Alternative 9-1-1 complexes have evolved to play essential roles in mammalian meiosis and function to activate the protein kinase ATR and promote key meiotic events necessary for fertility.

Two phosphorylation sites on 53BP1 are found to mediate interaction with TOPBP1-RAD9 and shown to be essential for assembling the G1 DNA damage checkpoint response apparatus.

During neurogenesis, Neurogenin 1 activates the microRNA miR-9, which directly targets the Jak-Stat pathway to inhibit astrogliogenesis.

Ca²⁺-free synaptotagmin-1 binds to neuronal SNARE complexes anchored on nanodiscs, and Ca²⁺ releases this interaction to induce tight, specific binding to PIP₂-containing membranes.

The OSM-9 TRPV channel is differentially regulated due to developmental programming via modulation by TGF-β signaling, endogenous RNAi and chromatin remodeling pathways.

An in-depth map of ATR signaling during mouse meiosis is revealed using a combination of genetic and pharmacological approaches coupled to quantitative mass spectrometry.

An adenylyl cyclase isoform is shown to dynamically traffic to endosomes after activation by G protein in mammalian cells, contributing to cellular cAMP signaling by internalized GPCRs.

In a Ugandan birth cohort, early childhood infection-exposure, notably to malaria, helminths, and diarrhoea, is associated with lower prevalence of atopy and allergy-related diseases in later childhood.

Cryo-EM structure of the mammalian respiratory supercomplex containing complexes I, III and IV shows a functional asymmetry of complex III, providing strong evidence for directed electron flow in the respirasome.

Plasmodium falciparum aminopeptidase PfA-M17 is essential to parasite survival and plays a role in hemoglobin digestion, providing a rationale for further development of inhibitors against this enzyme.