Structural, biochemical, and cellular data reveal the mechanism by which the clamp loader attaches sliding clamps at gapped and nicked DNA to support DNA damage repair.

Cryo-EM structures of the eukaryotic clamp loader illustrate the large conformational changes that the clamp loader ATPase undergoes to open the circular sliding clamp and place it onto primer–template DNA.

Plasmodium falciparum kelch13 mutations that cause artemisinin resistant malaria in Southeast Asia show markedly different patterns of evolutionary selection in Africa.

The de novo selection of a mutation responsible for Plasmodium falciparum in vitro artemisinin resistance is confirmed in Guyana, making artemisinin combination therapies vulnerable to complete resistance in this region.

KLHL41 acts as a poly-ubiquitin dependent chaperone that prevents the formation of pathogenic nebulin aggregates associated with muscle disease.

Single-particle cryo-EM structures reveal a multistep process of how DNA is loaded into the DNA sliding clamp proliferating cell nuclear antigen by the canonical clamp loader replication factor C.

Large-scale genetic surveillance of malaria implemented by National Malaria Control Programmes informs public health decision makers about the spread of strains resistant to antimalarials.

Novel disease pathways underlie disease pathogenesis in Kelch-related nemaline myopathy through proteomic remodeling.

A function-based genetic screen using the Caenorhabditis elegans axotomy model identifies new regulators and an inhibitory role for NAD⁺ in axon regeneration, expanding the understanding of axon injury responses and regeneration.