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The modelled structure of a membrane protein supports the hypothesis that it has a new fold with a channel that allows a chemical group to cross the membrane to decorate surface structures.

Dominant mutations in Arl3, linked to inherited retinal dystrophy, disrupt the active Arl3-GTP ciliary gradient and cause a defect in rod photoreceptor nuclear migration that can be rescued by elevating ciliary Arl3 activity or reducing aberrant non-ciliary Arl3 activity.

The dimer destabilizers cause a dimer-to-monomer equilibrium shift favoring the human thymidylate synthase monomer more degradable by the proteasome, thus breaking the long-standing link between inhibition and enhanced expression of the protein to fight cancer drug resistance.

A common genomic deletion in various human cancers disrupts mitochondrial protein homeostasis in a way that might be targeted by existing drugs.

High throughput metabolome profiling of yeast cells that are dynamically perturbed with the drug rapamycin can be used to implicate new genes in the key cellular process of TOR signaling, including the gene of unknown function CFF1.

Ostrich eggshell from the Liushu Formation in northwestern China push ancient protein preservation into the Miocene.

The integration of multiple omics panels obtained from bone tissue could aid in the evaluation of the postmortem interval in forensic investigations, expanding the boundaries of forensic research.

Calcium drives interactions for both calcium-binding domains of calmodulin in complex with KCa2.1 peptides and both domains are required for normal channel function.

Two zebrafish Keap1-paralogs are equally adept at electrophile-sensing but manifest divergent and co-regulatory electrophile-signaling behaviors.

N6-methyladenosine (m6A) reader Pho92 is directed by Paf1C to meiotic mRNAs in an m6A-dependent and independent manner and promotes CCR4-NOT-mediated mRNA decay of m6A modified transcripts contingent on translation.