Fig. 6: UvrA ID repositioning over the ATP-binding domain II and close to UvrB could promote the transfer of the lesion from UvrA to UvrB. | Nature Communications

Fig. 6: UvrA ID repositioning over the ATP-binding domain II and close to UvrB could promote the transfer of the lesion from UvrA to UvrB.

From: Mechanistic understanding of UvrA damage detection and lesion hand-off to UvrB in Nucleotide Excision Repair

Fig. 6: UvrA ID repositioning over the ATP-binding domain II and close to UvrB could promote the transfer of the lesion from UvrA to UvrB.

a The image on the left represents the models of both the UvrA-UvrB heterodimers observed in the MtUvrA2UvrB2-DNA* structure; the UBDs were not represented for a better visualization. The image on the right corresponds to an equivalent heterodimeric component within the BstUvrA2UvrB2 structure. The ID, the ATP-binding domain II (ATP-II) and UvrB are differently colored and labeled. The distances between ID and ATP-II, and the tip of α-hairpin381-405 and Asn117 of UvrB (Ans116 in BstUvrB) are indicated as double arrows. b Structure-based hypothetical model for the lesion hand-off (two 180° rotated images are shown). Upon optimal superposition, the ID of MtUvrA2UvrB2-DNA* structure was superposed and replaced with the ID and the DNA of MtUvrA2-DNA structure; the DNA and the UvrB β-hairpin98-116 were shifted to avoid clashes and marked with black arrows. Important elements in the model are highlighted and labeled. The missing region in one DNA strand is represented with a dashed line. The green arrow indicates the direction of the short-range translocation of UvrB on the DNA.

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