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Table 3 Correlation between experimental validations and nodes in the FA/BRCA BNM

From: Fanconi anemia cells with unrepaired DNA damage activate components of the checkpoint recovery process

Process Nodes in the Experimental markers Validated role References
  FA/BRCA BNM used in this study in the BNM  
DNA damage ICL MMC FA cells are [21, 25, 26]
induction    hypersensitive  
    to ICL inducing  
    agents  
Upstream FAcore Non-evaluated ICL recognition [14, 16, 17]
FA/BRCA FANCD2I   proteins  
pathway NUC1    
  NUC2    
DNA repair ADD γH2AX, ICLs are unhooked [13, 21]
intermediaries DSB CA in metaphase by FA core-recruited  
   spreads DNA-endonucleases  
    that generate a DSB  
    and an ADD  
Downstream TLS Non-evaluated The ADD and DSB [14, 15, 18, 54]
FA/BRCA FAHRR   are repaired by TLS  
pathway    and FA-dependent  
    downstream homologous  
    recombination repair,  
    respectively. FA cells  
    accumulate DSBs  
Alternative HRR2 Non-evaluated FA cells use [49, 56]
DNA repair NHEJ   alternative DNA  
pathways    repair pathways,  
    mainly NHEJ  
    HRR2 is a  
    criptic repair choice  
Checkpoint ATR Cell cycle arrest Upon DNA damage [27, 28, 31]
  ATM in G2, pCHK1-S341, normal and FA  
  p53 p21 gene expression, cells activate  
   MYT1, WEE1, p21 the G2/M checkpoint  
   proteins   
Checkpoint CHKREC MPM2 mitotic index, The checkpoint [83, 84] and this work
recovery   cytokinesis block assay, is inactivated by  
   G2/M transcriptional CHKREC after  
   program, WIP1, PLK1, DNA repair  
   CDC25, Aurora A FA cells seem to have  
   proteins a lower threshold for  
    CHKREC activation  
    compared to normal cells