Signal Transduction Flashcards
SAME signal on SAME R on DIFF cell will ellicit a ____ response (same/diff)
DIFF
What are two types of intracellular signalling P’s?
How are these regulated?
Kinases
G-P’s (GTP-binding P’s)
Reg by PHOSPHORYLATION
GPCR steps
1) Ligand bind 2 R → GP bind to R
2) R change conformation & G P ACTIVATED
3) GDP→ GTP on alpha =DISSOCIATE
4) alpha interacts with EFFECTOR
5) alpha hydrolyse GTP → GDP
6) REASSOCIATION of subunits
Which GP subunit has GTPase activity?
ALPHA
Activated PKA has 2 routes. What are they?
1) can PHOS target proteins
2) can ENTER NUC to PHOS TFs
T/F: G-P alpha subunit is responsible only for stimulating effector to ↑ [cAMP]
FALSE: alpha subunit has BOTH STIMULATORY AND INHIBITORY effects
T/F cholera and pertussis have different outcome
FALSE → BOTH ↑ ↑ cytosolic [cAMP]
Cholera LOCKS Gs (stimulatory) in ACTIVE STATE (ATP) & BLOCKS GTPase activity
Pertussis LOCKS Gai in GDP-bound STATE (inactive)
Mechanism of Cholera and outcome
LOCKS Gas (stim) in ACTIVE STATE with GTP
BLOCKS GTPase activity
= ↑ cytosolic [cAMP]
Mechanism and outcome of PERTUSSIS
LOCKS Gai in GDP-bound / INACTIVE state
= ↑ cytosolic [cAMP]
what is the action is IP3
And DAG?
What is their effector protein?
IP3 → ↑ Ca++ release → PKC Activation
DAG → PKC activation → TF activation
Effector P = PLC (phosolipase C)
Retinitis pigmentosa is a mutation in what?
What is the treatment?
RHODOPSIN
Vit A SLOWS progression
How are RTKs activated?
Dimerization
What are the 3 effector p’s of RTK
1) PI3-K
2) PLC
3) GRB2
RTK: PLC path
Same as Gq:
Breaks ↓ inositol phosophates to IP3 & DAG
DAG = PKC & TF IP3 = Ca++ & PCK
RTK: PI3K path
RTK dimerizes → PHOS PI3-K → changes PIP2 to PIP3 PIP3 acts PKB/Akt PKB -inhibs- BAD/BID BAD -inhibs- Bcl2 Bcl2 -inhibs - BAX/BAC BAX forms pores in mito Pores = activate caspase = cell SURVIVAL
RTK: PI3-K path::
When ligand bound and path active, does that = cell survival or APOP?
Cell SURVIVAL
RTK: GRB2 what is the fn & path
Fn = REVEAL DOCKING SITE 4 P’s
ligand bind RTK → GRB2 (Adapter) → SOS (GEF) → Ras (Effector)
RTK → GRB2 → SOS → Ras → Raf → Mek → MAP-K → response!
RTK: GBR2 path simplified
Ligand → RTK → adaptor → GEF → GTPase → Effector
Specific = RTK → GBR2 → SOS → Ras
In GBR2 path, what is the:
Adaptor, GEF, GTPase?
Adaptor = GBR2 GEF = SOS GTPase = Ras
Non insulin dependent diabetes mellitus cause?
↓ reg of insulin R
↓ R PHOS & TK activity
↓ 2nd messengers in pathway
Steroid H R’s
Where are the receptors?
What does H bind to? And what is unique about this type of signalling
INTRAcellular nuc R’s
All TF R’s will be in nuc or cytoplasm
Steroid H bind HRE in DNA →
ACTIVATES it DIRECTLY
