This is what I was thinking as well, because it is not amplified as much as Rad51, which is a direct response protein. I would have to continue to look at the exact function of the gene to figure this out.
I think that if the Pcirf gene plays a role in DNA damage repair, it is a possibility that new drugs could be synthesized to decrease function of this gene to slow cellular reproduction in cancer.
I would find genes in the superfamily with similar characteristics to the Pcirf gene (size, location, exon/intron makeup) and repeat this experiment. DUF4246 genes are found in bacteria and fungi, so I could isolate them the same way we did T. Therm genes.
Do you think targeting cancer via this specific pathway will become viable either on its own or in conjunction with other treatments that target the damage repair of cancer cells? Were there things you could have added in the experiment that halted the efficiency of this pathway?
Can hydroxyurea be used as an antibiotic to slow down sickle cell anemia?
I don’t think it’s an antibiotic, but it is sometimes used as treatment for sickle cell anemia.
Could your possibly be a secondary or tertiary pathway/response for DNA damage response?
This is what I was thinking as well, because it is not amplified as much as Rad51, which is a direct response protein. I would have to continue to look at the exact function of the gene to figure this out.
What uses do you think the Pcirf gene function could have to treat diseases?
I think that if the Pcirf gene plays a role in DNA damage repair, it is a possibility that new drugs could be synthesized to decrease function of this gene to slow cellular reproduction in cancer.
Hey this was a great presentation. How would you go about studying the DUF4246 superfamily?
I would find genes in the superfamily with similar characteristics to the Pcirf gene (size, location, exon/intron makeup) and repeat this experiment. DUF4246 genes are found in bacteria and fungi, so I could isolate them the same way we did T. Therm genes.
As you mentioned in your future directions, would you predict the proteins from the genes to have a greater effect on the DNA damage response?
Do you think targeting cancer via this specific pathway will become viable either on its own or in conjunction with other treatments that target the damage repair of cancer cells? Were there things you could have added in the experiment that halted the efficiency of this pathway?