Unit 17: Cell Signaling
How a molecule that never enters a cell still changes its behavior: receptors, second messengers, kinase cascades, and the amplification built into every step.
7 topics · 27 questions
Each topic is a path, not a menu: work down it in order and every question builds on the one above. Click any of them to watch the answer draw itself.
Signal Transduction from Ligand to Response
- How it worksHow does a ligand binding a cell-surface receptor set off a chain of intracellular events without ever entering the cell?
- Common mistakeWhy doesn't a signaling molecule directly change a target cell's behavior all by itself?
- Going furtherWhat happens to a cell's response when it lacks the receptor for a hormone circulating throughout the whole body?
Your turn1 of 2
A hormone circulates through the bloodstream and binds a receptor on a target cell's surface, and that cell then changes its behavior. A student pictures the hormone molecule itself as reaching inside the cell and directly flipping the switch that changes the cell's behavior. Why doesn't a signaling molecule directly change a target cell's behavior all by itself?G-Protein-Coupled Receptors and Heterotrimeric G Proteins
- How it worksHow does ligand binding cause a GPCR to swap GDP for GTP on its partner G protein?
- How it worksWalk me through how the activated G protein's subunits split apart and go on to activate downstream enzymes.
- Common mistakeWhy isn't a G protein permanently active once it's been turned on by a receptor?
- Going furtherWhat happens to G protein signaling when a mutation locks the G protein in its GTP-bound active state, as in cholera toxin?
Your turn1 of 2
A ligand binds a GPCR, and this triggers its partner G protein to swap GDP for GTP, activating it. A student assumes once this G protein is turned on, it should stay permanently locked in its active state indefinitely. Why isn't a G protein permanently active once it's been turned on by a receptor?Second Messengers: cAMP and Protein Kinase A
- How it worksHow does adenylyl cyclase convert ATP into cyclic AMP once a G protein activates it?
- How it worksHow does cyclic AMP activate protein kinase A to phosphorylate downstream target proteins?
- Common mistakeWhy isn't cyclic AMP itself the final effector that directly carries out the cell's response?
- Worked exampleFind the total number of cAMP molecules produced if one activated adenylyl cyclase makes 100 cAMP per second over 10 seconds.
Your turn1 of 2
Find the total number of cAMP molecules produced if one activated adenylyl cyclase makes 218 cAMP per second over 27 seconds.Calcium and IP3 Signaling
- How it worksHow does phospholipase C split a membrane lipid into IP3 and diacylglycerol after receptor activation?
- How it worksHow does IP3 trigger the release of stored calcium from the endoplasmic reticulum into the cytosol?
- Worked exampleFind how many-fold intracellular calcium concentration rises when it jumps from a resting 100 nanomolar to an activated 1 micromolar.
- Common mistakeWhy isn't calcium simply a structural ion with no role as a genuine intracellular signal?
- Going furtherWhat happens to a signaling response when the ER's calcium stores are experimentally depleted beforehand?
Your turn1 of 2
Find how many-fold intracellular calcium concentration rises when it jumps from a resting 120 nanomolar to an activated 1798 nanomolar.Receptor Tyrosine Kinases and the RAS-MAPK Cascade
- How it worksHow does ligand-induced dimerization let a receptor tyrosine kinase phosphorylate its own partner receptor?
- How it worksWalk me through how that phosphorylation recruits Ras and fires off the MAPK kinase cascade.
- Common mistakeWhy isn't Ras permanently active once a growth factor has turned it on?
- Going furtherWhat happens to cell growth signaling when a Ras mutation locks the protein in its active GTP-bound state?
Your turn1 of 2
A growth factor binds its receptor tyrosine kinase, which activates Ras, which then fires off the MAPK kinase cascade to promote cell growth. A student assumes Ras must remain permanently switched on once it's been activated by this signal. Why isn't Ras permanently active once a growth factor has turned it on?Signal Amplification Through Kinase Cascades
- How it worksHow does each enzyme in a kinase cascade activate many copies of the next enzyme, multiplying the signal at every step?
- Common mistakeWhy isn't signal amplification just the original signal molecule being copied over and over?
- Ties togetherHow does this same amplification logic explain both the cAMP cascade and the MAPK cascade producing an outsized response from a tiny stimulus?
Your turn1 of 2
One hormone molecule binding one receptor can end up activating thousands of downstream target molecules by the time a kinase cascade finishes relaying the signal. A student pictures this amplification as the original signal molecule somehow being copied over and over into thousands of identical copies. Why isn't signal amplification just the original signal molecule being copied over and over?Negative Feedback and Signal Termination
- How it worksHow does a phosphatase reverse a kinase cascade's phosphorylation to return proteins to their resting state?
- How it worksHow does receptor internalization remove an activated receptor from the cell surface to end a signal?
- Common mistakeWhy doesn't a signaling pathway simply run forever once it's been switched on?
- Worked exampleFind how many minutes it takes a phosphorylated receptor's signal to fall below threshold if a phosphatase halves it every 3 minutes and two half-lives are needed.
Your turn1 of 2
Find how many minutes it takes a phosphorylated receptor's signal to fall below threshold if a phosphatase halves it every 7 minutes and 4 half-lives are needed.