Thank you for your amazing explanation! I have no background in the subject but you made it so clear ☺
@JoeDeMasiScience17 күн бұрын
You’re welcome!
@estherfaith385018 күн бұрын
Very clear explanation.
@user-sz6hf5gc6r22 күн бұрын
Very helpful, thank you!
@RockerProf26 күн бұрын
Excellent!!! Superb explanation.
@ruheelbhat125528 күн бұрын
Sir but cip family inhibit E CDK n A CDK not D CDK
@user-dv5bh3qq6mАй бұрын
Wow, thanks. Your videos are excellent!!!
@aadil7302Ай бұрын
Thanks .Consice and useful
@aadil7302Ай бұрын
Thanks you
@aadil7302Ай бұрын
It’s really good
@aj-uo3uhАй бұрын
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.
@lehu85292 ай бұрын
Great video! What’s the mechanism that the RNA polymerase can ignore the stop codon in the Cu to also transcribe the Cdelta segment?
@lehu85292 ай бұрын
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
@linayasmine99752 ай бұрын
Really helpful thank you !
@adriensaouma32452 ай бұрын
Thanks
@yoyaoo82672 ай бұрын
wow amazing explanation just subscribed! thank you for making learning free and accessible to all
@darianacintron99372 ай бұрын
Your explanations are great! You have no idea how useful these videos are, seriously thank you!!!
@JoeDeMasiScience2 ай бұрын
Thanks for the feedback! Glad to hear that it was helpful!
@uhthin2 ай бұрын
Sweet! This is exactly what I was looking for! Well done. Thank you!
@JoeDeMasiScience2 ай бұрын
Happy I could help!
@noorsharabi53992 ай бұрын
Amazing
@02riyabhiwandkar432 ай бұрын
Great explanation. Thanks a lot for such an amazing video.😄
@saranawzad70192 ай бұрын
😊😊😊😊😊
@Caelicorn3 ай бұрын
very easy to understand, thank you!
@ivanvetcher3 ай бұрын
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.
@jacksonmulwa94064 ай бұрын
Am happy
@marinahovakimyan93874 ай бұрын
Thank you!
@canhung72184 ай бұрын
And are all D-type cyclin genes upregulated in cancer.
@canhung72184 ай бұрын
Could signalpathways PI3K/AKT/PTEN, Ras/Raf and Wnt make CCND2 upregulation ?
@user-oo8fd2ov5m4 ай бұрын
Thanks so much for the video! so helpful what textbook should we read to fully understand these topics?
@user-oo8fd2ov5m4 ай бұрын
thanks so much
@user-oo8fd2ov5m4 ай бұрын
thanks so much You are awesome man
@user-oo8fd2ov5m4 ай бұрын
9:55 What are the other signals that could make cell divide other than growth factors?
@user-oo8fd2ov5m4 ай бұрын
thanks so much
@user-oo8fd2ov5m4 ай бұрын
so if we put one single cell in a culture media without any growth factors, it won't do mitosis?
@Viridian884 ай бұрын
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?
@fatimahusseini20565 ай бұрын
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
@fatimahusseini20565 ай бұрын
Thnks alot, Sorry, Whats the name av previous video?
@torres126115 ай бұрын
What should you take to eat if you have one good pten gene and one mutated pten gene ?
@hannahbailey26 ай бұрын
Thank you so much !!! this makes so much more sense
@raniadaher9546 ай бұрын
thank youuu
@raniadaher9546 ай бұрын
amazing
@JoeDeMasiScience6 ай бұрын
Glad you liked it! Please subscribe and share!
@raniadaher9546 ай бұрын
thank youu
@hypnotoad04356 ай бұрын
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.
@JoeDeMasiScience6 ай бұрын
Thanks! All hail hypnotoad! Another futurama fan!
@muhammadsaif34996 ай бұрын
Thanks a lot , This one helped me a lot
@JoeDeMasiScience6 ай бұрын
You are welcome!
@robertserge24316 ай бұрын
Totally agree- you made this so easy to understand!
@robertserge24316 ай бұрын
Super clear explanation! Thank you!
@chaimachaifaoui80107 ай бұрын
I can't understand how can antibody of abo attacks hla of donner
@kendall20047 ай бұрын
Thank you a lot,this really helped me☺️
@user-vz4um3xx5r7 ай бұрын
J
@georgekriplon59537 ай бұрын
Thanks, profesor🎉🎉
@mariamali40048 ай бұрын
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!!!!
@JoeDeMasiScience8 ай бұрын
Wonderful! You are welcome!
@ikranahmed87988 ай бұрын
omg, one rare, informative video, that I'm lucky to have found. Thank you sir