TRAF-interacting protein is a protein that in humans is encoded by the TRAIPgene.[6][7]
This gene encodes a protein that contains an N-terminal RING finger motif and a putative coiled-coil domain. A similar murine protein interacts with TNFR-associated factor 1 (TRAF1), TNFR-associated factor 2 (TRAF2), and cylindromatosis. The interaction with TRAF2 inhibits TRAF2-mediated nuclear factor kappa-B, subunit 1 activation that is required for cell activation and protection against apoptosis.[7]
Mitotic DNA synthesis (MiDAS) is thought to be a DNA repair mechanism to salvage DNA that has not finished replication during S phase, which may be due to DNA replication stress (RS).[9] Intrinsic sources of RS include transcription-replication conflicts and “difficult-to-replicate’’ regions.[9] Extrinsic RS includes exposure to genotoxic agents, depletion of dNTPs, and premature S phase activity which can occur in precancerous cells after oncogene activation.[9] Some MiDAS pathways require the TRAIP protein to disassemble the replication complex at the stalled replication fork in cases where RS causes the fork to stall during replication.[9]
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