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H2AFX — XRCC6

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

• IRef Biogrid Interaction: XRCC6 — H2AFX (direct interaction, pull down) Kobayashi et al., PloS one 2012*
• IRef Biogrid Interaction: XRCC6 — H2AFX (physical association, affinity chromatography technology) Mischo et al., J Biol Chem 2005*
• IRef Biogrid Interaction: XRCC6 — H2AFX (physical association, affinity chromatography technology) Heo et al., Mol Cell 2008*
• IRef Biogrid Interaction: XRCC6 — H2AFX (direct interaction, pull down) Heo et al., Mol Cell 2008*
• IRef Biogrid Interaction: XRCC6 — H2AFX (physical association, affinity chromatography technology) Lee et al., EMBO J 2010
• MIPS CORUM GammaH2AFX-NDHII-Ku70-DNA complex: GammaH2AFX-NDHII-Ku70-DNA complex complex (DHX9-H2AFX-XRCC6) Mischo et al., J Biol Chem 2005*
• IRef Corum Interaction: Complex of DHX9-H2AFX-XRCC6 (association, anti bait coimmunoprecipitation) Mischo et al., J Biol Chem 2005*
• IRef Dip Interaction: Complex of 15 proteins (anti tag coimmunoprecipitation) Gottschalk et al., Proc Natl Acad Sci U S A 2009
• MIPS Negatome - no physical interaction between proteins Interaction: XRCC6 — H2AFX (Absence of interaction, anti bait coimmunoprecipitation) Mischo et al., J Biol Chem 2005*

Text-mined interactions from Literome

Burma et al., J Biol Chem 2001 : The minimal H2AX phosphorylation in Atm-/- fibroblasts can be abolished by low concentrations of wortmannin suggesting that DNA-PK , rather than ATR, is responsible for low levels of H2AX phosphorylation in the absence of ATM
Cowell et al., Biochem Pharmacol 2005 (Breast Neoplasms) : ATM inhibition reduced the initial average intensity of gammaH2AX foci while inhibition of DNA-PK had only a small effect on the initial phosphorylation of H2AX
Chowdhury et al., Mol Cell 2005 : The effect of PP2A on gamma-H2AX levels is independent of ATM, ATR, or DNA-PK activity
Mukherjee et al., DNA repair 2006 : Interestingly, we find here that DNA dependent protein kinase (DNA-PK) is solely responsible for H2AX phosphorylation during apoptosis while ATM is dispensable for the process
Guirouilh-Barbat et al., Mol Biol Cell 2008 : In contrast to DNA-PK, ATM phosphorylated H2AX both in NER-proficient and -deficient cells, but its full activation was dependent on H2AX as well as DNA-PK , suggesting a positive feedback loop : DNA-PK-gamma-H2AX-ATM. Knocking-out H2AX or inactivating DNA-PK reduced Et743 's antiproliferative activity, whereas ATM and MRN tended to act as survival factors
Solier et al., Mol Cell Biol 2009 : H2AX phosphorylation was dependent on DNA-PK , while Chk2 phosphorylation was dependent on both ATM and DNA-PK
Zhu et al., Cancer Res 2011 (Cell Transformation, Neoplastic) : RSK2 and DNA-PK , but not ATM or ATR, are required for EGF induced phosphorylation of H2AX at Ser139 ; however, only RSK2 is required for phosphorylation of H2AX at Ser16
Solier et al., Proc Natl Acad Sci U S A 2012 : We also show that DNA-PK is a client of HSP90a and that HSP90a is required for full DNA-PK activation, ?-H2AX formation, DNA fragmentation, and apoptotic body formation
Baritaud et al., Cell death & disease 2012 : AIF mediated caspase independent necroptosis requires ATM and DNA-PK induced histone H2AX Ser139 phosphorylation ... Employing a pharmacological approach and gene knockout cells, we also demonstrate in this paper that the phosphatidylinositol-3-OH kinase related kinases ( PIKKs ) ATM ( ataxia telangiectasia mutated ) and DNA dependent protein kinase (DNA-PK) mediate ?H2AX generation and, consequently, MNNG induced necroptosis ... Further, DNA-PK contributes to H2AX Ser139 phosphorylation
Urushihara et al., Biochem Biophys Res Commun 2012 : DNA-PK inhibition causes a low level of H2AX phosphorylation and homologous recombination repair in Medaka ( Oryzias latipes ) cells
Meyer et al., Nucleic Acids Res 2013 : Clustered DNA damage induces pan-nuclear H2AX phosphorylation mediated by ATM and DNA-PK