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GPR88 inhibits G-protein signaling of nearby GPCRs, and dampens b-arrestin recruitment by all GPCRs tested, likely by sequestration in intracellular compartments.

After two heart attacks in three years, an associate professor discusses the challenges of faculty life.

A temperate bacteriophage reprograms the oxygen response of a bacterial signaling system by replacing a host-encoded promoter with a phage-encoded promoter.

Cardiomyocyte Nox4 is a crucial physiological mediator of Nrf2 activation during acute exercise, triggering an adaptive response that preserves redox balance, mitochondrial and cardiac function to support normal physical exercise.

A novel thermoregulatory mechanism in blood-sucking insects, vectors of human disease, is described using a functional-morphological approach.

A heat exchange mechanism in the head of kissing bugs helps to prevent stress and regulate their temperature while they feed on warm blood.

Intrinsic tolerance of Mycobacterium tuberculosis toward the world's most successful antibacterials, β-lactams, is dependent on cytoplasmic redox potential and an intracellular redox-sensor WhiB4.

Phosphoproteomics identifies β-arrestin 2 phosphorylation at Thr383 by MEK as a key step of GPCR-induced Erk½ activation, thus providing new insight into the molecular mechanism underlying β-arrestin-dependent GPCR-operated signaling.