Deletion of Arginase 1 in myeloid cells delays tumor formation in pancreatic cancer.

The PRMT1 protein mediates arginine methylation of KCNQ2 channels to control neuronal excitability.

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.

Poly-PR and poly-GR interact with importin β, disrupt importin-cargo loading, and inhibit nuclear import in permeabilized cells in a manner that can be rescued by RNA.

Signaling pathway mTOR can sense its principal activator amino acid arginine via a different mechanism than that previously described for other amino acids.

The results presented here indicate that IL-10-producing CD4⁺ T cells express genes associated with chronically activated T_H1-like cells, undergo clonal expansion, and inhibit antiviral T cell responses via the secretion of arginase-1, facilitating viral persistence in mice infected with MCMV.

A mutation in the lineage-determining regulator C/EBPα that increases the factor’s affinity for its partner PU.1 dramatically accelerates the velocity of B cell to macrophage transdifferentiation.

Fly vision depends on a member of the SLC22 transporter family for recycling the histamine neurotransmitter following its uptake by glia and its modification into the transport metabolite carcinine.

The N-terminal domain in histone 2A serves as an evolutionary tool to enable greater chromatin compaction when genome size is disproportionately larger than the nuclear volume across eukaryotes.

The time it takes to secrete a protein is dominated by diffusion of positively charged arginines through the channel across the membrane, but lysines avoid this problem as they are neutralised before transport.