It is. It's an oncogene because when it's disrupted, it leads to failure to express the tumour suppressor protein. An ooncogene is one that when mutated contributes to the pathology of cancer.
Great to know that DNA polymerase recognize the parent strand by its extramethylation, also it's very important what you mentioned regarding how many hits required to develop cancer either in proto-oncogene or tumor suppressor gene. Thinking about it, it's very hard for any cell to develop cancer due to all checkpoints present and strikingly even when a cell senses an extra and abnormal stimulation for proliferation via Myc signaling for example, it automatically shuts down any progression to cell division!
Congrats on 1m! Well earned. Except (hey, if I’m not being honest, I’m not helping you, right?) after we get into the video (at about 6:30) you encourage us to watch your Cell Cycle Checkpoints video located in your Biology playlist. That’s a great tip… but PLEASE put the link in the description of THIS video so students don’t have to poke around searching for it. Copy link, paste link, voila, Medicosis leaps up to a new superstratospheric level of user friendliness. Or, to borrow an expression, watching the right videos in the right order is so easy once you give us the links to what the flip you are talking about! 😂❤
I dont understand why leading strand more error prone than leading strand, doesnt ligase work on both strand, and since DNA pol of lagging strand polimerizing DNA in small chunk does that reduce error prone
ligase doesn't work for both strands, only the lagging strand because it's replicated discontinuously. ligase is needed to basically connect the okazaki fragments together, the leading strand doesn't need it cus it's replicated continously. ligase lacks proofreading abilities making it error prone
There is no break in the production of the leading strand, ligase is used, but much less frequently. For the lagging strand ligase and dna polymerase works, but ligase must work more than in the leading strand to join the replicated dna strand fragments("okazaki fragments") produced from the lagging strand by dna polymerase. Due to the direction of the lagging strand 3'-5', snd the directionally with which dna polymerase works, 5',3 prime, dna replication must feed into the replication fork(the split in the original dna double strand created by dna helicase to allow access of replication machinery) Wherefore on the leading strand, dna pol extends the the new complementary strand away from the replication fork continuously.
No. You develop mutations throughout your life and usually cell defense mechanisms deal with abberrant cells quite effectively. The accuracy dna repair is also phenomenal.
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when discovred your videos started enjoying studying
I am glad!
Thank you as usual!
I noticed you mentioned that Rb is a tumor suppressor gene but on the next slide, you put it as a oncogene
It is. It's an oncogene because when it's disrupted, it leads to failure to express the tumour suppressor protein. An ooncogene is one that when mutated contributes to the pathology of cancer.
Great to know that DNA polymerase recognize the parent strand by its extramethylation, also it's very important what you mentioned regarding how many hits required to develop cancer either in proto-oncogene or tumor suppressor gene.
Thinking about it, it's very hard for any cell to develop cancer due to all checkpoints present and strikingly even when a cell senses an extra and abnormal stimulation for proliferation via Myc signaling for example, it automatically shuts down any progression to cell division!
Well phrased!
Congrats on 1m! Well earned.
Except (hey, if I’m not being honest, I’m not helping you, right?) after we get into the video (at about 6:30) you encourage us to watch your Cell Cycle Checkpoints video located in your Biology playlist. That’s a great tip… but PLEASE put the link in the description of THIS video so students don’t have to poke around searching for it.
Copy link, paste link, voila, Medicosis leaps up to a new superstratospheric level of user friendliness. Or, to borrow an expression, watching the right videos in the right order is so easy once you give us the links to what the flip you are talking about! 😂❤
Thank you!
Here: Checkpoints of the Cell Cycle:
ua-cam.com/video/17jXE3QQBq0/v-deo.html
Thank you for your excellent work and channel.
Definitely subscribing
Thank you so much!
The best explanation. You´re simply the best. Thank you so much. The ancient egyptian Gods and The Bangles bless you, Dr. Medicosis 💜
Thank you!
Hey! I got a seat in the front row 😊
Thank you 😊
That’s an amazing explaining THANK YOU ALOT
You’re most welcome, Monica!
Would you please help me by sharing?
@@MedicosisPerfectionalis yes👍🏻
ممكن تعمل سلسلة محاضرات عن ال genetic oncology موضوع معقد جدا وشكرا
Veeery well explained
Thank you 🙏
I love you and I keep loving you, you're one of the blessed soul
this is perfection!
NICE BRO ::::: CONTINOUS
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I dont understand why leading strand more error prone than leading strand, doesnt ligase work on both strand, and since DNA pol of lagging strand polimerizing DNA in small chunk does that reduce error prone
ligase doesn't work for both strands, only the lagging strand because it's replicated discontinuously. ligase is needed to basically connect the okazaki fragments together, the leading strand doesn't need it cus it's replicated continously. ligase lacks proofreading abilities making it error prone
There is no break in the production of the leading strand, ligase is used, but much less frequently. For the lagging strand ligase and dna polymerase works, but ligase must work more than in the leading strand to join the replicated dna strand fragments("okazaki fragments") produced from the lagging strand by dna polymerase. Due to the direction of the lagging strand 3'-5', snd the directionally with which dna polymerase works, 5',3 prime, dna replication must feed into the replication fork(the split in the original dna double strand created by dna helicase to allow access of replication machinery) Wherefore on the leading strand, dna pol extends the the new complementary strand away from the replication fork continuously.
should have watch this video 4 weeks ago
What about leukoplakia
Does all precancer always turn to cancer????? Please answer please
No. You develop mutations throughout your life and usually cell defense mechanisms deal with abberrant cells quite effectively. The accuracy dna repair is also phenomenal.
can you please make a series on cancer genetics (colon, breast, pancreas,...) it's very complex topic,, thanks.
Thank you for letting me know!
Don’t forget to check my “Oncology-Cancers” playlist.
@@MedicosisPerfectionalis I’m an oncosurgeon, and I’m addict to your videos 😊
6:25 ..
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Xeroderma PigmentoSUM
Hit the bell. That's what my girlfriend said.
Will lung ever ever re grown after pneumonectomy ?
No, but the remaining lung lobes may grow to compensate.