The PI3K/AKT signalling pathway

The phoshatidylinositol-3 kinase (PI3K) can be activated by binding directly or via the protein IRS-1 to the activated receptor tyrosine kinase. Alternatively, PI3K can be activated by binding to the GTP-bound form of the membrane bound protein Ras. Active PI3K catalyzes the formation of membrane bound PIP3. The second messenger PIP3 activates the serine-threonine kinase AKT. Active AKT phosphorylates many proteins, which leads to the inhibition of apoptosis and to the activation of translation and proliferation.

[@flames1000000]

Thank you for this incredible video; it goes into a lot of depth, however it was explained clearly and as a teenager I understand it so well done.

[@abbyleyva5745]

I love this video! So easy to understand, thank you!

[@jackpistone8015]

this video is amazing, thank you so much!!!!

[@Liiipoutou]

Thank you sooooo much !! I'm a french medical student and altough i have not a very good level of english, I understood everything ! Thanks to your videos, it's so much easier to learn my lessons now =D

[@mjgc8755]

The narrator sounds like Carrie Fisher! Thanks for the upload, Carrie!

[@plucky2115]

Great video, and yes the reading program does just what is supposed to do. Thank you for posting.

[@juan280100]

Muy buen video , para comprender un poco mas acerca de la hipertrofia es necesario conocer esta via ..

[@kzenonos1]

Excellent video (at least for my level). Thank you very much indeed!

[@johnmandrake8829]

this was awesome thanks

[@funnyviralespn5878]

excellent video

[@katewinslet7670]

Mammalian target of rapamycin (mTOR), also known as FKBP12-rapamycin-associated protein (FRAP), is a 280 kDa serine/threonine kinase which plays a key role in regulating critical cellular processes such as growth, proliferation, cytoskeletal organization, transcription, protein synthesis and ribosomal biogenesis by integrating three major inputs-nutrients (amino acids), growth factors (insulin), and cellular energy status.

[@elfassimariam250]

Great video ! Thank u

[@carolinegreen4771]

#AKT is involved in cellular survival pathways, by inhibiting apoptotic processes. AKT is also able to induce protein synthesis pathways, and is therefore a key signaling protein in the cellular pathways that lead to general tissue growth. Since it can block apoptosis, and thereby promote cell survival, AKT has been implicated as a major factor in many types of cancer. AKT was originally identified as the oncogene in the transforming retrovirus, AKT8. AKT comprises three highly conserved isoforms in mammals, designated AKT 1/PKBα, AKT 2/PKBβ, and AKT 3/PKBγ. Although each isoform is expressed differentially in a tissue-specific manner, they all contain an N-terminal pleckstrin homology (PH) domain, which mediates lipid protein or protein protein interactions, a kinase domain, and a C-terminal regulatory domain. -Creative BioMart

[@immadisarojini2775]

I wish I had this teaching 60 years ago

[@evil-robot]

A very clear and informative animation. My only qualm is that I would have liked to see PIP2 and PIP3 illustrated as simplified versions of their molecular formulae (rather than boxes) to differentiate them from proteins (and would make it much easier to mentally consolidate this pathway with the PLC-beta/PKC pathway).

[@anitabalazs5947]

Great, now my brain pictures a purple cat agent explaining science. Thanks Princess Carolyn for the narration! :D

[@molekularac]

excellent!

[@samifoz2350]

Thank You!

[@samifoz2350]

However, I do not think that insulin RTKs are dimerising receptors because it is a class two heterodimer structure at the membrane before signal binding. Binding of IGF-1 causes the B-subunits of the RTK to increase in proximity to allow autophosphorylation.

[@mohamedkalaaji]

Very nice, really helps :) thanks!!

[@hinrichconradsiedenburg554]

Rivista erotik

[@hinrichconradsiedenburg554]

Rivista erotik vintage magazine

[@Vishal5171]

Omg ... thanks for upload ...

[@kemelhadjer2137]

thank you

[@edu859biology]

Superb ...very easy

[@ati071087]

Good video, does miss a few things out. Just to clarify that PIP3, as stated has three phosphate groups which acts as a ligand for protein kinases (Akt) that have a pleckstrin homology domin. Also another pathway that activated Akt causes is the ubiquitylation of glycogen synthase kinase Beta. GSK-Beta, causes the inhibition of a protein called Beta-catenin which acts as transcription factor by binding the tcf/lef promoters and this activates the transcription of cyclin D1. ;)

[@immadisarojini2775]

Yes so useful

[@danman2007]

thanks!

[@arpitapriyadarshini30]

Awesome

[@ahaz588]

Great

[@sanjaisrao484]

thanks

[@dgwear69]

what do you guys study?

[@mexicanfish21]

Akt doesn't directly activate Rheb, it phosphorylates TSC2 and suppresses the inhibitory effect of TSC2 towards Rheb, yet in the video it does mention "multi-step", so that's fine.

[@hraqhraq]

very good but still simple.
Check Molecular Cell Biology or the Molecular Biology of the Cell both have extensive info about this.

[@mjgc8755]

It's like Carrie Fisher is teaching us

[@marcoshenrique5917]

Muitoo bomm

[@fernsader9261]

Can I ask what softwares are being used to make these motion illustrations?

[@nishantsingh361]

??

[@ALASKAOO7]

Nel Video non viene spiegato il ruolo di PDK1 e degli enzimi PTEN e IP3K per la formazione di PIP2 e PIP3

[@AmericanTradgety]

Like if you came from the bio cell presentation of Uottawa... and your exam is like, soon lol.

[@munifthegreat842]

yep... saturday exam. Looking at random videos online about that stuff

[@1986mayday]

Once activated, does PI3K actually dissociate and migrate to PIP2, or do they interact while PI3K is still bound to its activator (a RTK or Ras/GTP)?

[@PastTheFacade]

We are taught at our university the scaffold assembles on the RTK creating a microdomain of activity

[@kommienzuspadt]

@Tallturk I think a computer synthesized voice is speaking.

[@osservatorescettico88]

Sure better than Robbins’ Pathology

[@Dezwix]

@sb2jan
Well, you have Bad and Bax in this pathway

[@haribladeo6686]

Wow

[@user-rh7ph9ms5w]

Is this called survival pathway?

[@Klaukardenas]

Question: If the GAP complex that normally inactivates RAS is damaged, this signal pathway would be altered.....what would be the effects ???? Please answer me! I'm doing a Neurofibromatosis 1 expo and i need to undestand this so i can explain pathophysiology of NF1.

[@forgetuandme2011]

Claudia Cárdenas Hernández Yh

[@stuudyplan9196]

So good

[@General0208]

Good luck to my exam :(

[@splenter3500]

So u are a doctor now??

[@kommienzuspadt]

Pro-Tee-Ay-Zees.

[@arnauvizcarramiserachs6318]

THIS IS WRONG !!!!! S6K is not a transcription factor, it is a kinase which goes on to phosphorylate ribosomal protein s6 to facilitate protein TRANSLATION

[@christophwagener4698]

You are right, the p70S6 kinase (S6K) phosphorylates the small ribosomal subunit protein S6 to increase the rate of protein synthesis. For this reason, we choose the term 'translation factor' (not 'transcription factor').

[@arnauvizcarramiserachs6318]

Oh I did not realise that, my fault. Sure because im sooooooo used to hearing this mistake.

[@sanasnostraightfringe3117]

in conclusion i wanna die but akt don't let me

[@ChristinaCanavati]

...........

[@General0208]

Today

[@user-xb6fl9ri6g]

can't deal with the droning monotone of the narration sorry :/

[@daladangames516]

picz3k

[@charnalking]

I love how stupid this sounds in an American accent! "kinaysees" :-)

[@frankliang4323]

George Diggory I cannot play this video。

[@7amido12]

+George Diggory epuptosis

[@JackT13]

the way she says 'phospho..TIDYL.. inooooositoooool' is like someone running their fingernails down a blackboard

[@99F]

sorry we can't have a good accent like from islamic republic of great britain

[@frybucket]

Small quip- A-K-T not “act”.

[@ameliac504]

This is just too much at once...