane bound, and it directly stimulates increased gene expression in the nucleus (involved highly in cell growth and division
Which pathway does glucagon trigger and what does this do?... how does this compare with insulin?
Glucagon trigger the cAMP pathway which activates kinases…..whereas insulin via the SH@ protein activates protein phosphatase
What is the effect of insulin on glycogen phosphorylase and glycogen synthase, and is the active form phosphorylated and not phosphorylated?
Insulin dephosphorylates both glycogen synthase and dephosphorylase, which activates glycogen synthase and inactivates glycogen phosphorylase
What is the effect of insulin on glycogen phosphorylase and glycogen synthase, and is the active form phosphorylated and not phosphorylated?
Glycogen activates glycogen phosphorylase and deactivates glycogen synthase. It does this by phyosphorylating these enzymes
What is always insulins mode of action?
What is always glucagon’s mode of action?
Why are G proteins called G proteins?
They bind GTP to change their activity.
Where does GTP and GDP binding occur on the G proteins?
Alpha subunit
What diseases’s mechanism is ADP ribosylation of G proteins?
Cholera toxin…..E. Coli toxin…… and Pertussis toxin
In disease states, where on the G protein does the ADP ribosylation occur?
Alpha subunit of the G proteins.
What is the specific mechanism of cholera toxin?
ADP ribosylation of the alpha subunit of the Gs protein leaves it is a constantly stimulated state, thus greatly increasing cAMP which leads to phosphorylation of chloride channels….thus leading to the release of Chloride into the lumen of the intesting…this chloride traps Sodium in the lumen also…thus raising the osmolarity of the luman and causing it to retain and draw too much water.
What is the mechanism for E.Coli enterotoxin?
same as cholera toxin
What is the mechanism for the pertussis toxin?
ADP ribosylation of Gi. Instead of exaggerating the inhibition, the ADP ribosylation completely shuts down Gi inhibition adenyl clcyase and cAMP production increases
What is the disease associated with pertussis toxin, and what is the mechanism?
the disease is whooping cough and the mechanism is not well known.
What is a ras protein and thus ras gene associated with?... what is the significance?
the signal transduction of growth factors…remember the insulin growth factor receptors... thus if there is a mutation in the ras genes, they can directly effect cell growth and division
What is the name for genes that produce compound that can trigger cell growth and division?
What is an oncogene that is functioning normally?