[BSCI 1511] - Midterm Exam Guide - Comprehensive Notes for the exam (25 pages long!)

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Vanderbilt
BSCI 1511
MIDTERM EXAM
STUDY GUIDE
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SHORT ANSWER CONCEPTS
BIOLOGY 1511 EXAM 1
GPCRs
G protein functions as molecular switch that is either on or off depending if GDP OR
GTP is attached
When GDP is bound, G protein Is inactive
Receptor and G protein work together with another protein, usually an enzyme
When signal binds to receptor, receptor is activated and changes shape, inactive G
protein binds to receptor and GTP displaces GDP, activating the G protein
Activated G protein dissociates from the receptor and binds to an enzyme, causes
shape change, enzyme triggers the rest of the cellular response
G protein acts as GTPase enzyme, GDP returns and G protein returns to original state
Example: epinephrine/cAMP pathway (see second messengers, G protein activates adenylyl
cyclase)
RTKS
RTKs exist as monomers within the membrane
Binding of the ligand causes the monomers to associate together to form a dimer
(dimerization)
Dimerization activates tyrosine kinase region of each monomer, each tyrosine kinase
adds a phosphate to a tyrosine on other monomer
Receptor is now fully activated, recognized by specific relay proteins inside the cell, each
protein binds to specific phosphorylated tyrosine, and each activated protein relay
protein then triggers an STP leading to a response
Example: Insulin pathway
Ion Channel receptors
Receptor gate is closed until ligand binds to the receptor
When it binds, gate opens and specific ions can flow through the channel
When ligand dissociates, gate closes and ions no longer enter the cell
Example: neurotransmitters between synapses in neurons
TRANSDUCTION
Example: phosphorylation cascade
1. Relay molecule activates protein kinase 1
2. Active protein kinase 1 transfers phosphate to inactive molecule of kinase 2, thus
activating it
3. Active kinase 2 phosphorylates kinase 3
4. Active protein kinase 3 phosphorylates a protein that brings about the cells response to
the original signal
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* phosphatases can dephosphorylate the kinases, and they provide the mechanism for turning
off the STP when the initial signal is no longer present, also make the kinases available for reuse
Second Messengers
1) cAMP to break down glycogen from epinephrine
adenylyl cyclase converts ATP to cAMP in response to epinephrine
epinephrine binds to receptor, receptor protein activates adenylyl cyclase, which
catalyzes the synthesis of cAMP, normal concentration of cAMP can be boosted 20
fold in a matter of seconds
usually activates serine/threonine kinase called protein kinase A
example of a problem: cholera
produces a toxin in the small intestine
toxin modifies the G protein involved in regulating salt and water secretion
modified G protein cant hydrolyze GTP back to GDP, remains stuck in active form,
continuously stimulating adenylyl cyclase to make cAMP, causes intestinal cells to
secrete high volumes of salt into intestines, with water following by osmosis, quickly get
really bad diarrhea
2) calcium ions
increasing cytosolic concentration causes muscle cell contraction, cell division,
secretion of stuff, etc.
second messenger in GPCR and RTK pathways
transported out of the cell and imported into the ER from cytosol by protein pumps
concentration in ER is usually much higher than that in the cytosol
STP- cytosolic calcium level may rise, usually by releasing it from the ER
3) Calcium and IP3 in signaling pathways
Signal molecule binds to receptor, activating phospholipase C
Phospholipase C cleaves PIP2 into DAG and IP3
IP3 quickly diffuses through cytosol and binds to IP3 gated channel in the ER
membrane, causing it to open
Calcium ions flow out ER raising calcium levels in cytosol
Calcium ions activate the next protein in 1+ signaling pathways
Cascades
If leaf cells are losing too much water, ABA is released, ABA opens calcium channels in
membrane of guard cells, calcium rushes in and releases more calcium from vacuole by
CICR, high calcium opens ion efflux channels in membrane that allow ions/salts to leave
the guard cells and closes ion influx channels, so then water follows by osmosis and then
the guard cells close so they stop losing water
RTK pathway
o Ras/MAP kinase pathway: activation of RAS stimulates cell division, a few ligands
can lead to millions of response molcules, mutations or RAS in cancers happens
when it cannot hydrolyze GTP to GDP, leading to continuous cell division
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