Thank you for posting. Surprised that PALB2 (which was almost named BRCA3 but is more like BRCA1.5 since it putatively joins BRCA 1&2 at some point) was not mentioned, especially since pathogenic mutations in that often results in cancer or prophylactic surgeries. Was looking for how it functions & any partial redundancies it may have w/ RAD 51 (C&D?) in conjunction w/ BRCA2 in HR/DSB repair...
Your video is still helpful for many. Esp those working backwards from a genetic diagnosis.The clinical recommendations for people who hold DS repair gene pathogenic mutations are evolving (increasing) relatively rapidly for breast, ovarian, pancreatic (&?). The role of PARP inhibitors may also be an interesting upper level undergrad-ish level discussion, highlighting the functions of deleterious version of these genes. Even if students don't end up having big careers in medicine/biotech, having the ability to assimilate these concepts can add up to potentially life saving personal decisions. [read: finally, my education is paying off more than any science job I've had, LOL]
First, I really thank you for making this useful video. I watched this video from South Korea, and I'm highschool student interesting in brca gene. I know human use some methods when reparing DNA, and I thought that the one you mentioned in video is HR. Is it right? If it is right, if we use brca gene for dna reparing, does it always do its role with HR? Why it do not use NHEJ? If we have gene mutation either brca 1or brca 2, not both, is the possibility of cancer same?And what are other reasons causing dna mutation? If a person is inherited mutated gene, why breast cancer(or other else) happend in realtive old age, not in childhood?I'm sorry for my poor english...But I would really appreciate if you would leave some comments with my questions. Thank you!!
Very cool that you're studying this in high school. Was looking for words to respond to your question when I saw this in wiki: "When a double strand DNA lesion is repaired by NHEJ there is no validating DNA template present so it may result in a novel DNA strand formation with loss of information." That loss of information can still result in the production of a different protein or truncation of the protein that was supposed to have been produced. In individuals well past the embryonic stage [meaning anyone who can read this ;-) ], there are limitations to delivery of any repair mechanisms.
Thank you so much. I searched everywhere for explanation like this. Would appreciate more of ur works
there is an entire genetics course here: www.youtube.com/@janineleblanc-straceski3181
Thank you. It was very nice talk and a good summary about BRCA1, BRCA2
Thank you so much for this explanation. It was very straight-forward and helpful! Please keep making videos!
Very helpful and clear! Thank you for making and publishing this video.
I'm glad it helped!
Thank you for posting. Surprised that PALB2 (which was almost named BRCA3 but is more like BRCA1.5 since it putatively joins BRCA 1&2 at some point) was not mentioned, especially since pathogenic mutations in that often results in cancer or prophylactic surgeries. Was looking for how it functions & any partial redundancies it may have w/ RAD 51 (C&D?) in conjunction w/ BRCA2 in HR/DSB repair...
I may add some details in a future version of the video. There is a good Wikipedia entry on it.
Your video is still helpful for many. Esp those working backwards from a genetic diagnosis.The clinical recommendations for people who hold DS repair gene pathogenic mutations are evolving (increasing) relatively rapidly for breast, ovarian, pancreatic (&?). The role of PARP inhibitors may also be an interesting upper level undergrad-ish level discussion, highlighting the functions of deleterious version of these genes. Even if students don't end up having big careers in medicine/biotech, having the ability to assimilate these concepts can add up to potentially life saving personal decisions.
[read: finally, my education is paying off more than any science job I've had, LOL]
Thank you so much. Best regards from Colombia.
You are welcome! Nice to know it has a global reach.
First, I really thank you for making this useful video. I watched this video from South Korea, and I'm highschool student interesting in brca gene. I know human use some methods when reparing DNA, and I thought that the one you mentioned in video is HR. Is it right? If it is right, if we use brca gene for dna reparing, does it always do its role with HR? Why it do not use NHEJ? If we have gene mutation either brca 1or brca 2, not both, is the possibility of cancer same?And what are other reasons causing dna mutation? If a person is inherited mutated gene, why breast cancer(or other else) happend in realtive old age, not in childhood?I'm sorry for my poor english...But I would really appreciate if you would leave some comments with my questions. Thank you!!
Very cool that you're studying this in high school. Was looking for words to respond to your question when I saw this in wiki: "When a double strand DNA lesion is repaired by NHEJ there is no validating DNA template present so it may result in a novel DNA strand formation with loss of information." That loss of information can still result in the production of a different protein or truncation of the protein that was supposed to have been produced.
In individuals well past the embryonic stage [meaning anyone who can read this ;-) ], there are limitations to delivery of any repair mechanisms.