Exam 17: Cell Signaling

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NF- κ\kappa B activates the gene for I κ\kappa B, which feeds back and inhibits NF- κ\kappa B activity.

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CREB is activated by

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Activated CREB protein

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How would a mutation in the TGF- β\beta type I receptor that prevented it from being phosphorylated affect the cell?

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Signaling by neurotransmitters is an example of _______ signaling.

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Which statement correctly describes how protein kinase A can activate genes?

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Binding of integrins to the extracellular matrix stimulates the FAK protein-tyrosine kinase.

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Ras is a membrane-bound _______ when activated.

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Binding of integrins to the extracellular matrix leads to integrin clustering and activation of the nonreceptor tyrosine kinase

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MAP kinase is an abbreviation for _______ protein kinase.

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Nitric oxide is considered a paracrine signal molecule because it

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In signaling pathways, the duration of a single activated pathway (for example, short versus long periods of time) often leads to completely different cellular responses.

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Which of the following is not a commonly observed consequence of the binding of a signaling molecule to its cell surface receptor?

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The G protein that activates adenylyl cyclase is a

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The alpha subunit of the G protein that is associated with the epinephrine receptor, Gs,

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Which of the following is an example of endocrine signaling?

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Steroid hormones usually act via receptors that

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As a cell biologist for a pharmaceutical company, you are charged with developing a drug to inhibit the cAMP response element binding protein (CREB) pathway. Briefly describe the cascade leading to CREB activation and where one might target a drug to block its activation.

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What is the basis for the different responses of nerve cells versus heart muscle cells to acetylcholine?

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β\beta -arrestin binds to phosphorylated G protein-coupled receptors, binding Raf, MEK, and ERK into the complex and linking the G protein-coupled signal pathway to the ERK signal pathway. This is an example of inhibitory crosstalk.

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