{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Joshi IV"],"funding":["National Institute of Allergy and Infectious Diseases","Intramural NIH HHS","Government of the United Kingdom","National Institutes of Health","Division of Intramural Research"],"pagination":["107127"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11065749"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["300(4)"],"pubmed_abstract":["Regulators of G protein signaling (RGS) proteins constrain G protein-coupled receptor (GPCR)-mediated and other responses throughout the body primarily, but not exclusively, through their GTPase-activating protein activity. Asthma is a highly prevalent condition characterized by airway hyper-responsiveness (AHR) to environmental stimuli resulting in part from amplified GPCR-mediated airway smooth muscle contraction. Rgs2 or Rgs5 gene deletion in mice enhances AHR and airway smooth muscle contraction, whereas RGS4 KO mice unexpectedly have decreased AHR because of increased production of the bronchodilator prostaglandin E2 (PGE2) by lung epithelial cells. Here, we found that knockin mice harboring Rgs4 alleles encoding a point mutation (N128A) that sharply curtails RGS4 GTPase-activating pr"],"journal":["The Journal of biological chemistry"],"pubmed_title":["RGS4 controls airway hyperresponsiveness through GAP-independent mechanisms."],"pmcid":["PMC11065749"],"funding_grant_id":["ZIA AI000939","ZIA AI000939-19"],"pubmed_authors":["Druey KM","Lack JB","Liu C","Chan EC","Joshi IV"],"additional_accession":[]},"is_claimable":false,"name":"RGS4 controls airway hyperresponsiveness through GAP-independent mechanisms.","description":"Regulators of G protein signaling (RGS) proteins constrain G protein-coupled receptor (GPCR)-mediated and other responses throughout the body primarily, but not exclusively, through their GTPase-activating protein activity. Asthma is a highly prevalent condition characterized by airway hyper-responsiveness (AHR) to environmental stimuli resulting in part from amplified GPCR-mediated airway smooth muscle contraction. Rgs2 or Rgs5 gene deletion in mice enhances AHR and airway smooth muscle contraction, whereas RGS4 KO mice unexpectedly have decreased AHR because of increased production of the bronchodilator prostaglandin E2 (PGE2) by lung epithelial cells. Here, we found that knockin mice harboring Rgs4 alleles encoding a point mutation (N128A) that sharply curtails RGS4 GTPase-activating pr","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Apr","modification":"2026-05-26T20:11:43.528Z","creation":"2025-08-27T03:08:36.3Z"},"accession":"S-EPMC11065749","cross_references":{"pubmed":["38432633"],"doi":["10.1016/j.jbc.2024.107127"]}}