7 Receptor and Effector Mechanisms Flashcards
Describe a receptor with intrinsic enzymatic activity
Ligand binding activates enzyme activity that phosphorylates the receptor itself and other substrates.
Define a ligand-gated ion channel
The intrinsic pore of a receptor opens when a complementary ligand binds to the receptor.
Give examples of ligands GPCRs respond to
Ions
Neurotransmitters
Hormones
Large glycoproteins
Describe the common basic structure of a GPCR
Single polypeptide chain
7 transmembrane spanning regions
Extracellular N terminal
Intracellular C terminal
Where can a ligand bind to a GPCR?
Between the 2nd and 3rd transmembrane domain
The N-terminal region
What is a G-protein made up of?
3 subunits, alpha, beta, gamma
How does a G-protein work?
When a ligand binds to the GPCR:
GTP => GDP
The ‘a-By’ complex then dissociates.
Each G subunit interacts with effector proteins
GDP => GTP (via GTPase)
‘By’ then regains affinity for ‘a’ to reform the G-protein complex
What is the result of Ga and GBy subunits being specific to effector proteins?
1 type of GPCR will activate 1 type of G-protein and therefore 1 effector to produce a response.
Describe the actions of adenyl cyclase
ATP => cyclic AMP
How does cyclic AMP cause a cellular response?
cAMP binds to the regulatory area of AMP-dependent protein kinase (PKA). The catalytic area then detaches to create an effect.
How does Phospholipase work in the cell? What is the final response?
PIP2 => IP3 + DAG
Ca2+ released from intracellular stores
How does adrenaline and noradrenaline increase inotropy?
Interact with ventricular B1-adrenoceptors
PKA phosphorylates VOCC so more Ca2+ enters the cell on depolarisation. This increases the contraction of the heart.
How is neurotransmitter release modulated by GPCRs?
The GBy subunit inhibits some VOCCs, reducing Ca2+ influx and neurotransmitter release.
