Hello Friends
to continue with signal transduction
The first signal transduction pathway to discuss today is cAMP pathway.
High level of epinephrine induce or stimulate this pathway.
In this pathway epinephrine is primary messanger and cAMP is secondary messanger.
When epinephrine bind to G protein coupled receptor, the GDP is exchanged with GTP and alpha subunit of trimeric G protein is released from it and interacts with adenyl cyclase and starts producing cAMP.
cAMP activates protein kinase A. Protein kinase A is a tetramer of two regulatory and two catalytic subunits.So when cAMP binds to regulatory subunit it gets confirmation change in regulatory subunit and separates from catalytic subunit which results in activated protein kinase A.
Protein kinase A activates phosphorylase kinase A.
Activated Phosphorylase kinase A activates glycogen phosphorylase. Glycogen phosphorylase is enzyme used to convert glycogen to glucose.
Protein kinase A also phosphorylate glycogen synthase. Phophorylation of glycogen synthase inactivates this enzyme and inhibit glycogen synthesis.
Increase in cAMP leads to
Enhanced degradation of storage feuls, increase of acid secretion by gastric mucosa,
decrease in aggregation of blood platelets.
In odorant receptors of nose are coupled to G protein coupled receptors.
Stimulus leads to increase in cAMP level and cAMP directly act on sodium ion channel in plasma membrane and causes depolarisation of membrane and initiation of nerve impulse.
G protein are also involved in cholera and whooping cough.
In cholera, the part of cholera toxin has enzymatic activity and inhibits hydrolysis of GTP, So GTP is permanently bound which leads to constant salt secretion, water secretion and ultimately to dehydration.
Hope this will help you all. See you all with next topic.
Thankyou for reading.
to continue with signal transduction
The first signal transduction pathway to discuss today is cAMP pathway.
High level of epinephrine induce or stimulate this pathway.
In this pathway epinephrine is primary messanger and cAMP is secondary messanger.
When epinephrine bind to G protein coupled receptor, the GDP is exchanged with GTP and alpha subunit of trimeric G protein is released from it and interacts with adenyl cyclase and starts producing cAMP.
cAMP activates protein kinase A. Protein kinase A is a tetramer of two regulatory and two catalytic subunits.So when cAMP binds to regulatory subunit it gets confirmation change in regulatory subunit and separates from catalytic subunit which results in activated protein kinase A.
Protein kinase A activates phosphorylase kinase A.
Activated Phosphorylase kinase A activates glycogen phosphorylase. Glycogen phosphorylase is enzyme used to convert glycogen to glucose.
Protein kinase A also phosphorylate glycogen synthase. Phophorylation of glycogen synthase inactivates this enzyme and inhibit glycogen synthesis.
Increase in cAMP leads to
Enhanced degradation of storage feuls, increase of acid secretion by gastric mucosa,
decrease in aggregation of blood platelets.
In odorant receptors of nose are coupled to G protein coupled receptors.
Stimulus leads to increase in cAMP level and cAMP directly act on sodium ion channel in plasma membrane and causes depolarisation of membrane and initiation of nerve impulse.
G protein are also involved in cholera and whooping cough.
In cholera, the part of cholera toxin has enzymatic activity and inhibits hydrolysis of GTP, So GTP is permanently bound which leads to constant salt secretion, water secretion and ultimately to dehydration.
Hope this will help you all. See you all with next topic.
Thankyou for reading.
No comments:
Post a Comment