< GPCR News < GPCRs in Oncology and Immunology Ascitic Shear Stress Activates GPCRs and Downregulates shear stresses are not well understood. upper range of fluid shear stress generated by the accumulation of ascites. We show that ovarian cancer cells exposed to ascitic shear stresses display heightened G protein-coupled These findings along with a shear-induced immunomodulatory secretome position elevated shear stress as

A functional analogue of GBP, stress-responsive peptide (SRP), was also identified in the same species Enhancement of GBP2 expression was observed in both Drosophila larvae and S2 cells under heat stress Authors Masaya Ono , Takashi Matsumura , Eui Jae Sung , Takashi Koyama , Masanori Ochiai , Stephen B Shears

Samples of synovial fluid and peripheral blood were analyzed for CD45+CD3+CD4+GPR15+ and CD45+CD3+CD8 Also, the frequency CD4+/CD8+ GPR15+ T lymphocytes are higher in synovial fluid of established RA patients

Methods: Relative levels of CXCL10(1-73) and intact CXCL10(1-77) were determined in synovial fluids of Results: Natural CXCL10(1-73) was more abundantly present compared to intact CXCL10(1-77) in synovial fluids

physiological contexts…one being our discovery that GPR56 is the platelet receptor that senses collagen and shear

GPCRs, Software, and Fluid Dynamics Yamina Berchiche and Aurelien Rizk discussed the complexities of The discussion ended with Aurelien Rizk sharing his current work on numerical simulations of fluid dynamics

Metabolic cage experiments demonstrated no differences in fluid intake, urine volume, urinary pH or urine systematically characterized the function of sodium/hydrogen exchanger 3 in the intestine and kidneys for fluid

The Leiser laboratory is focused on the molecular mechanisms of aging, with an emphasis on stress response Recent research in his laboratory focuses on how organisms perceive and respond to environmental stress

his laboratory has two main axes of research: 1) Studying interindividual vulnerability to chronic stress

Collectively, our findings suggested that Peptidase M84 triggered PAR-1-mediated oxidative stress to

of emergent vulnerabilities associated with adaptation pathways required to buffer cancer associated stress

his laboratory has two main axes of research: 1) Studying interindividual vulnerability to chronic stress

evolved to encompass their roles in regulating immune cell response to acute cardiac injury or chronic stress

tumor suppressor gene, has received increasing attention owing to its close relationship with oxidative stress

required for the restoration of glutamatergic synapses in prefrontal cortical neurons of chronically stressed

They stressed the necessity of making their research goals clearer, avoiding replication, and adopting

They stressed the necessity of making their research goals clearer, avoiding replication, and adopting

Yamina expressed interest in understanding how Badr’s experiences influenced his current role, and Badr stressed

John also mentioned his university application process, which was less stressful than the US system.