Experimental results suggest a previously unknown regulatory mechanism for GLP-1 production in L cells, which could offer new insights into diabetes treatments.

Non-native synthetic short-chain glycosphingolipids fused to GLP-1 enable intestinal absorption with high bioavailability in vivo.

A genetically encoded sensor and a photocaged peptide together enable precise investigation of human glucagon-like peptide-1 receptor activation with high spatiotemporal resolution.

C. elegans germline stem cells become quiescent under starved conditions, and this quiescence maintains the stem cell state even in the absence of GLP-1/Notch signaling, which is otherwise essential for stem cell maintenance.

Repression of gene expression by the histone methyltransferase G9a is guided by two zinc finger proteins that can recognize consensus sequences in DNA.

The cotranslational membrane integration of three multispanning Escherichia coli inner membrane proteins is followed using force profile analysis, uncovering unexpected complexities in the membrane integration process.

Leptin acts cell autonomously on brainstem neurons that express GLP-1 to suppress development of excitatory viscerosensory inputs to the hypothalamus.

The innate immune DNA sensor IFI16 is in association with H3K9 methyltransferases SUV39H1 and GLP under physiological conditions in the nucleus which facilitates the epigenetic silencing of foreign viral DNA.

By controlling the SUMOylation of the protein CAR-1, the aging-regulating pathways downstream of the Insulin/IGF signaling cascade and of the germ cells of the nematode Caenorhabditis elegans are integrated.

Autophagic flux assays in the nematode Caenorhabditis elegans suggest that autophagy decreases during normal aging, whereas long-lived daf-2 and glp-1 mutants maintain autophagic capacity in distinct spatiotemporal-specific manners to extend lifespan.