I’m a mantle cell lymphoma patient and this is of tremendous interest to me. MCL occurs (almost always) due to a chromosome translocation which place the cyclin-d gene right after the immunoglobulin h genes. Too much cyclin-d is produced in my B lymphocytes and the cell cycle is disregulated. I reckon that groovy P21 protein just can’t handle the cyclin-d overload!
great video and thank you so much for sharing your knowledge. I have 1 question. In some books it says that p21 inhibits cdk2 could you clarify if this is the case or does p21 inhibits cyclin D as you stated in the video.
doesn't hereditary intrinsic mutation of retinoblastoma lead to two tumorous eyes and spontaneous extrinsic mutation result in one eye or am i interpreting knudson's two hit model incorrectly? Thorough video nonetheless
Since mutations in the retinoblastomas are recessive (Rb is a tumor suppressor gene), it is rare that individuals inherit a mutation from both parents, so the occurrence of a retinoblastoma tumor is a stochastic event in each eye. there is no guarantee that a heterozygote will develop a tumor in both eyes. Thanks for your interest!
I have found these video lectures vary helpful with my biomedical course, but is there a reason why there is to videos on Apoptosis and sorry if this is irrelevant to this post.
At 11.50 your saying that with 1 good copie and 1 bad copie of P53 protein you get no tumor. p53 is a homo-tetrameer complex and it only functions with all four subunits intact. So if 1 subunit is defect by a L.O.F the other units wont take over and the protein wont do its job meaning increased cell division.
@snorro- if half of the subunits are defective and half functional, 1/16 of the tetramers will be fully functional, which is apparently enough to provide for normal cell cycle regulation, as p53 behaves as a recessive tumor suppressor.
This video is actually VERY helpful. I was lost with cdk and cyclines function and now they make perfect sense! Thank you.
thank you so much for your unselfish deeds
This is awesome! thanks for putting this together
Very useful and clear explanation. Thank you!
I’m a mantle cell lymphoma patient and this is of tremendous interest to me. MCL occurs (almost always) due to a chromosome translocation which place the cyclin-d gene right after the immunoglobulin h genes. Too much cyclin-d is produced in my B lymphocytes and the cell cycle is disregulated. I reckon that groovy P21 protein just can’t handle the cyclin-d overload!
Very productive video that helped me ALOT..Thanks allot dmflyboy....
wow! great video. please keep on with your videos, they are very helpful.
GREAT EXPLANATION!
Thank you for explain retinoblastoma
very good and useful videos! may I ask what video editing software you use?
awesome explanations! i wish i had you for biochemistry
This is fantastic thank you!
thank you for your interest!
The intro music is really creepy
Educative indeed!
Thanks for that was a very useful introduction :)
Amazing video
hey! great video! :) may I know who is the narrator in the video and is this video under an incorporated publisher? Thanks a lot! :)
great video and thank you so much for sharing your knowledge. I have 1 question. In some books it says that p21 inhibits cdk2 could you clarify if this is the case or does p21 inhibits cyclin D as you stated in the video.
According to Robbins' "Pathologic Bases of Disease", p21 inhibits Cdk4 and Cdk6.
thanks for the comment - I will update this in the near future
actually no p16 inhibits cyclin D- cdk4/6 and p21 inhibits the other complexes
Thanks so much for this
really helplful !
thank you!!
Hello, I really like your way to explain. I have question, Can you please tell me which program did you use in explanation in TH-cam. Thank you.
Thanks a lot !
great video, thanks, helped a lot.
doesn't hereditary intrinsic mutation of retinoblastoma lead to two tumorous eyes and spontaneous extrinsic mutation result in one eye or am i interpreting knudson's two hit model incorrectly? Thorough video nonetheless
The diagram in the first half of the video is great. Is there anywhere online I could find it?
thanks for you interest
Since mutations in the retinoblastomas are recessive (Rb is a tumor suppressor gene), it is rare that individuals inherit a mutation from both parents, so the occurrence of a retinoblastoma tumor is a stochastic event in each eye. there is no guarantee that a heterozygote will develop a tumor in both eyes.
Thanks for your interest!
Thank you sir.
Thanks...I teach this course every Fall. Updates will be posted then.
Best lec....
OH MY GOD THANK YOU
thanks!
I have found these video lectures vary helpful with my biomedical course, but is there a reason why there is to videos on Apoptosis and sorry if this is irrelevant to this post.
Is it just me or did his shirt change colour halfway through?
At 11.50 your saying that with 1 good copie and 1 bad copie of P53 protein you get no tumor. p53 is a homo-tetrameer complex and it only functions with all four subunits intact. So if 1 subunit is defect by a L.O.F the other units wont take over and the protein wont do its job meaning increased cell division.
@snorro- if half of the subunits are defective and half functional, 1/16 of the tetramers will be fully functional, which is apparently enough to provide for normal cell cycle regulation, as p53 behaves as a recessive tumor suppressor.
thanks for your interest... I use Camtasia software.
I thought that Cyclin D is continuously present throughout the cell cycle
thanks sir
Phosphorylation
Thank you for explain retinoblastoma
thank you for your interest!
thank you for your interest!
thanks for your interest!
thanks for your interest!
thanks for your interest!
thanks for your interest!
thanks for your interest!
thanks for your interest!