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Note for: RAD18 and RAD54 cooperatively contribute to maintenance of genomic stability in vertebrate cells (doi: 10.1093/emboj/cdf534) Major pathway for post-replcational DNA damage; 1. TLS 2. HR Rad18- conserved from lower eukaryotes to vertebrates. double KO, synthetic lethal --> ach has nearly normal kinetic (in term of proliferation). Gap in this study; no one study the role of TLS in maintenance of chromosomal DNA. In yeast, S. cerevisiae; RAD6/RAD18 epistasis group (all in; 1. RAD6(UBC2) 2. RAD18 3. REV1 4. REV3 5. REV7 Rad6 -- E2 conjugating enzyme Rad18 -- has the DNA binding domain it is proposed that Rad18 recruited Rad6 and transferring Ub to the targeted proteins. Another gap --> so far, the targeted for Rad18+Rad6 is still unk, but it has been proposed that it could bind to DNA polymerase that play activity in TLS. Mammals, 2 homologs of RAD6 --> HR6A and HR6B 1 homolog RAD18 --> RAD18 AA comparison; ...

Paper: A novel Rad18 function involved in protection of the vertebrate genome after exposure to camptothecin (10.1016/j.dnarep.2006.05.045) S. cerevisiae; Rad18 function in PRR consist of 1.error-free damage bypass (Rad30 -Poln) 2.error-prone damage bypass (Rev3/7 -Pole) DT40; RAD18(-/-) cell 1. hypersensitivity to CPT but not RAD30(-/-)+REV3(-/-) 2. higher levels of H2Ax phosphorylation 3. higher in chromosomal aberration; gaps and breaks (after exposure to CPT) 4. no function in elongation without stimulant; but with CPT it showed more break In conclusion; this paper showed the role of RAD18 in replication fork when there is the lesion generate by CPT Context: CPT inhibit topoisomerase-I which is required for unsolve secondary structure during DNA replication Inhibition of CPT can cause the db strand break during replication, therefore, initiate the ATR/ATM dependent phosphorylation of H2Ax. There is evident showed DSB generated by CPT - being repair by HR. I...