Test Flashcards
Cell signalling: What is a morphogen?
Exist aroudn cells as gradients in development to tell the cell what to turn into. Ex morphogen gradients make neuronal precursors become neurons
What is ‘allosteric’?
Protein alteration due to binding of a molecule
Cell signalling: Molecules A and B are in equilibrium at 1000 molecules/cell.
each A survives 10 seconds on average
each B survives 100 seconds on average
A signalling molecule comes in to double synthesis rates of both A and B
What do the concentrations look like?
How does this relate to half-life?
A increases in concentration way faster, because it has a faster turnover rate
The time required for A to shift halfway from its old to its new equilibrium concentration is equal to the time it takes it to halve its concentration
Cell Signalling: What is the turnover of cAMP like in the cell?
How is this relevant?
Fast
cAMP can make signals propegate super quickly
Cell Signalling: What proteins are responsible for cAMP’s fast turnover (creation and destruction)?
Synthesize: Adenylyl cyclase
Destruction: cAMP phosphodiesterases
Cell Signalling: How is adenylyl cyclase activated so it can make cAMP?
GPCRs bound to Gs get a ligand
Cell Signalling: What kinase does cAMP bind once adenylyl cyclase makes it?
PKA. Needs 4 cAMP molecules to bind before it releases its two active subunits
Cell Signalling: When a protein gets GTP added, what class of enzyme does this?
What about when it gets GTP removed?
Added: GEFs (Guanine Nucleotide Exchange Factors)
Removed: GAPs (GTPase-Activating Proteins)
Cell Signalling: Which of the following is a major consequence of activation of phospholipase C-B (PLCB) by the Gq trimeric GTPase?
- What protein causes this and how?*
a) Elevation of intracellular cAMP levels, leading to activation of PKA
b) Elevation of PIP3 levels in the plasma membrane, leading to activation of PKB
C) Elevation of intracellular Ca2+ levels, leading to activation of PKC
D) Elevation of IP3 in the plasma membrane, leading to the activation of PKD
C), IP3 goes down to the ER and binds to open calcium channels, creating calcium waves that activate PKC if diacylglycerol is also bound
Cell Signalling: What protein does the activated GCPR activate in the PKC pathway?
How?
Gq
Adds GTP to it
Cell Signalling: What are the two parts of Gq?
Why are they important?
The a-subunit and the BY complex
The a-subunit binds to phospholipase C-B
Not sure what BY does
Cell Signalling: What protein activates PI 4,5-bisphosphate?
How?
Phospholipase C-B (after Gq activates it)
It hydrolizes PI 4-5 bisphosphate to break it in two
Cell Signalling: What type of receptor is the mitogen receptor (results in transition to S-phase)?
Receptor tyrosine kinase
(A type of enzyme-coupled receptor)
Membrane Traffic: What changes the balances of phosphoinositide types on membranes?
What does this balance do in terms of coat formation?
PI kinases
PI phosphatases
PI-binding proteins recognize particular patterns of PI signals
Where do COPI-coated vesicles travel?
Where do COPII-coated vesicles travel?
Where do Clathrin coated vesicles travel?
COPI: Golgi > ER, Golgi > plasma membrane
COPII: ER > Golgi
Clathrin: Plasma membrane > golgi, Golgi > endosome
Membrane Traffic: What protein helps disentangle SNARES after vesicle fusion?
NSF
Binds to SNARE, hydrolyzed ATP to pry apart complexes
Membrane traffic: What kind of signal tags transmembrane proteins for degradation?
Where?
Ubiquitin
Goes to lysosome
Endosomes: What is the function of ESCRT complexes?
Bind to ubiquitin tags on membrane proteins
Bring the membrane proteins inside the endosome, into intralumenal vesicles
Membrane Traffic: What is another function of endosomes besides bringing stuff to lysosomes? (in regards to membrane proteins)
They can carry membrane proteins inside of them
Ready to jump on to membrane if needed
What markers diverts proteins to lysosomes (via endosomes) in clathrin-coated transport vesicles?
Mannose-6 phosphate
