All right. So here in this video, we're going to do a summary of biosignalling by revisiting our map of the lesson on biosignalling, which we have down below right here. But notice that this map is a lot more comprehensive than our previous map, and that's because this map is including a lot more images and more memory tools to make this a better summary for you guys. So one of the first things that you'll notice about this map is that it's got these 3 different colored backgrounds to create these 3 different types of biosignalling pathways. We've got this green background over here on the left-hand side, which represents the biosignalling pathways that utilize G protein-coupled receptors or GPCRs. And then we have this pink background over here, which represents the biosignalling pathways that utilize receptor tyrosine kinases, or RTKs. And then we have this yellow background over here on the right-hand side, which represents biosignalling pathways that utilize lipid hormones. And so, of course, we know that when we explore this biosignalling map that we explore the leftmost branches first. And so we started off talking about G protein-coupled receptors or GPCRs, which we know consists of the GPCR itself, which is the receptor that has 7 transmembrane alpha helices and associates or couples itself with a heterotrimeric G protein, which contains 3 different subunits, the alpha, beta, and gamma subunits.
Then we talked about really 2 specific types of GPCR signal transduction pathways. We talked about the adenylate cyclase GPCR signal transduction pathway, which utilizes the beta-adrenergic GPCR. And we also talked about the phosphoinositide GPCR signal transduction pathway, which utilizes the alpha-adrenergic GPCR. And notice up above here we have the signal transduction pathway for the adenylate cyclase pathway, and over here on the right, we have the signal transduction pathway for the phosphoinositide signaling pathway. Recall with the adenylate cyclase signaling pathway that the effector enzyme that would get activated by the stimulatory G protein was adenylate cyclase. And adenylate cyclase would generate the secondary messenger cAMP, and then cAMP would act as an allosteric activator to the protein kinase A or PKA, which would then generate the cell response.
When it came to the adenylate cyclase GPCR signal transduction pathway, we talked about how adenylate cyclase was symbolized as a car, our story. cAMP was symbolized as the campsite in our story, and PKA was symbolized as the parking of the Acura. And hopefully, these will help jog your memory of what we talked about in our previous lesson videos. Then we talked more specifically about the stimulatory pathway when it comes to adenylate cyclase, which involved Gs, the stimulatory G protein. And we also talked about the inhibitory pathway, which involved the inhibitory G protein Gi. The stimulatory pathway leads to the production of the secondary messenger cAMP, and cAMP acts as an allosteric activator to protein kinase A or PKA. PKA, recall, exists as a heterotrimeric protein that has 2 regulatory subunits and 2 catalytic subunits, and 4 cAMP molecules are required to bind the regulatory subunits to release 2 catalytically active PKA subunits. So, basically, we reviewed this from our previous lesson videos. And when we talked about the inhibitory pathways, we talked about specific drugs and toxins that affect GPCR signaling, more specifically, cholera, which is going to pretty much overstimulate the Gs protein, the stimulatory G protein, leading to the disease cholera, which is characterized by extreme diarrhea and dehydration, which is why we have this toilet over here. And we also talked about the pertussis toxin, which acted as the inhibitor that inhibited the inhibitor. So pertussis would inhibit Gi, the inhibiting G protein, and that would lead to whooping cough, which is why we have this character coughing over here.
Then for the phosphoenacetonaltransduction pathway, recall from our previous lesson videos that the alpha hero was used to represent the alpha subunit of the heterotrimeric G protein, and the beta blaster and gamma gadget were used to represent the beta and gamma subunits of the G protein respectively. Recall from our story that the alpha hero sees the evil villain Pip and his two weapons. And so Pip and his two weapons represent pip2. And the alpha hero needs to alarm the police and the police is going to be represented by the effector enzyme phospholipase C. And so then, the police are going to taser Pip's two weapons to separate them into the two secondary messengers: the dagger or DAG and the 3 ice picks or IP3. And of course, IP3, notice we have its structure over here. DAG or diacylglycerol, we have its structure here. And we know IP3 would stimulate the release of calcium from the endoplasmic reticulum or the release of Captain Marvelous. You will from our story. And the calcium would associate with calmodulin, which would then activate other cytosolic protein kinases. And then the DAG part of the cleave substrate would ultimately make its way to PKC, the packed crowd of spectators, and activate PKC along with calcium. So, all of that was things that we had talked about in our previous lesson videos for GPCRs.
Now when it came to receptor tyrosine kinases, we talked about how these are receptors that have tyrosine kinase domains that phosphorylate tyrosine residues. And we talked about the insulin and insulin receptor which would generate the IRS1, the insulin receptor substrate, which was active and phosphorylated. And then IRS1, we know, acted as a branch point, which would lead to 2 different insulin signaling pathways: the insulin RTK signaling on glucose metabolism, which involved PI3K or the pi with a fake 3K label on it, PIP3, PKB, and PDK1, and these would lead to an increase in PIP savings or an increase in glycogen synthesis, as well as the bank tellers ordering some gluten-free doughnuts or an increase in GLUT4 expression. And then, of course, we also talked about another insulin RTK signaling pathway as a growth factor, and this would include 2 other mini pathways, the RAS pathway and the MAPK pathway. The RAS pathway involved the cell ordering 2 orders of Grubhub, putting some hot sauce on there, and ending up getting a rash. And so it involved GRB2, SOS, and RAS, the monomeric G protein. And so here we have a reminder of I got a rash here of our little mnemonic for memorizing that pathway. And then, of course, when the cell got a rash, you would call doctor RAF, who would mix something to make the irking pain go away. And so RAF1 followed by MEK followed by ERK represents the MAPK pathway here. And so we've got doctor RAF and the ERK pill here to remind you of those mnemonics.
Then, after that, we talked about another variation of the RTKs, which was the JAK-STAT signaling pathway. Really what defined these or what differentiated the JAK-STAT pathway from other RTKs was that it does not have a covalently bound tyrosine kinase domain. Instead, it needs to recruit a separate cytosolic tyrosine kinase which was JAK, and it also involved the recruitment of the STAT transcription factors. And so we talked about EPO, Erythropoietin Cytokine being the ligand, JAK being the Tyrosine Kinase, and STAT being the transcription factors. And so recall we talked about a little mnemonic here, which was that lucky Jack's pig spotted polka-dotted truffles, and that reminded us of the 7 steps in the JAK-STAT signaling pathway.
Last but not least, we talked about lipid hormone signaling, and really the biggest thing the biggest takeaway from this was that lipid hormones, because of their hydrophobic nature, are capable of diffusing directly through plasma membranes and having a more direct effect on metabolic responses and gene expression responses. And so this here concludes our summary of biosignalling and we'll be able to get a little bit more practice as we move forward in our course. So I'll see you guys in our next video.
