Receptors Flashcards
Gs
Stimulates adenylate cyclase by activating it with alpha-GTP so that cAMP is generated. CAMP will go on to activate PKA that will phosphorylate other things.
PDE will inactivate adenylate cyclase
Gt
Stimulates cGMP phosphodiesterase. Light activated GPCR that will then activate cGMP phosphodiesterase that will inactivate cGMP into 5’-GMP
Gi
Inhibits adenylate cyclase. Signal molecule binds and inhibits adenylate cyclase. CAMP is not activated so neither is PKA
Gq
Activates phospholipase C which will turn into IP3 that will cause calcium to be released or DAG that will activate PKC and phosphorylate target proteins
Epinephrine signal type with beta adrenergic
Es
Dopamine receptor type
Gi
Histamine receptor type
Gs
Epinephrine/norepinephrine with alpha adregneric receptor
Gi
Acetylcholine receptor type
Gq
Light receptor type
Gt
Cholera
Covalent modifcation of the alpha subunits ADP ribosylation of arginine will decrease GTPase activity so Gs remains active and will continuously stimulated adenylate cyclase. The over abundance of cAMP will open CL- channels and cause a loss of electrolytes and water, resulting in diarrhea
Whooping cough
ADP ribosylation of cysteine of Gi prevents activation and dissociation of the alpha subunit from the G protein complex. There will be less inhibtion of AC and an overproduction of cAMP. Loss of fluid and excess mucus in airway epithelial cells
RAS and cancer
Mutant RAS will decrease GTPase activity to lock in the active GTP bound state.
Neurofibromatosis
Growth of tumors from nerve tissue. Caused by inactivitng mutation in NF-1 gene that encodes GAP. RAS will be uncontrollably active
Cytoplasmic receptors
For lipophillic, signal will travel to cytoplasm where a receptor is bound to HSP 90. When ligand binds, HSP 90 will dissociate and then the complex will travel to the nucleus and bind to hormone response elements (HRE) in the DNA promoter sequence
