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Cyclic adenosine monophosphate is a secondary messenger that, if increased, has shown memory improvements.
The name has no relationship to Cyclic adenosine monophosphate (cAMP).
Cyclic adenosine monophosphate (cAMP) molecules bind directly to f-channels and increase their open probability.
The mutation activates cAMP (cyclic adenosine monophosphate), causing an increase in the cells' function and growth.
One hormone that is used by many fungi is Cyclic adenosine monophosphate (cAMP).
Inside the cell, cyclic adenosine monophosphate (cAMP) has been shown to be an important second messenger of pigment translocation.
Melatonin and cyclic adenosine monophosphate modulate the expression of NF-YB.
Cyclic adenosine monophosphate (cAMP)
Cyclic adenosine monophosphate causes increase activation of protein kinase A (PKA).
This in turn leads to the inactivation of the secondary messenger Cyclic adenosine monophosphate and induces smooth muscle and blood vessel constriction.
Stimulation of these receptors causes a cascade of events ultimately leading to increase cyclic adenosine monophosphate (cAMP) within the cell.
This results in stimulation of membrane-bound adenylyl cyclase and increased intracellular cyclic adenosine monophosphate (cAMP).
Excitation of this receptor protein results in the formation of cyclic adenosine monophosphate (cAMP) as a second messenger.
The mechanism behind the aggregation of the amoebae relies on Cyclic adenosine monophosphate (cAMP) as a signal molecule.
Ribonucleotides can be converted to cyclic adenosine monophosphate (cyclic AMP) to regulate hormones in organisms as well.
Like parathyroid hormone it also increases nephrogenous cyclic adenosine monophosphate (AMP) and decreases the tubular phosphate threshold.
Cyclic adenosine monophosphate (cAMP) is present in low levels of glucose, and binds to CAP which changes to an active conformation.
Although these adrenoceptors share the same messenger, cyclic adenosine monophosphate (cAMP), the specific transduction pathway depends on the receptor type (alpha or beta).
Both receptors are 7-transmembrane G-protein coupled receptors (GPCRs) which inhibit the accumulation of cyclic adenosine monophosphate within cells.
The PDE4 degrades the phosphodiester bonds in the second messenger molecule cyclic adenosine monophosphate (cAMP), which is one of the ways the brain relays information.
The alpha subunit of the G protein activates adenylyl cyclase, which catalyzes the production of cyclic adenosine monophosphate (cAMP).
PDE4 hydrolyzes cyclic adenosine monophosphate (cAMP) to inactive adenosine monophosphate (AMP).
Release of the hormone glucagon triggers production of cyclic adenosine monophosphate (cAMP), which activates a cAMP-dependent protein kinase.
GPCRs modulate the inhibition of adenylyl cyclase and accumulation of the second messenger, cyclic adenosine monophosphate (cAMP).
