12. Biosignaling
Recap of Insulin Signaling As A Growth Factor
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Recap of Insulin Signaling As A Growth Factor
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all right, so in this video, we're going to do a recap or a review of insulin signaling as a growth factor. And so, really, there's nothing new that we're going to cover in this video that we haven't already covered in our previous lesson videos. And so if you're already feeling really, really good about insulin signaling as a growth factor, then feel free to skip this entire video if you'd like. Because again, it's not going to cover anything new that we haven't already covered in our previous lesson videos. However, if you're struggling with this even just a little bit, then stick around because a recap or a review could potentially be really, really helpful for you guys. All right, so if we take a look at our large image down below, notice that it's pretty much recapping everything that we covered in our previous lesson videos regarding insulin signaling as a growth factor. And so if we start at the top left up here, of course, we know that the 51 amino acid residue peptide hormone insulin is going to act as the like and here in the situation and bind to the insulin receptor which we know is an arty K or a receptor Tyrosine kindness. And so when insulin binds to the receptor tyrosine kindness here, the insulin receptor it's going to cause the auto phosphor relation of the insulin receptor here and that is going to fully activate the insulin receptor so that it can phosphors its substrate, the insulin receptor substrate one or I. R s. One. And so we have the phosphor relation or the activation of I. R s one here. And of course I R s one is going to be phosphor elated on tyrosine residues since the tyrosine kinase domains, phosphors, late tyrosine residues. And so next What we have is another adaptor protein called GRB two is going to bind toe iris one using its S H two domain. Then Thea s. H three domain of GRB two is going to bind to the guanine exchange factor called sauce or the GEF called sauce. And because it is a gaffe, a guanine exchange factor, it's going to assist rass in exchanging it's g d. P with the high energy GTP, and so sauce is going to help activate wrasse and rass will then activate a map KKK called wrath. One wrath one. Well, then activate another map. KK called Mac phosphor relating it to become active. And then, uh, Mac is a map KK that will phosphor relate the map k irk activating ERC. And then, of course, IRK will make its way into the nucleus so that it can regulate transcription factors that are involved in cell growth. And so what you'll notice is that these red arrows that you see here, here, here, here and here are really just representing the removal of phosphate groups. And so, uh, here you can see that the removal of phosphate groups is gonna be, uh, occurring via the action of phosphate aces. And this helps to terminate the signal and notice that this arrow right here, eyes showing the GTP, hydraulics, ISS activity of wrasse, which we know is really, really slow and can really only occur under, uh, the help of gap proteins, which are GTP ace activating proteins. And so the gap proteins will help accelerate the inactivation of wrasse to help terminate the signal. And so recall from our previous lesson videos that we actually introduced this crazy story to help you guys memorize the most important components of this insulin, signaling a za growth factor in the correct order. And so recall that the story started off with I. R s one activation. And so the Internal Revenue Services is going to give a tax refund where the cell can get this cash and use the cash to order, uh, two orders of grubhub. And then, of course, when the food arrives, the sell ads hot sauce to the food, and that hot sauce ends up activating a rash. And so the cell calls Dr Ralf and Dr Rath says, You know what? I'm gonna make the parking pain go away. And so hopefully that will help you with, uh, the insulin signaling as a growth factor. And so really, this year concludes our recap or our review of insulin signaling as a growth factor and as we move forward, will be able to get a little bit more practice. So I'll see you guys in our next video
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Problem
ProblemHow is Ras activity turned off?
A
It is turned off by phosphorylation.
B
It is turned off by hydrolysis of its bound GTP to GDP.
C
It is turned off by hydrolysis of its bound GDP to GTP.
D
It is turned off by hydrolysis of its bound GTP to GMP.
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Problem
ProblemIn a tumor cell line, Raf-1 is mutated such that it is constitutively activated by Ras even in the absence of insulin signaling. How can you inhibit the growth of this tumor cell line?
A
Blocking insulin receptor autophosphorylation.
B
Inhibiting the kinase activity of ERK.
C
Preventing the production of cAMP.
D
Blocking the recruitment of PI3K to the plasma membrane by IRS-1.