Biosignaling 2 - Video Tutorials & Practice Problems
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Biosignaling 2
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Let's turn our attention to camp that secondary messenger generated by a dental eel. Cyclists Now camp activates protein kindness A, which is a protein kindness that's very important in signaling pathways. And it activates protein kinase assay by al hysterically binding to the regulatory sub unit. And if you can picture, um, protein kindness A. For a second here, I'm drawing it as a sort of I don't know, blue blobby thing. So this is protein kinda say, and it has this regulatory sub unit that is bound into the active site. So our that's our regulatory sub unit, and it's bound into the active site so that, um, the enzyme cannot perform its function. Now. Camp causes the regulatory sub unit to be released from the active site when it binds, and this allows peek A or protein kinda se Teoh boss for late stuff, which is basically what it does now. It's important to realize that camp is actually secondary messenger for many different systems. Um, you know, including hormones and neurotransmitters. Um, so, you know, we're really only focusing on one little role that it has. Um and don't let that give you the impression that it's not really involved in anything else. It's involved in a ton of other stuff, Uh, additionally, you know you don't want or if you think about it, if it's involved in so many signaling pathways, you really need a way to control how much campus present. And so it's important that there is this cyclic, nucleotide fostered Iast race or PDS, sometimes the abbreviation for fostered Iast race. And basically this breaks down camp into AM P right theme, non cyclist version. And it's super important to have this enzyme around, because we, you know this ourselves really need to control theory levels of camp in order to give off the appropriate responses. And, um, have their signaling pathways function normally. So protein kindness a regulates a ton of different enzymes, and it does this by co violently modifying searing or three ning residues with a phosphate group, right? It's a kindness it's gonna cost for light stuff. It's gonna cost for late stuff at a searing or three inning. And it's important to note that, you know, we're talking about all these different things. There's the G protein coupled receptor. There's this protein kindness. There's the identical cyclists you know, you might be wondering. Well, how does all this stuff get together in the cell? You know, these air proteins, the cell is way bigger than proteins. How does that happen? It's actually, um because there are these anchoring proteins, and they basically hold together in the receptor. Right. So here, in our image, um, let's call this our sector. So we're gonna have anchoring proteins that are going to hold together. The receptor are this is a dental liel cyclists. I'm just going to abbreviate it a c and are protein kinda say so. These air all gonna be held together. Bye. An anchoring protein, and basically, that's just gonna, you know, join them together to ensure that they're able to interact easily. Right? Um, you know, we see this in metabolic pathways. How enzymes that you know, our the carry out reactions in a sequence will be linked together by some sort of scaffolding protein to ensure efficiency. Well, same thing with this. This is basically just a measure to ensure efficiency. You keep all the stuff that needs to interact with each other, close together so that it's easy for it to interact now. Protein kindness A You know, we said it. Foster relates a lot of stuff, and it basically it leads to what we call phosphor relation cascades. And these, you know, this is where you have a cascading effect where things were getting phosphor, elated and defrost for related. And this activates and deactivates Siris of proteins. So basically, you know, you're just transferring around these phosphate groups and this causes, uh, various proteins in a signaling pathway. Thio basically like, turn on or turn off and there is sort of a cascading effect to it. We'll look at an example right now, So let's use epinephrine as our example. Epinephrine is another hormone. We're gonna talk about a bunch of hormones. Epinephrine, the hormone. Uh, you probably know it as adrenaline. Um, but in America, we call it epinephrine. I don't know why adrenaline is the commonly his name in the media, but doesn't matter. So epinephrine, the hormone, it's actually synthesized from tyrosine, and it binds to a G protein coupled receptor, and it leads to the activation of protein kinase a. So looking at our example here, you know we have our receptor are dental cyclists are protein kinda say so Let's call this yellow molecule here This molecule here cyclic a m p and call this protein kinda say so. Cyclic A m p is going to allow for the activation of protein. Kinda say so. Here it is. It's active form and this is going Thio cause a phosphor are a possible relation Cascade So protein kind I say eyes going thio phosphor late. Uh huh. Phosphor Alice B. Kindness be which I'm going to just abbreviate p b k b and that be on the end there. That means it's thean active form. So it's going to get phosphor related by a protein kindness A into phosphor Lisbie kindness a the active form. So that's what we have over here. That's PK. I'm sorry. PB p b k. So again that be means inactive that a means active form And then, uh, fast for at least be kindness. A is going thio foster for late glycogen phosphor lace. So that's what we have over here. This is glycogen, boss for lace. Oops, glycogen phosphor Ellis. And that's the, um Excuse me. That's the B form inactive form, right? The inactive. You just jump out of the image here, so it's easier to see. And then we have glycogen bus for lace A. The active forms. That's a phosphor relation cascade, right? You see how? See how it works. Now we have one thing getting phosphor related, leading to another thing getting phosphor related. And you know, you're turning in this case, returning on a Siris of proteins. Could be that were deactivating certain proteins by foster relating them. Of course, that's not what we're seeing this example, but it is possible on just as a side note, people very frequently confused foster relation defrost. Correlation is always being. You know, if you phosphor relate something, you activate it. If you defrost for relating, if you're deep phosphor relating something, then you're in activating it. But that's not always the case. Sometimes phosphor relating, something will actually inactivated. So, you know, uh, in a foster relation cascade things could be activated court inactivated in our example. They're all being activated, however, so anyways, essentially what we have here, So I've forgot to label epinephrine here. This is our epinephrine bound to our receptor. So basically what we have here is epinephrine binding to a receptor, and the downstream result is that we activate glycogen, phosphor Ellis and glycogen phosphor. Ellis is going to break down glycogen into glycogen one phosphate. And then, uh, that's gonna be released, his glucose into the blood. And, you know, you don't really need to worry about how glycogen one phosphate becomes glucose and is released to the blood. That's, you know, or like, med school stuff. But, uh, basically, all you need to know is that when glycogen phosphor lace breaks down glycogen, it actually doesn't break it down. As plain old glucose, it breaks it down as glucose. One phosphate on that epinephrine leads to the activation of glycogen phosphor lace, and that that glucose one phosphate will be released into the blood as glucose. And you know, bringing this back to you, epinephrine or adrenaline. You know, that's that, uh, hormone that gives you that fight or flight response, right? And so one of the things that it's gonna do is it's gonna put more glucose in your blood because if you need to fight or flee, you're going to need that glucose, that energy to do. So So that's, um you know, one of the things that this hormone will do in the body. So let's turn our attention to amplification a little bit here. So, uh, one molecule of epinephrine actually can lead thio about 100,000 molecules of glucose getting released, which is pretty crazy, right? I mean, that is some serious amplification there. And, you know, I'm kind of showing, uh is obviously very simplified version of the image going on here. But, you know, this is, like our amplification and basically start off with one and then, you know, you get in this case we're going to then before, But of course. In actuality, we're talking about one leading Thio more than just to no, you know, ultimately, one molecule of epinephrine is going to lead Thio, you know, with 100,000 molecules of glucose. But, you know, this image is just sort of give you a rough idea what that would look like. Anyhow, um, you know, one of the other features of signal transaction we mentioned is adaption and our epinephrine signal pathway is going thio, use this This, uh, kindness. It looks like it's bark. I like just thinking of it as bark. It's actually beta arc. So it's beta Adrianne ergic receptor kindness the beta Adrianne ergic receptors, the receptor that's picking up on that epinephrine. And what beta arc does, is it, uh, fost for lates writes a kindness. So it cost for relates the epinephrine receptor so that it won't work anymore. And this is sort of how you know, our cells are our signal. Transaction pathways in ourselves adapt. Um, additionally. So after beta arc phosphor awaits the receptor, you have this other protein called beta arrest in, and it combined to the phosphor related terminal of the receptors. So after they've been phosphor related by beta arc beta arrest and combine them and this will actually signal the membrane trafficking system to pull those receptors back into the cell where they're stored is end ISMs. And that's that's sort of what I'm trying to show in this image here. I want you to ignore, you know, this whole coded pit coat protein thing. Um, I'm sort of appropriating a new image that is meant to be used for something else to illustrate this, because what I really want to show is here are receptors, right? So this is our beta adrianne ergic receptor, right? here, you know, also labeled right here. And, um, basically, when it gets phosphor, elated, think of this red stuff as being the beta arrest in, and it's gonna bind the phosphor related terminal of the receptor. And what that's gonna do is it's gonna signal the membrane thio pinch inward like you see here. It's actually gonna, um, pinch inward and pull some of these receptors inward. Right? See how we have these receptors in here in this and his own. So that's that's gonna adapt our signal transaction pathway because now we're gonna have fewer receptors for epinephrine. So it's going thio mod, or it's going to attenuate how the signal comes out when epinephrine Bynes. So that is a nice example of um, you know both how amplification works and also how Theodore option of thes signal pathways works. One last note I wanna talk about before we move on is cholera toxin, and what cholera toxin does is takes n a D plus, which we're going to be talking about a lot more later when we get into, like, college assist So it takes n a d plus and it breaks it down and it co violently links it as ADP ribose, um co violently links that to G protein. I didn't mean to go green there, so it's gonna link it to G protein. And what this is going to do is it's actually gonna co violently modified g protein and cause it to be stuck in its active form. Right? So think about it. You know, we were just talking about how the cell needs to control these signal pathways. Well, this is a signal pathway going out of control work, but, you know, basically sticking g in the on position and just letting it go crazy. And that's gonna lead to way too much camp being produced. And what this is going to you end up doing is because remember, camp has a variety of roles. Well, this is going to result in excess chlorine and sodium getting pumped out of the cells, and this is specifically happening in intestinal cells. Uh, and so, ah, lot. Ah, loss of these assaults, these ions and intestinal cells is going to cause ah, lot of water to be lost to because, uh, you know, as I'm sure you're aware from what we talked about in the last unit water tends to follow solve utes. And so, pumping out all these salt molecule or salt ions is going thio result in a large loss of water. Water is gonna follow them out into the Lumen of the intestine. And that's going to result in some pretty awful watery diarrhea. And actually the, you know, main concern for people being affected by cholera is dehydration. They just lose so, uh, so much fluid from their bodies. And it's because of this signal transaction pathway going haywire from the toxin. All right, let's flip the page.