Hoatlin: Fundamentals: Difference between revisions
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*XP patients have a defect in one of the many genes involved in NER (nucleotide excision repair) e.g., XPA, XPC, XPC, XPG etc. Thus, XP patients cannot repair DNA damage (cyclobutane pyrimidine dimers) caused by exposure to sunlight. The XP-V patients have a different defect but the same phenotype. They have a defective bypass polymerase, called Pol eta. Normally, Pol eta can synthesize (error-free) past a thymine dimer by inserting two A residues. In XP-V patients, other bypass Pols are substituted that are not error-free for this lesion. Also, in XP-V patients, the upstream XPA-XPG proteins are functional and NER repair is intact. Only the bypass polymerase is defective. | *XP patients have a defect in one of the many genes involved in NER (nucleotide excision repair) e.g., XPA, XPC, XPC, XPG etc. Thus, XP patients cannot repair DNA damage (e.g., photoproducts like cyclobutane pyrimidine dimers) caused by exposure to sunlight. The XP-V patients have a different defect but the same phenotype. They have a defective bypass polymerase, called Pol eta. Normally, Pol eta can synthesize (error-free) past a thymine dimer by inserting two A residues. In XP-V patients, other bypass Pols are substituted that are not error-free for this lesion. Also, in XP-V patients, the upstream XPA-XPG proteins are functional and NER repair is intact. Only the bypass polymerase is defective. | ||
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Revision as of 08:09, 31 January 2011
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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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