Scopus Publication Detail
The publication detail shows the title, authors (with indicators showing other profiled authors), information on the publishing organization, abstract and a link to the article in Scopus. This abstract is what is used to create the fingerprint of the publication.
Irving C. Allen; Amy J. Pace; Leigh A. Jania; Julie G. Ledford; Anne M. Latour; John N. Snouwaert; Virginie Bernier; Rino Stocco; Alex G. Therien; Beverly H. Koller (Profiled Authors: Beverly H Koller; Julie Ledford)
American Journal of Physiology - Lung Cellular and Molecular Physiology. 2006;291(5):L1005-L1017.Abstract
A genetic contribution to asthma susceptibility is well recognized, and linkage studies have identified a large number of genes associated with asthma pathogenesis. Recently, a locus encoding a seven-transmembrane protein was shown to be associated with asthma in founder populations. The expression of the protein GPRA (G protein-coupled receptor for asthma susceptibility) in human airway epithelia and smooth muscle, and its increased expression in a mouse model of asthma, suggested that a gain-of-function mutation in this gene increased the disease risk. However, we report here that the development of allergic lung disease in GPRA-deficient mice is unaltered. A possible explanation for this finding became apparent upon reexamination of the expression of this gene. In contrast to initial studies, our analyses failed to detect expression of GPRA in human lung tissue or in mice with allergic lung disease. We identify a single parameter that distinguishes GPRA-deficient and wild-type mice. Whereas the change in airway resistance in response to methacholine was identical in control and GPRA-deficient mice, the mutant animals showed an attenuated response to thromboxane, a cholinergic receptor-dependent bronchoconstricting agent. Together, our studies fail to support a direct contribution of GPRA to asthma pathogenesis. However, our data suggest that GPRA may contribute to the asthmatic phenotype by altering the activity of other pathways, such as neurally mediated mechanisms, that contribute to disease. This interpretation is supported by high levels of GPRA expression in the brain and its recent identification as the neuropeptide S receptor. Copyright © 2006 the American Physiological Society.
This section shows information related to the publication - computed using the fingerprint of the publication - including related publications, related experts with fingerprints representing significant amounts of overlap between their fingerprint and this publication. The red dots indicate whether those experts or terms appear within the publication, thereby showing potential and actual connections.
Samir N. P. Kelada; Mark S. Wilson; Urraca Tavarez; Kari Kubalanza; Bhavesh Borate; Greg S. Whitehead; Shuichiro Maruoka; Michelle G. Roy; Michelle Olive; Danielle E. Carpenter; et al.American Journal of Respiratory Cell and Molecular Biology. 2011;45(4):817-824.
P. Marraccini; D.M. Brass; J.W. Hollingsworth; S. Maruoka; S. Garantziotis; D.A. SchwartzClinical and Experimental Allergy. 2008;38(9):1526-1535.
Julia K. L. Walker; Adriana Ahumada; Bryan Frank; Renee Gaspard; Katherine Berman; John Quackenbush; David A. SchwartzAmerican Journal of Respiratory Cell and Molecular Biology. 2006;34(6):711-718.
Appears in this Document