NER * Helix distortion * ERCC6 and 8 mutation -- Cockayne's syndrome * XP proteins (XPE or DDB2, XPC, XPA) mutated in xeroderma pigmentosum. * TFIIH, the same helicases as seen in DNA replication.

BER * For non-helix distorting base lesions. * Base is not present, a gap is present in DNA. * Specific DNA glycosylases used for identification. * APEX1 and APEX2 (AP endonucleases): responsible for end processing * An AP site (apurinic/apyrimidinic site). * The exposed 3' OH is available to a replicative polymerase. * Ligation performed by ligase * Short or long patch BER is possible.

In HR, * MRN -- begginings of dsDNA resection. * The PARP1 protein is active on ssDNA. * Free 3' ends made available, crucial for later DNA pol binding. * RPA binds, coats, the ssDNA.<br /> * Rad51 searches for strand for invasion. * Strand invasion carried out by sister chromatid, etc. * D-loop formation.

May have. * DSBR * SDSA * BIR

NHEJ relies on microhomologies. Doesn't require homologous sequence from another source. * Ku protein instrumental in identification of DSB and recruits DNA-PKcs. * DNa-PKcs autophosphorylates. * DNA ends processed by Artemis. * LIG4 and XCRR4 are needed for strand ligation.

NHEJ and HR can be compared.

lit review

extensive review