AKT Signaling Pathway Regulation and Downstream Effects. hey, everyone, this lesson is on AKT signaling. So in this lesson, we’re going to introduce the AKT signaling pathway, and we’re going to look at the downstream effects of the act signaling pathway as well as how the pathway is regulated. So to begin, what is AKT is also known as protein kinase B, and it is a serene and threeonine kinase.
The AKT signaling pathway is a key regulator of cellular proliferation and survival. However, the role of AKT in regulating downstream effects is unknown. In this article, we identify a new role for AKT in regulating downstream effects of the Wnt signaling pathway. We discovered that AKT overexpression reduced the expression of downstream targets of the Wnt signaling pathway, including cyclin D1 and c-Myc.
The AKT signaling pathway is essential for cell growth and survival. Pathway regulation is important for maintaining the correct balance of AKT activity, which can have downstream effects on cellular signaling and gene expression. Misregulation of the AKT pathway can lead to cancer. There are several known pathways that can regulate AKT activity, and further research is needed to understand the full scope of AKT pathway regulation.
The AKT signaling pathway is a key regulator of cell growth and division. Dysfunction in the AKT pathway has been linked to a number of diseases, including cancer. However, the downstream effects of AKT signaling are not well understood. In this article, we explore the role of AKT signaling in regulating downstream pathways and how this affects cell behavior.
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Which means that it leads to the phosphorylation of serine and threatenine residues on target proteins. Now, there are actually three isoforms of AKT, AKT one, also known as protein kinase B Alpha, AKT two, also known as protein kinase B beta, and AKT three, also known as protein kinase B gamma. And we’ll get into the specific details and the specific actions each of these ice worms has in another lesson.
akt phosphorylation
So this lesson will be primarily focusing on AKT one signaling. So AKT is regulated by growth signals, and it is involved in various disease States, including cancer, insulin resistance, type two, diabetes, cardiovascular diseases, and autoimmune diseases. And when we look into the signaling pathway, we’ll be able to understand why AKT is associated with these types of diseases. So how does AKT signaling occur in the cell? Well, it all begins at the cell membrane with the activation of either a receptor tyrasine kinase or a G protein coupled receptor.
Now, these are two different types of receptors, but both lead to the activation of act. Now, as I mentioned before, growth signals activate AKT signaling, and one of the growth signals or growth factors is insulin. So I’ve talked about insulin signaling before in another lesson. If you haven’t watched that lesson, I would suggest you watch that to better understand insulin signaling. Now, when either of these receptors are activated, they lead to the recruitment of a Pi three kinase or a phosphatyl anosodol three kinase.
AKT Signaling Pathway Regulation and Downstream Effects
Now, Pi three K leads to an increase in Pip three levels or fossil nasodol triphosphate, which leads to the recruitment of PDK one. Now, PDK one can directly phosphorize act at 308 to activate AKT, or it can actually activate mTOR complex two indirectly, which itself can actually AKT at Seren four, seven, three to activate AKT. So these are two important phosphorrelation sites on act, which lead to its activation. So when AKT is activated, what does AKT do in the cell? One of the main things that act does is it actually inhibits as 160 through phosphorylation.
Now, as 160, as you may have learned in my insulin signaling video, is a negative regulator of glute for translocation, which means that when act inhibits as 160, the cell is able to translocate glute four containing vesicles, which leads to glute four being deposited in the membrane and allowing glucose to enter the cell and undergo glycolysis. Another thing at does in the cell is that it actually inhibits tubersclerosis complex one and two through phosphorylation. So you may be thinking, okay, what is Tse one and two? Well, TSC one and two is actually a negative regulator of mTOR complex one. So normally Tse one and two actually inhibits Reb or Rheb, which is an activator of mTOR complex one.
pi3 kinase akt pathway
So by AKT actually inhibiting Tse one and two, it actually activates mTOR complex one, which leads to the activation of P 70 X six kinase and ribosomal s six, which actually leads to protein synthesis. So AKT activation actually leads to increases in protein synthesis. Now, another thing mTOR complex one does is it actually inhibits autophagy and it inhibits autophagy by several mechanisms. And if you want more information on those mechanisms, I suggest you check out my macro autophagy video and my mTOR signaling videos. So because AKT activates mTOR complex one, it up regulates protein synthesis and downregulates autophagy.
Now, another major protein that AKT regulates is FOXO, and it actually inhibits FOXO through phosphorylation. Now, FOXO actually inhibits self survival and proliferation, which means that act actually increases self survival and proliferation. Now, another protein that act actually inhibits through phosphorylation is GSK three or glycogen synthase kinase three. Glycogen synthase kinase three, as his name suggests, actually phosphorylates glycogen synthase to inactivate glycogen synthase through phosphorylation. Glycogen synthase, as we learned before, is critical or needed for glycogen synthesis.
pi3k signaling pathway
So this means that because AKT actually inhibits an inhibitor of glycogen synthesis, it actually activates glycogen synthesis. So AKT actually activates glycogen synthesis.
And finally, AKT actually activates ATP citrate Lyte and ATP citrate Liase is important for fatty acid synthesis. So AKT actually activates fatty acid synthesis as well through ATP citrate lioness. So, because of the many functions of the act signaling pathway, we now can understand why AKT is so important in diseases such as insulin resistance and diabetes, as well as cancer. Now, when the act signaling pathway is complete, how does this pathway actually shut off? Well, there’s actually a couple of ways that the act pathway can actually turn off.
And one of those ways is at the beginning of the pathway, P ten, which is a phosphatease actually downregulates Pip three, and it does so by actually converting Pip three to Pip two. So this can actually shut off this step so that PDK one is not recruited and activated. Another way that AKT signaling is actually turned off is through another phosphatease phlppp, and this phosphate actually deposit’s AKT at Seren four, seven, three. So this is another way that the cell can actually turn off act signaling. And finally, the last phosphatease that can actually turn off act signaling is protein phosphatase two A or PP two A, which actually B.
pi3k akt signaling
Phosphorrelates act at. So these are a few ways the act signaling pathway can be turned off. So now that we’ve seen the act signaling pathway, we can summarize what the pathway actually performs. And one of the things that it actually does is it actually increases glucose uptake and utilization. As we’ve mentioned before, it actually leads to the inhibition of as 160, which leads to glute four translocation and glucose uptake and utilization in glycolysis.
It also leads to glycogen synthesis because it leads to the activation of Glycogen synthase. So that means that the cell can uptake glucose more readily and also store the glucose as glycogen for later use. Agd signaling also increases fatty acid synthesis through ATP Citrate Lionesse activation and it also increases protein synthesis through mTOR complex one activation. And then finally AKT signaling leads to increases in cell survival and proliferation through negative regulation on foxoproteins.
So as you can see AKT signaling leads to the synthesis of macromolecules and leads to cell survival and peripheration and finally act signaling leads to the inactivation or suppression of autophagy through mTOR complex one signaling. So if we could describe AKT signaling in one statement, what could we say? Akt signaling actually does well, AKT signaling actually increases metabolism and decreases metabolism so we can see that it increases anabolism through the synthesis of macromolecules in Glycogen fatty acids and proteins and it also decreases catabolism by decreasing functions and processes such as autophagy.
Anyways, guys, I hope you found this video helpful if you did please like and subscribe for more videos like this one and as always thank you so much for watching and I’ll see you next time.
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In conclusion
the AKT signaling pathway is important for cell growth and survival. Abnormal AKT signaling can lead to a wide variety of diseases, so it is important to understand how it works and what can go wrong. There are many ways to regulate AKT activity, and this knowledge may be helpful in the development of new treatments for diseases.
