+AK LECTURES (Andrey K) same. idk what i'd do without AK me and my friend always say the following after lecture: "time for AK to teach us what just happened"
Hello Andrey, I just wanted to start off by saying I ABSOLUTELY LOVE YOU. Your lectures are so well put together and conceivable. I am currently studying for the MCAT while taking biochemistry at university, and your videos supplement my studying like no other resource known to man. So thank you for your time and effort and passion for the sciences, because it is rubbing off on me like no other.
Medical student from Russia. Thank you a lot for these well explained and high informational lectures! I will recommend you to biochemistry teachers and students here.
Med Student from Bogotá, Colombia, and i want you to know that this video makes me so happy because it was what i were looking for, thank you so much!!
THANK YOU You are saving me the hussle of having to figure out an entire chapter on my own! I love every single video! You make everything sound so logical and easy... Thank you for sharing your wisdom in this perfect way!
You are a gifted person, capable of explaining such a complex matter in a clear, organized, and understandable way. Thank you very much for your video and congratulations on your teaching skills.
I love your lecture so much, they are so clarify and easy to understand. I'm second language, but your pronunciation is really good that I can understand the whole video without any problems. Thank you so much for posting these useful video.
Long time ago i thought ur lectures will not be useful to me But today when i actually watched one till the end i thought mm wrong.... U r seriously a fab teacher.. 🙃❤️
Excellent videos; all of them. Could you one day do one on insulin resistance, and the role of Threonine/serine receptors, DAG and adipose tissue hormones like resistin, on such insulin resistance? Thanks a bunch
Your lecture are awesome. Just a tiny bit of correction in this one. Protein kinase B [AKT here] gets bound to PIP-3, when PIP2 gets phosphorylated by PI3K. When so bound to PIP3, then PDK-1 acts on it phosphorylating it. {source: Lehninger- 6ed, page-456}. Cheers for your awesome videos!
Thanks for taking the time to make such a comprehensive lecture. One question: what turns off the pathway? In GPCR systems the GTP is degraded to GDP - how about RK systems?
Awesome video but I think there may be a mistake towards the end? Forgive me if I'm wrong. I've learned that Insulin leads to the activation of certain protein phosphatases, which will ultimately dephosphorylate various enzymes: glycogen synthase (active when dephosphorylated) PFK-2/FBase-2 complex (PFK-2 active when dephosphorylated in the liver cell, producing more F26BP and thus allosterically upregulation PFK-1 for glycolysis) glycogen phosphorylase (inhibiting glycogen breakdown) phosphorylase kinase (inhibiting the activation of glycogen phosphorylase) towards the end, you mention that AKT will phosphorylate enzymes that synthesize glycogen from glucose molecules. Are we talking about a different enzyme than glycogen synthase? Thanks! edit: looks like you were likely referring to the phosphorylation of glycogen synthase kinase, deactivating it, and subsequently keeping glycogen synthase in its active form.
