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

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.

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.

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

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

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.

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.

Degradation products of polysaccharides trigger partial population dispersal and alter cellular metabolism, shaping the marine biomass decomposition by foraging bacteria.

Salt stress triggers excessive hydrolysis of arginine-derived urea in Arabidopsis thaliana, raising cytoplasmic pH and inhibiting seed germination and seedling growth, providing new insights into the relationship between seed nitrogen mobilization and seed germination inhibition.

JMJD6 helps BRD4 to recruit CDK9 to RNA Polymerase II by disrupting 7SK snRNP complex.