DNA-dependent ATPase and 5'-3' DNA helicase (PubMed:12748189, PubMed:17416902). Can also unwind DNA-RNA hybrid duplexes. Is active on D-loops and R-loops, and on forked structures (PubMed:17416902). May be involved in recombinational DNA repair and the resumption of replication after DNA damage (PubMed:17416902). The redox cluster is involved in DNA-mediated charge-transport signaling between DNA repair proteins from distinct pathways. DinG cooperates at long-range with endonuclease III, a base excision repair enzyme, using DNA charge transport to redistribute to regions of DNA damage (PubMed:24738733). ATP + H2O = ADP + H(+) + phosphate Binds 1 [4Fe-4S] cluster. The iron-sulfur cluster is essential for protein stability and helicase activity. ATPase activity is 15-fold stimulated by single-stranded DNA (ssDNA). ATP-dependent DNA helicase activity requires divalent cations (Mg(2+), Ca(2+) or Mn(2+)) but is not detected in the presence of Zn(2+) (PubMed:12748189). Reduction of the [4Fe-4S] cluster reversibly switches off helicase activity. Remains fully active after exposure to 100-fold excess of hydrogen peroxide, but the [4Fe-4S] cluster can be efficiently modified by nitric oxide (NO), forming the DinG-bound dinitrosyl iron complex with the concomitant inactivation of helicase activity (PubMed:19074432). Monomer in solution. DNA damage-inducible. Transcriptionally regulated by LexA. Deletion of the gene results in a slight reduction of UV resistance. Belongs to the helicase family. DinG subfamily. Type 1 sub-subfamily. Truncated N-terminus.