Hoatlin: Fundamentals: Difference between revisions
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==Questions and Answers== | ==Questions and Answers== | ||
;Question | |||
*I am still having trouble understanding PARPi's mechanism. Can you explain to me the normal interactions and mutated interactions of PARP and BRCA along with PARPi's function? | |||
;Answer | |||
*The essence of the idea in the PARP/BRCA example, very briefly, is that the BRCA-deficient tumor cell has a defect in repair of DNA double strand breaks by a repair process called homologous recombination (HR). PARP1 is in charge of repairing single strand DNA breaks, which become DNA double strand breaks during replication. Thus, if PARP1 is inhibited, the DNA ss breaks convert to DNA ds breaks and must be repaired by HR. If HR is defective, the cell accumulates so much damage that it cannot survive. HR is defective in the tumor cell...but not in the wild-type cell! | |||
That's how PARP1 inhibitors are relatively selective in killing the HR deficient tumor cell but not the wild-type cell (which is competent for HR) | |||
;Question: | ;Question: | ||
*1) When you talk about the number of base pairs in a genome, the number 3 x 10^9 was mentioned and I wanted to double check, is this for the haploid genome? And just out of curiosity, why is it reported for the haploid genome? | *1) When you talk about the number of base pairs in a genome, the number 3 x 10^9 was mentioned and I wanted to double check, is this for the haploid genome? And just out of curiosity, why is it reported for the haploid genome? |
Revision as of 11:59, 29 January 2011
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Questions and Answers
That's how PARP1 inhibitors are relatively selective in killing the HR deficient tumor cell but not the wild-type cell (which is competent for HR)
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