What makes a good second messenger

In other words, what can a secondary messenger do in the body that a first messenger cannot? Secondary messengers are able to bind to membranes, anchoring themselves in one place, whereas primary messengers float freely throughout the cell body and are unreliable. Secondary messengers can take up extra space in a cell, thus limiting the ability of other chemical reactions to interfere with cell processes. Secondary messengers help primary messengers cross the phospholipid bilayer by making them hydrophilic or hydrophobic.

Secondary messengers are capable of crossing the phospholipid bilayer cell membrane, whereas primary messengers often are not. The primary ability of secondary messengers is their ability to leave the cell membrane and travel through the phospholipid bilayer by being selectively hydrophilic or -phobic, allowing egress.

This enables, for example, a cascade effect that greatly amplifies the strength of the original primary messenger signal. All of the examples listed are considered second messengers except for protein kinase C, which interacts with second messenger pathways as an effector; however, it is not a second messenger itself.

Recall that second messengers are used to amplify signals within the cell. A ligand may bind to a receptor on the cell surface in order to activate a signaling cascade. Second messagers will help propagate this cascade throughout the cytosol. The messengers essentially help transfer the signal from the receptor on the cell membrane to the proteins in the cytosol that will ultimately be affected.

Second messenger cascades can be triggered by the binding of an extracellular ligand to a membrane-spanning G-protein coupled receptor GPCR. The GPCR undergoes a conformational change, making a binding site available for a G-protein within the cytosol. The GPCR is released from the membrane and enters the intracellular space to trigger downstream signaling cascades. G-protein coupled receptors begin the signal transduction pathway by interacting with intracellular G-proteins.

This interaction isn't possible until a ligand forces a conformational change in the GPCR, thereby freeing up a site for the G-protein to bind. Which of the following is NOT a primary benefit of utilizing second messengers to transduce signals within a cell? Second messengers permit fine-tuned modulation of the signal through various intracellular enzymes.

Second messengers give cells direct access to extracellular material by permeabilizing the membrane. The ligand binds the receptor on its extracellular terminus; therefore the ligand itself never enters the cell or passes through the membrane.

Second messengers let the cell 'know' what is happening on the outside, but these extracellular molecules do not directly enter the cell. Second messengers are intracellular signaling molecules. Epinephrine is a hormone that is released into the bloodstream and is thus never inside the cell.

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Hanley Rd, Suite St. Louis, MO Subject optional. Email address: Your name:. Possible Answers: Secondary messengers are able to bind to membranes, anchoring themselves in one place, whereas primary messengers float freely throughout the cell body and are unreliable.

None of these describe the unique role of secondary messengers. Correct answer: Secondary messengers are capable of crossing the phospholipid bilayer cell membrane, whereas primary messengers often are not. Explanation : The primary ability of secondary messengers is their ability to leave the cell membrane and travel through the phospholipid bilayer by being selectively hydrophilic or -phobic, allowing egress.

Report an Error. Which of the following is NOT an example of a second messenger molecule? Possible Answers: Protein kinase C.

Correct answer: Protein kinase C. Explanation : All of the examples listed are considered second messengers except for protein kinase C, which interacts with second messenger pathways as an effector; however, it is not a second messenger itself. However, its level in the cell can rise dramatically when channels in the plasma membrane open to allow it in from the extracellular fluid or from depots within the cell such as the endoplasmic reticulum and mitochondria.

Some factors at work:. John W. This content is distributed under a Creative Commons Attribution 3. Binding of the hormone to its receptor activates a G protein which, in turn, activates adenylyl cyclase. The resulting rise in cAMP turns on the appropriate response in the cell by either or both : changing the molecular activities in the cytosol, often using P rotein K inase A PKA — a c A MP-dependent protein kinase that phosphorylates target proteins turning on a new pattern of gene transcription.

Figure 4. It recruits P rotein K inase C PKC — a c alcium-dependent kinase that phosphorylates many other proteins that bring about the changes in the cell. As its name suggests, activation of PKC requires calcium ions. These are made available by the action of the other second messenger — IP 3. The rise in intracellular calcium triggers the response. Example : The calcium rise is needed for NF-AT the "nuclear factor of activated T cells" to turn on the appropriate genes in the nucleus.

The drugs block this. Receptor-operated channels These are found in the post-synaptic membrane and open when they bind the neurotransmitter.