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Genetic interaction between DNA repair factors PAXX, XLF, XRCC4 and DNA‐PKcs in human cells

29 May 2019

Abstract excerpt

DNA double-strand breaks (DSBs) are highly cytotoxic lesions, and unrepaired or misrepaired DSBs can lead to various human diseases, including immunodeficiency, neurological abnormalities, growth retardation, and cancer. Nonhomologous end joining (NHEJ) is the major DSB repair pathway in mammals. Ku70 and Ku80 are DSB sensors that facilitate the recruitment of downstream factors, including protein kinase...

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PMID: 31141305
DOI: 10.1002/2211-5463.12681

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Genetic interaction between DNA repair factors PAXX, XLF, XRCC4 and DNA‐PKcs in human cellsPMID 31141305Read ↗

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Deficiency of XLF and PAXX prevents DNA double-strand break repair by non-homologous end joining in lymphocytesSemantic proximity Read ↗

PAXX, a paralog of XRCC4 and XLF, interacts with Ku to promote DNA double-strand break repairSemantic proximity Read ↗

Repair of ionizing radiation-induced DNA double-strand breaks by non-homologous end-joiningSemantic proximity Read ↗

Update on DNA-Double Strand Break Repair Defects in Combined Primary ImmunodeficiencySemantic proximity Read ↗

Ku regulates the non-homologous end joining pathway choice of DNA double-strand break repair in human somatic cells.Semantic proximity Read ↗

The conserved Tpk1 regulates non-homologous end joining double-strand break repair by phosphorylation of Nej1, a homolog of the human XLFSemantic proximity Read ↗

Identification of Genes Involved in Repair of DNA Double-Strand Breaks in Mammalian CellsSemantic proximity Read ↗

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Structural insights into the role of DNA-PK as a master regulator in NHEJSemantic proximity Read ↗

DNA-PKcs suppresses illegitimate chromosome rearrangementsSemantic proximity Read ↗

XRCC4 deficiency in human subjects causes a marked neurological phenotype but no overt immunodeficiency.Semantic proximity Read ↗

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