#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
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
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.
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).
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. ;)
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.
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.
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
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').
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.
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.
The narrator sounds like Carrie Fisher! Thanks for the upload, Carrie!
#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
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
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.
I wish I had this teaching 60 years ago
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).
this video is amazing, thank you so much!!!!
Muy buen video , para comprender un poco mas acerca de la hipertrofia es necesario conocer esta via ..
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. ;)
Great video, and yes the reading program does just what is supposed to do. Thank you for posting.
I love this video! So easy to understand, thank you!
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.
Great, now my brain pictures a purple cat agent explaining science. Thanks Princess Carolyn for the narration! :D
Great video ! Thank u
excellent video
Yes so useful
Like if you came from the bio cell presentation of Uottawa... and your exam is like, soon lol.
yep... saturday exam. Looking at random videos online about that stuff
Very nice, really helps :) thanks!!
Rivista erotik
Rivista erotik vintage magazine
Sure better than Robbins’ Pathology
It's like Carrie Fisher is teaching us
this was awesome thanks
Nel Video non viene spiegato il ruolo di PDK1 e degli enzimi PTEN e IP3K per la formazione di PIP2 e PIP3
Awesome
Thank You!
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.
very good but still simple.
Check Molecular Cell Biology or the Molecular Biology of the Cell both have extensive info about this.
Superb ...very easy
thank you
thanks
Omg ... thanks for upload ...
excellent!
Is this called survival pathway?
@Tallturk I think a computer synthesized voice is speaking.
what do you guys study?
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
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').
Oh I did not realise that, my fault. Sure because im sooooooo used to hearing this mistake.
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)?
We are taught at our university the scaffold assembles on the RTK creating a microdomain of activity
Can I ask what softwares are being used to make these motion illustrations?
??
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.
Claudia Cárdenas Hernández Yh
So good
Great
@sb2jan
Well, you have Bad and Bax in this pathway
thanks!
in conclusion i wanna die but akt don't let me
Muitoo bomm
Wow
This is just too much at once...
Good luck to my exam :(
So u are a doctor now??
can't deal with the droning monotone of the narration sorry :/
Small quip- A-K-T not “act”.
I love how stupid this sounds in an American accent! "kinaysees" :-)
George Diggory I cannot play this video。
+George Diggory epuptosis
the way she says 'phospho..TIDYL.. inooooositoooool' is like someone running their fingernails down a blackboard
sorry we can't have a good accent like from islamic republic of great britain
Pro-Tee-Ay-Zees.
Today
...........
picz3k
Excellent video (at least for my level). Thank you very much indeed!