Disruption of P2Y2 signaling promotes breast tumor cell dissemination by reducing ATP-dependent calcium elevation and actin localization to cell junctions.

The tumor microenvironment and wound healing after injury both contain extremely high concentrations of the extracellular signaling molecule, adenosine triphosphate (ATP) compared to normal tissue. P2Y2 receptor, an ATP-activated purinergic receptor, is typically associated with pulmonary, endothelial, and neurological cell signaling. Here we report its role and importance in breast epithelial cell signaling and how it is altered in metastatic breast cancer.

Conserved residues in the extracellular loop 2 regulate Stachel-mediated activation of ADGRG2.

Cleavage and dissociation of a large N-terminal fragment and the consequent unmasking of a short sequence (Stachel) remaining on the N-terminus have been proposed as mechanisms of activation of some members of the adhesion G protein-coupled receptor (aGPCR) family. However, the identity of residues that play a role in the activation of aGPCRs by the cognate Stachel remains largely unknown. Protein sequence alignments revealed a conserved stretch of residues in the extracellular loop 2 (ECL2) of all 33 members of the aGPCR family.

The Emerging Role of Adhesion GPCRs in Cancer.

Aberrant expression, function, and mutation of G protein-coupled receptors (GPCRs) and their signaling partners, G proteins, have been well documented in many forms of cancer. These cell surface receptors and their endogenous ligands are implicated in all aspects of cancer including proliferation, angiogenesis, invasion, and metastasis. Adhesion GPCRs (aGPCRs) form the second largest family of GPCRs, most of which are orphan receptors with unknown physiological functions.

An experimental paradigm examining the influence of frustration on risk-taking behavior.

The present study examined the impact of frustration on risk-taking in college students with low and high ADHD symptomatology (L-ADHD and H-ADHD). Participants completed the Balloon Analogue Risk Task (BART) following induced frustration from a mood manipulation task (experimental session) and following no mood manipulation (control session). A manipulation check revealed a significant three-way interaction where the H-ADHD group reported higher frustration levels compared to the L-ADHD group, particularly in response to the frustration induction in the experimental condition.