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The α1 isoform of synGAP restricts the binding of AMPA-receptors and other regulatory proteins to PSD-95, and thus regulates synaptic strength.

Mice doubly deficient for Naa10 and Naa12 display embryonic lethality, with both enzymes compensating for each other with amino-terminal acetylation of proteins in mouse development.

ARL13B regulates cell ciliation and cilia length from within cilia and Sonic hedgehog response from outside of cilia indicating the two processes can be spatially uncoupled.

Primary-cilia-mediated processing of the Gli3 transcription factor enables the formation of subtypes of projection neurons in appropriate numbers during the development of the cerebral cortex.

Alteration of host gut microbiota by antibiotic exposure in early life remodeled host intestinal immune development and metabolism and enhanced the induction of type 1 diabetes in genetically predisposed animals.

A signalling cascade involving PI3K/Akt1 remodels the extra-cellular matrix to achieve atypical cellular responses and control cell fate specification within the embryonic endoderm.

Alternatively spliced C-terminal protein sequences encoded by the Syngap1 gene exhibit unique biochemical and functional properties in vivo, which explain in part how individual isoforms can promote cognitive functions and seizure protection.

Analysis of the tumor microenvironment reveals that pancreatic tumors experience metabolic stress caused by immune cell degradation of the amino acid arginine, and that pancreatic cancers cope by synthesizing arginine to provide access this amino acid despite low tumor availability.

Genetic and biochemical analysis reveal a variant in HSF2BP causing POI and C19ORF57/BRME1 as an interactor and stabilizer of HSF2BP by forming a complex with BRCA2, RAD51, RPA and PALB2.