Lecture: 23 Flashcards
G-protein couple receptor (GPCR) function?
Passes on a signal (message) from outside the cell by producing a second messenger inside the cell
CAMP Pathway
-glucagon and catecholamines (Epinephrine, norepinephrine)
Pathway:
1) (Heptahelical receptors) GPCR passes on a signal from outside the cell by producing a second messenger inside the cell
2) Epinephrine/norepinephrine or glucagon binds to GPCR = binding it to G-S-Beta-2
3) GDP bond to Gs falls off and GTP comes out activating it
4) Gs moves to adenylyl cyclase = activation
5) Adenylyl cyclase forms cAMP
6) cAMP can activate Protein kinase A + PKA phosphorylates of cellular proteins = cellular response
(CREB, CREB-P = Change in gene expression) ALSO turns ATP to SER/THR)
7) Or cAMP can be degraded by cyclic phosphodiesterase (Hydrolyzes cAMP to 5’ -AMP)
Cholera
(Toxin)
What it does:
-ADP-Ribosylates G-ALPHA-S resulting in continuous = CONTINUOUSLY ACTIVE G- ALPHA-S (BC GTP constantly activated)
CAMP effects:
-INCREASES in intestines
Pertussis
(Toxin)
What it does:
-ADP-Ribosylates G-ALPHA-I resulting in continuous = CONTINUOUSLY INACTIVE G- ALPHA-I
CAMP effects:
-INCREASED in respiratory-tract cells
Effects:
- Respiratory distress
- Whooping cough
E. Coli
-Can produce a toxin that ADP-Ribosylates G-ALPHA-I = INCREASED CAMP
IP3, DAG, Ca2+ Pathway
Pathway: (Phosphoinositide System:)
1) (Heptahelical receptors) GPCR passes on a signal from outside the cell by producing a second messenger inside the cell
2) Epinephrine/Norepinephrine binds to GPCR = binding it to G-Q-Alpha-1
3) G-Q-Alpha activates phospholipase C (PLC)
4) PLC cleaves PIP2 to IP3 and DAG
5) IP3 and CA2+ activate the Protein Kinase C = cellular response
(Protein Kinase C requires DAG, Ca2+ and Phospholipid for maximal activity)
G-Q-Alpha-1
Increases IP3/DAG, Ca2+, Protein kinase c (PKC)
G-I-Alpha-2
Decreases cAMP, IP3/DAG (everything)
G-S-Beta-1
Increases cAMP, Ca+
G-S-Beta-2
Increases cAMP, Protein kinase A (PKA)
relaxation smooth muscle