akt最新在哪发布

hey， everyone， this lesson is on akt signaling so in this lesson， we're gonna introduce the akt signaling pathway and we're gonna look at the downstream effects of the akt signaling pathway as well as how the pathway is regulated so to begin what is akt well， akt is also known as proteinkind a's b and it is a syrian and three onion chinese， which means that it leads to the phosphorelation of siri and three onion residues on target proteins now， there are actually three isoforms of akt akt one also known as proteinkinasb alpha， akt two also known as protein kindas be beta and akt three also known as protein kindas be gamma and we'll get into the specific details and the specific actions each of these dice forms has in another lesson， 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 agati 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 tires in chinese or a g protein coupled receptor now these are two different types of receptors， but both lead to the activation of akt now， as i mentioned before growth signals activate akt signaling and one 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's signaling now when either of these receptors are activated they lead to the recruitment of a p i three kinese or a fossil title a nasa tall three kinese now p i three k leads to an increase in pip three levels or fossil nasa tall tri phosphate， which leads to the recruitment of p d k one now pdk one can directly phosphorily akt at three and three await to activate akt or it can actually activate m tor complex to indirectly， which itself can actually phosphorily akt at searing force seven three to activate akt， so these are two important foss relations sites on akt， which lead to its activation so when akt is activated what does akt do in the cell one of the main things that akt does is it actually inhibits as one sixty through voss relation now as one sixty as you may have learned in my insulin signaling video is a negative regulator of glute for translocation， which means that when a k t inhibits as one sixty 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 akiti does in the cell is that it actually inhibits tuberoscores complex one and two through foster relation so you may be thinking okay what is tsc one and two well tsc one and two is actually a negative regulator of m tour complex， one so normally tsc one and two actually inhibits reb or rheb， which is an activator of m tour complex， one so by akt actually inhibiting tsc one and two it actually activates m tour complex， one which leads to the activation of p seventy six chinese and ribosomal s six， which actually leads to protein synthesis so akt activation actually leads to increases in protein synthesis now another thing in tor 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 macrotophogy video and my mtor signaling videos so because akt activates mtor complex， one it up regulates protein synthesis and down regulates atophagy now another major protein that akt regulates is foxo and it actually inhibits foxo through foster relation now foxo actually inhibits self survival and proliferation which means that akt actually increases self survival in proliferation now another protein that akt actually inhibits through fos relation is gsk three or glycogen synthese kaine's three glycogen synthese kineys three as his name suggests actually phosphorulates glycogen synthese to enactivate glycogen synthese foster relation glycogen synthese as we've learned before is critical or needed for glycogen synthesis 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 lies and atp citrate lies is important for fatty acid synthesis so akt actually activates fatty acid synthesis as well through atp citrate lies so because of the many functions of the akt signaling pathway we are now can understand why akt is so important in diseases such as insulin resistance and diabetes as well as cancer now when the akt signaling pathway is complete how does this pathway actually shut off well， there's actually a couple of ways that the akt pathway can actually turn off and one of those ways is at the beginning of the pathway p ten which is a phospha tay's actually down regulates pip three and it does sew by actually converting pip three into 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 phosphotes， phl， pp and this foster days actually defoster relates akt at searing four seven three so this is another way that the cell can actually turn off akt and finally the last foster days that can actually turn off a k t signaling is protein foster days two a or p p two a which actually defos relates a k t at three and in three away so these are a few ways the akt signaling pathway can be turned off so now that we've seen the a k t 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 in utilization as we've mentioned before it actually leads to the inhibition of as one sixty， which leads to glute for translocation and glucose uptake and utilization in glycolosis it also leads to glycogen synthesis because it leads to the activation of glycogen synthes so that means that the selkan uptake glucose more readily and and also store the glucose as glycogen for later use agd signaling also increases fatty acid synthesis through atp citrate lies activation and it also increases protein synthesis through m tor complex one activation and then finally akt signaling leads to increases in cell survival and proliferation through negative regulation on foxo proteins so as you can see akat signaling leads to the synthesis of macro molecules and leads to self survival imploreriferation and finally akt signaling leads to the inactivation or suppression of atophagy through m tor 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 enablism and decreases catabolism so we can see that it increases enablism 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。

我用 uc 浏览器下载的月下和卡福卡， 打开后会显示网页无法打开， 卡服卡的也一样， 根本找不到教程中的那个叫那个被解压东西的又也找到，有没有知道？