Second messengers are molecules that act within cells to either increase or decrease activity or amount of a final molecule. All of the answer choices are second messengers in various pathways.

When a ligand binds to its associated receptor, the signal is passed into the cell and on to a distinct final molecule (often DNA transcription factors). Second messengers allow for significant amplification of a single ligand/receptor signal in order to cause mass change within a cell, and therefore within the body.

Often following the activation of a G protein, ATP is converted to the second messenger, cAMP, by adenylate cyclase. This propagates the amplification of the signal transduction.

After adenylate cyclase converts ATP to cAMP, this second messenger goes on to bind to protein kinase A. Unactivated protein kinase A requires cAMP in order to become activated, at which point it can phosphorylate certain threonine and serine residues on target molecules.

In order for protein kinase A to become activated, cAMP must bind to it. PKA has a structure composed of two regulatory subunits and two catalytic subunits all bound together. The catalytic units are active on their own, so in order to work they must simply become dissociated from the regulatory subunits. Thus, cAMP will bind to only the regulatory subunits of PKA which then allows dissociation of the already catalytic subunits.

The function of phospholipase C is to cleave phosphatidylinositol biphosphate (PIP2) into the two second messenger molecules, diacylglycerol (DAG) and inositol triphosphate (IP3). These can then act within signal transduction pathways to amplify ligand/receptor signals.

Atrial natriuretic factor (ANF) and nitric oxide use cGMP as a second messenger to exert their effects. The ANF has guanylyl cyclase activity which converts GTP (guanosine-5'-triphosphate) to cGMP (cyclic guanosine monophosphate). This in turn activates protein kinase G and leads to relaxation of smooth muscle. IP3, calcium and DAG are second messengers in activation pathways of G protein-coupled receptors, as is the case of the epinephrine receptor.

Phospholipase C catalyses the formation of DAG (diacylglycerol) and IP3 (inositol triphosphate) from PIP2 (phosphatidylinositol-4,5-bisphosphate). IP3 promotes the influx of calcium ions into the cytoplasm while DAG stimulates protein kinase C.

Nitric oxide is a gas second messenger.It is also a neurotransmitter in the brain. Nitric oxide is produced by 3 enzymes: endothelial, induced, and neuronal nitric oxide synthases. Nitric oxide synthases require a calcium ions for the enzyme activity. Nitric oxide does act thru the cyclic guanosine monophosphate activation pathway.

In this question, we're asked to identify a statement that is not connected with intracellular signal transduction pathways (STP). To do so, we'll need to look at each answer choice individually.

Upon binding of a ligand to a G protein-coupled receptor (GPCR), the conformational change of this receptor is transmitted to a G-protein that is on the inner leaflet of the plasma membrane. This causes the individual sub-units of the G-protein to dissociate from each other, which then goes on to activate other components of the signal transduction pathway.

Activation of GPCR can also result in a signal transduction pathway in which a particular intracellular enzyme is activated. This enzyme is responsible for cleaving a specific fatty acid off of certain phospholipids from the plasma membrane. The fatty acid cleaved off is called phosphatidylinositol bisphosphate, which acts as a second messenger in STP's.

Another consequence of the activation of certain GPCR's is the activation of an enzyme called protein kinase A (PKA). This enzyme then goes on to phosphorylate other kinase enzymes. The end result is amplification of the entire signal.

One of the common second messengers in STP's is cyclic AMP (cAMP) and cyclic GMP (cGMP). One of the mechanisms in place to turn STP's off is to degrade these cyclic nucleotides. The class of enzymes responsible for this is called phosphodiesterases.

Beta-hydroxybutyrate is a ketone body that forms when excess acetyl-CoA is present. This molecule is not involved in signal transduction pathways.