BIOB11H3 Lecture Notes - Map Kinase Kinase Kinase, Receptor Tyrosine Kinase, G Protein–Coupled Receptor

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greenherring451

21 Apr 2013

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First we will talk about a very conserved pathway called the map kinase cascade. Then we will talk about pathway interactions and later we will talk about apoptosis. Last time we talked about receptor tyrosine kinase this type of communication isn"t the only thing this category of receptors does. Many of them are involved in governing cell cycle control, that is, governing cell division. When the appropriate signal comes in, it might be in the form of a growth factor type of hormone and it gets together with its receptor and this activates a couple of intermediates called ras and raf. The map kinase cascade for the most part deals with the commitment of cells to cell proliferation. Figure 15 20 shows what to gets the pathway rolling towards cell division. The growth factor comes in and binds to a receptor if it exists. Phosphorylation occurs and the receptor is then phosphorylated.

Related Questions

The EGF-receptor is a receptor tyrosine kinase that binds toepidermal growth factor (EGF). In response to EGF binding, theEGF-receptor stimulates a signaling pathway that involves Ras.Ultimately, this signaling pathway leads to the upregulation offactors that promote cell division. As a result, in response toEGF, cells that express the EGF-receptor undergo cell division toproduce more cells. If an inhibitor that inhibited all G proteinswas added to cells, how would this affect the ability of thesecells to respond to EGF?

1)The inhibitor would have no effect, because the EGF-receptoris not a G protein-coupled receptor.

2)While the receptor would dimerize and autophosphorylate in thepresence of the inhibitor, downstream signaling would be preventedbecause the inhibitor would affect Ras activity.

3)In the presence of the inhibitor, the receptor could bind toEGF and dimerize, but it would not be able to autophosphorylatebecause this requires the activity of a G protein.

amethystantelope937

QUESTION 1

Which of the following is an example of an extracellular signal molecule?

	a.	IP₃
	b.	cAMP
	c.	Insulin
	d.	Diacylglycerol

2 points

QUESTION 2

Nuclear hormone receptors _____

	a.	Bind to water soluble ligands
	b.	Activate second messengers
	c.	Regulate transcription in response to ligand binding
	d.	Are normally located on the plasma membrane

2 points

QUESTION 3

Which of the following does not occur when a receptor tyrosine kinase is bound by ligand?

	a.	Phosphorylation of the RTK
	b.	Cytoplasmic proteins bind the phosphorylated RTK
	c.	Dimerization of the RTK
	d.	The RTK binds to DNA to regulate transcription

2 points

QUESTION 4

Which of these is a logical signal-transduction pathway?

	a.	An intracellular receptor activates phospholipase C, which cleaves a membrane protein to form IP₃, which then activates the opening of an ER channel protein, which releases cyclic AMP into the cytoplasm, where it binds to an intracellular enzyme that carries out a response.
	b.	A G-protein-linked receptor activates G protein, which activates phospholipase C, which cleaves a membrane lipid to form IP₃, which binds to a calcium channel on the ER, which opens to release calcium ions into the cytoplasm, which bind to an intracellular enzyme that carries out a response.
	c.	An ion-channel receptor opens, allowing a steroid hormone to enter the cell; the steroid hormone then activates protein kinases that convert GTP to GDP, which binds to an intracellular enzyme that carries out a response.
	d.	A tyrosine-kinase receptor activates adenylyl cyclase, which activates phospholipase C, which converts ATP into cyclic AMP, which binds to an intracellular enzyme that carries out a response.

2 points

QUESTION 5

Which of the following is an example of signal amplification?

	a.	activation of an enzyme molecule
	b.	activation of a specific gene by a growth factor
	c.	Breakdown of many cAMP molecules
	d.	activation of 100 molecules by a single signal binding event

2 points

QUESTION 6

Consider a signal transduction pathway that utilizes cAMP as a second messenger to activate PKA (Protein Kinase A). Which of the following situations will result in the cellular response?

		The G protein releases GDP and binds to GTP
		The target protein (adenylyl cyclase) is inactive
		The regulatory subunits of PKA (Protein Kinase A) are bound to the catalytic subunits
		The appropriate G protein is bound to GDP

2 points

QUESTION 7

Which of the following is found in only some signal transduction pathways? [In other words, which is not found in all signal transduction pathways?]

		Receptor protein
		Extracellular signal molecule
		Intracellular signaling molecule
		Cellular response
		Effector protein

2 points

QUESTION 8

The enzyme that specifically catalyzes the conversion of ATP to cAMP is:

		Adenylyl phosphatase
		Adenylyl kinase
		Adenylyl dehydrogenase
		Adenylyl cyclase

2 points

QUESTION 9

If an animal cell suddenly lost the ability to produce GTP, what might happen to its signaling system?

		It would use ATP instead of GTP to activate and inactivate the G protein on the cytoplasmic side of the plasma membrane.
		It would not be able to activate and inactivate the G protein on the cytoplasmic side of the plasma membrane.
		It would employ a transduction pathway directly from an external messenger.
		It would be able to carry out reception and transduction but would not be able to respond to a signal.

2 points

QUESTION 10

A hormone signal is sent from the brain to other parts of the body via the bloodstream. Why do only certain cells respond to this signal?

		Hormones do not last long enough in the bloodstream to stimulate a cellular response
		Only cells that have a specific transcription factor gene will be able to respond to the signal
		Only cells in the immediate vicinity of the cell sending the signal will respond
		Only cells that have a receptor for the specific signal will be able to respond to it

cerisehedgehog846

1.In 1971, Dr. Judah Folkman published the âangiogenic hypothesisâ suggesting that a tumor cannot grow beyond 1â2 millimeters without the development of new blood vessels (angiogenesis) that provide access to oxygen and nutrients. During the 1990s, it was discovered that vascular endothelial growth factor (VEGF) stimulates migration and proliferation of the cells that form blood vessels, leading to the formation of new blood vessels. VEGF binds to receptor tyrosine kinases (RTKs) on the cell surface and causes the RTKs to dimerize and become active, thereby initiating an intracellular signaling cascade that stimulates cell division and inhibits apoptosis. Many cancer cells secrete high levels of VEGF and increased VEGF expression in a tumor is correlated with a poor medical outcome for the patient. You work for a biotechnology company that seeks to create anti-cancer drugs that prevent growth of tumors and/or cause tumors to shrink, while leaving normal cells relatively untouched. Your company has purchased the rights to therapeutic uses of VEGF derived proteins as anti-tumor drugs. You have found that the VEGF protein has 2 domains, one involved in receptor binding, the other is required for dimerization of VEGF. You propose to make mutant versions of the protein that will act as antagonists of the receptor to be given to patients as an IV treatment as a way to inhibit the endogenous VEGF secreted by the tumor.

a.Which of the 2 domains should you mutate (receptor binding or dimerization)?

b. How do you expect the introduction of the mutant protein into the bloodstream of patients to block tumor progression (in other words, why did you change the domain in part a)?

peachmoose600

BIOB11H3 Lecture Notes - Map Kinase Kinase Kinase, Receptor Tyrosine Kinase, G Protein–Coupled Receptor

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