Редактирование: XRCC5

X-ray repair cross-complementing protein 5 (EC 3.6.4.-) (86 kDa subunit of Ku antigen) (ATP-dependent DNA helicase 2 subunit 2) (ATP-dependent DNA helicase II 80 kDa subunit) (CTC box-binding factor 85 kDa subunit) (CTC85) (CTCBF) (DNA repair protein XRCC5) (Ku80) (Ku86) (Lupus Ku autoantigen protein p86) (Nuclear factor IV) (Thyroid-lupus autoantigen) (TLAA) (X-ray repair complementing defective repair in Chinese hamster cells 5 (double-strand-break rejoining)) [G22P2]

==Publications==

{{medline-entry
|title=Repairing DNA damage by [[XRCC6]]/KU70 reverses [[TLR4]]-deficiency-worsened HCC development via restoring senescence and autophagic flux.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/23518600
|abstract=Hepatocellular carcinoma (HCC) is among the most lethal and prevalent cancers in the human population. The initiation and progression of HCC is closely associated with chronic liver inflammation. Recent research indicates that nonhomologous end joining (NHEJ), one of the DNA repair mechanisms, autophagy and senescence are all involved in the pathogenesis of HCC induced by carcinogens or oxidative stress. DNA repair proteins including [[XRCC6]]/KU70 and [[XRCC5]]/KU80 are the critical NHEJ factors that play pivotal roles in genome-maintenance issues such as DNA replication and repair, telomere maintenance and chromosomal instability. Our studies indicate that a deficiency of toll-like receptor 4 ([[TLR4]])-mediated immune activities results in a decreased expression of [[XRCC5]] and [[XRCC6]] in response to insult by the carcinogen diethylnitrosamine (DEN). This effect causes a failure in DNA repair, and promotes the transformation of precancerous hepatocytes and HCC development. Ectopic expression of [[XRCC6]] protects against HCC initiation and progression by restoring the cellular senescent response and activation of immune networks, which induces an effective autophagic degradation, removes the accumulated reactive oxygen species (ROS), decreases DNA damage, attenuates proliferation, and promotes programmed cell death in [[TLR4]]-deficient livers. Our work indicates that repairing DNA damage by [[XRCC6]] reverses [[TLR4]]-deficiency-worsened HCC development via restoring immunity to support senescence and autophagy in liver cells.
|mesh-terms=* Animals
* Antigens, Nuclear
* Autophagy
* Carcinogenesis
* Carcinoma, Hepatocellular
* Cellular Senescence
* DNA Damage
* DNA Repair
* DNA-Binding Proteins
* Humans
* Ku Autoantigen
* Liver Neoplasms
* Models, Biological
* Reactive Oxygen Species
* Toll-Like Receptor 4
|keywords=* DNA damage repair
* KU70
* hepatocellular carcinoma
* selective autophagy
* senescence
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3672303
}}