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Very clear explanation.

Very helpful, thank you!

Excellent!!! Superb explanation.

Sir but cip family inhibit E CDK n A CDK not D CDK

Wow, thanks. Your videos are excellent!!!

Thanks .Consice and useful

Thanks you

It’s really good

Joe you are the best, often I come back here to review it and understand it better. What became more clear this time is that once the Rb is off the transcription factor, two things can happen with a certain chance: 1.The transcription factor will encounter a new active non phosphorylated Rb. 2.The transcription factor will encounter rna polymerase and start transcription. Step 1 will become less likely once the concentration of active Rb goes down. Also what is funny is that rna polymerase itself is restricted by active Rb, so once we get a less active Rb there will come more rna polymerase available and step 2 will become more likely.

Great video! What’s the mechanism that the RNA polymerase can ignore the stop codon in the Cu to also transcribe the Cdelta segment?

I think there might be a little mistake in the somatic recombination of light chains: I think there is no deletion or inversion of DNA between the J and C segment(s), the J-C intron is transcribed and then spliced out of the mRNA transcript

Really helpful thank you !

Thanks

wow amazing explanation just subscribed! thank you for making learning free and accessible to all

Your explanations are great! You have no idea how useful these videos are, seriously thank you!!!

Sweet! This is exactly what I was looking for! Well done. Thank you!

Amazing

Great explanation. Thanks a lot for such an amazing video.😄

😊😊😊😊😊

very easy to understand, thank you!

Thank you so much. My wife has breast cancer and I am learning a lot from watching your videos. We are in the 21st century and there is science behind something other than chop and burn. Please keep making more.

Am happy

Thank you!

And are all D-type cyclin genes upregulated in cancer.

Could signalpathways PI3K/AKT/PTEN, Ras/Raf and Wnt make CCND2 upregulation ?

Thanks so much for the video! so helpful what textbook should we read to fully understand these topics?

thanks so much

thanks so much You are awesome man

9:55 What are the other signals that could make cell divide other than growth factors?

thanks so much

so if we put one single cell in a culture media without any growth factors, it won't do mitosis?

Great explanation and effective use of sketch models, you definitely know what you’re doing. Thanks for sharing! Just a question: if a mutation on a single allele were to damage the tetramerization domain, what would happen? I’d say that you’d have a reduction in overall production of p53 but the wild type tetramer would still be able to form (and it’d the only homo tetramer to actually assemble) and so in this case we would not be calling about negative dominance effect - the cell would still retain a functional p53 (at least until heterozygosis is kept). Is this correct?

Do you know some article that you can suggest me? Sir!My thesis subject is about Macropinocytosis of regulation system on cancer and the protein we will work about is SHIP2, EPS8, and DYNAMIN2 , So I need the articles and have to understand that. Sorry for my bad english

Thnks alot, Sorry, Whats the name av previous video?

What should you take to eat if you have one good pten gene and one mutated pten gene ?

Thank you so much !!! this makes so much more sense

thank youuu

amazing

thank youu

your videos are great and your voice is so calming. i'm cramming for a stressful exam retake and it finally seems to make sense.

Thanks a lot , This one helped me a lot

Totally agree- you made this so easy to understand!

Super clear explanation! Thank you!

I can't understand how can antibody of abo attacks hla of donner

Thank you a lot,this really helped me☺️

J

Thanks, profesor🎉🎉

i cannot believe that you explained such a tough concept in 12 minutes, it took me one hour in my lecture and I still didn't get it, your explanation helped me ALOT thank you so much!!!!

omg, one rare, informative video, that I'm lucky to have found. Thank you sir

What about malaria?