do all peptide hormones use secondary messengers?

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youngrace

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okay so in my TPR book, it says that all peptide hormones operate through secondary messengers. and yet, in the very next paragraph, it says that insulin binds to a catalytic receptor (i.e., not a receptor that will lead to a secondary messenger chain)

what's up with this? are there exceptions to the rule, and if so, what are they? ty in advance 🙂
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The insulin receptor is a tyrosine kinase receptor. When bound, the receptor undergoes autophosphorylation and activates a downstream signaling cascade. It does lead to a secondary messenger chain.

http://en.wikipedia.org/wiki/Tyrosine_kinase_receptors#Signal_transduction

The phosphorylation of specific tyrosine residues within the activated receptor creates binding sites for Src homology 2 (SH2) domain- and phosphotyrosine binding (PTB) domain-containing proteins.[6] Specific proteins containing these domains include Src and phospholipase Cγ. Phosphorylation and activation of these two proteins on receptor binding lead to the initiation of signal transduction pathways. Other proteins that interact with the activated receptor act as adaptor proteins and have no intrinsic enzymatic activity of their own. These adaptor proteins link RTK activation to downstream signal transduction pathways, such as the MAP kinase signalling cascade.[2]
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thanks guys~

odd though, because the tpr book makes a big deal about the difference between secondary messenger receptors (which it basically summates as g-protein coupled receptors) and normal kinase receptors. as in, kinase receptors don't kick off a secondary messenger chain. which i assume is wrong?
 
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too much detail. as above, just know peptide hormones work via secondary messengers. thyroid hormones (t3, t4) are an exception as they are quite lipophilic and are able to pass through the cell membrane, but you probably don't need to know that. however, you can never know too much. The bio section always tends to have a few ridiculously detailed discretes thrown in.
 
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thanks muhali. i feel like i'm being a bit of an anal nightmare about this, but i read the wikipedia article for secondary messenger systems and apparently all of them are supposed to be triggered by g-protein coupled receptors. ("In all of these cases, a ligand binds to a membrane-spanning receptor protein molecule. The binding of the neurotransmitter to the receptor changes the receptor and causes it to expose a binding site for a G-protein.") as far as i know, the insulin receptor is just a protein kinase, not a GPCR. how does it end up triggering a secondary messenger then?

i want to clarify this just because i don't want my confusion over this issue tripping me up on what could be fairly easy questions. thanks again, you guys are the best. ♥
 
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