TRAF interacting protein
Protein-coding gene in the species Homo sapiens
From Wikipedia, the free encyclopedia
TRAF-interacting protein is a protein that in humans is encoded by the TRAIP gene.[6][7]
| TRAIP | |||||||||||||||||||||||||||||||||||||||||||||||||||
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| Aliases | TRAIP, RNF206, TRIP, SCKL9, TRAF interacting protein | ||||||||||||||||||||||||||||||||||||||||||||||||||
| External IDs | OMIM: 605958; MGI: 1096377; HomoloGene: 31343; GeneCards: TRAIP; OMA:TRAIP - orthologs | ||||||||||||||||||||||||||||||||||||||||||||||||||
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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]
Interactions
Role in mitotic DNA synthesis
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]
