Hi in this video we're gonna be talking about fossil or not tied or fossil hospital signaling pathways. So this pathway is confusing in the textbook because there seems to be all these different results that happen from them. But it doesn't like they're not very clear on why they're happening or what's activating it or how all these different things are being activated. So I tried to divide this into two groups. And this is because the phosphor and also tied signaling pathway may also see this as being a hospital phosphor lipid pathway. Same thing. Both of these can be activated by the G protein coupled receptors or the receptor tyrosine keenness. So the enzyme coupled receptors. So there's two main pathways in the each activate this pathway for different functions. So let's first focus on the G. P. C. R. So how the G PcR is activated is they activate. So once they are activated the receptors are activated they activate this G. Protein called G. Q. And this goes on to activate hospital. If they see now fossil life A. C. Is important because it cleaves this special lipid called in an hospital phosphor lipid. Once this cleavage happens it results in two products. The first is going to be called I. P. Three and the second is Dag. And if you're interested in what their names they're listed written right there. So I. P. Three goes on to cause calcium signaling in the Cida Plaza and dad goes on to activate this protein kinase C. Which then goes on to activate a lot of other proteins when calcium is present. So they interact. So the I. P. Three brings calcium into the cell and Dag activates proteins that are responsive to calcium. This all makes sense. And so the calcium surge in the cytoplasm triggers a lot of different events. Things like egg development, muscle contraction, nerve cell secretion. So calcium is a big signaling molecule. And so this is one of these pathways that the hospital fosca lipid pathway leads to the signaling of calcium. So here we have the example. So here um you've probably seen this picture before but just want to show it to you again. So here you have this lipid false Philip. K. C. Comes in and cleaves it it forms Dag and I. P. Three I. P. Three travels down here and releases calcium and Dag activates different proteins that are responsive to calcium to then go on and do a lot of different signaling things. Now on the other hand are T. K. S. And other types of receptors like cytokine receptors will also activate phosphor like they see for a different purpose but this is still the very similar pathway so far. So if they see in this case will recruit this P. I. Three kindness to the membrane P. I. Three K. And then once this kindness is here it can do a lot of things. So first it's a kindness so it's gonna add phosphates onto something. And so in this case it's gonna add it onto a fossil hospital lipid. So this is the same lipid that we talked about before and once. This is phosphor elated. It leads to a bunch of signaling cascades which can trigger cell division and prevent cell death. Um It also activates this protein called A. K. T. Which activates a variety of other proteins and P 10 phosphate taste. Remember phosphates are gonna remove phosphates. So um so this is how this is actually inactivated. It's through this P 10 pasta taste. So what this looks like is you have some type of receptors, tires and kindness. You then get pi three kinase activation. You can get act activation which is going to activate a lot of different things. And you can see that there's a ton of different other things that happened down here. You don't need to know these names. There's no these are signaling cascades, they're activating lots of things. So that's how the R. T. K. S activate the phosphor and hospital signaling pathways. So with that let's not move on.
The inositol signaling pathway can be activated by both GPCRs and RTKs.
Which of the following molecules removes phosphates from PI-3 kinase?