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Neuropeptide Y gene polymorphisms confer risk of early-onset atherosclerosis.
(PLoS Genet, 2009-01)
Neuropeptide Y (NPY) is a strong candidate gene for coronary artery disease (CAD).
We have previously identified genetic linkage to familial CAD in the genomic region
of NPY. We performed follow-up genetic, biostatistical, ...
Hybrid transgenic mice reveal in vivo specificity of G protein-coupled receptor kinases in the heart.
(Circ Res, 2000-01-07)
G protein-coupled receptor kinases (GRKs) phosphorylate activated G protein-coupled
receptors, including alpha(1B)-adrenergic receptors (ARs), resulting in desensitization.
In vivo analysis of GRK substrate selectivity has ...
Augmentation of cardiac contractility mediated by the human beta(3)-adrenergic receptor overexpressed in the hearts of transgenic mice.
(Circulation, 2001-11-13)
BACKGROUND: Stimulation of beta(1)- and beta(2)-adrenergic receptors (ARs) in the
heart results in positive inotropy. In contrast, it has been reported that the beta(3)AR
is also expressed in the human heart and that its ...
Gene expression signatures that predict radiation exposure in mice and humans.
(PLoS Med, 2007-04)
BACKGROUND: The capacity to assess environmental inputs to biological phenotypes is
limited by methods that can accurately and quantitatively measure these contributions.
One such example can be seen in the context of exposure ...
Gene expression signatures of radiation response are specific, durable and accurate in mice and humans.
(PLoS One, 2008-04-02)
BACKGROUND: Previous work has demonstrated the potential for peripheral blood (PB)
gene expression profiling for the detection of disease or environmental exposures.
METHODS AND FINDINGS: We have sought to determine the ...
beta-Arrestin1 mediates nicotinic acid-induced flushing, but not its antilipolytic effect, in mice.
(J Clin Invest, 2009-05)
Nicotinic acid is one of the most effective agents for both lowering triglycerides
and raising HDL. However, the side effect of cutaneous flushing severely limits patient
compliance. As nicotinic acid stimulates the GPCR ...
Differential mechanisms of morphine antinociceptive tolerance revealed in (beta)arrestin-2 knock-out mice.
(J Neurosci, 2002-12-01)
Morphine induces antinociception by activating mu opioid receptors (muORs) in spinal
and supraspinal regions of the CNS. (Beta)arrestin-2 (beta)arr2), a G-protein-coupled
receptor-regulating protein, regulates the muOR in ...
Enhanced rewarding properties of morphine, but not cocaine, in beta(arrestin)-2 knock-out mice.
(J Neurosci, 2003-11-12)
The reinforcing and psychomotor effects of morphine involve opiate stimulation of
the dopaminergic system via activation of mu-opioid receptors (muOR). Both mu-opioid
and dopamine receptors are members of the G-protein-coupled ...
When 7 transmembrane receptors are not G protein-coupled receptors.
(J Clin Invest, 2005-11)
Classically, 7 transmembrane receptors transduce extracellular signals by coupling
to heterotrimeric G proteins, although recent in vitro studies have clearly demonstrated
that they can also signal via G protein-independent ...
Beta-arrestin-mediated beta1-adrenergic receptor transactivation of the EGFR confers cardioprotection.
(J Clin Invest, 2007-09)
Deleterious effects on the heart from chronic stimulation of beta-adrenergic receptors
(betaARs), members of the 7 transmembrane receptor family, have classically been shown
to result from Gs-dependent adenylyl ...