Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

The biased M3 mAChR ligand PD 102807 mediates qualitatively distinct signaling to regulate airway smooth muscle phenotype.

The Journal of biological chemistry - 1 Oct 2023

Tompkins Eric, Mimic Bogdana, Penn Raymond B, Pera Tonio

Abstract excerpt

Airway smooth muscle (ASM) cells attain a hypercontractile phenotype during obstructive airway diseases. We recently identified a biased M3 muscarinic acetylcholine receptor (mAChR) ligand, PD 102807, that induces GRK-/arrestin-dependent AMP-activated protein kinase (AMPK) activation to inhibit transforming growth factor-β-induced hypercontractile ASM phenotype. Conversely, the balanced mAChR agonist,...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to AMP-Activated Protein Kinases
Share to Mechanistic Target of Rapamycin Complex 1

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Methacholine Chloride

Share to Multiprotein Complexes

Share to Muscle, Smooth

Share to Myocytes, Smooth Muscle

Share to Receptor, Muscarinic M3

Share to TOR Serine-Threonine Kinases

Source

Open in PubMed Open full text

Identifiers

PMID: 37660916
DOI: 10.1016/j.jbc.2023.105209
PMCID: PMC10520882

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

The biased M3 mAChR ligand PD 102807 mediates qualitatively distinct signaling to regulate airway smooth muscle phenotype.PMID 37660916Read ↗

Up-regulation of KCa3.1 promotes human airway smooth muscle cell phenotypic modulation.Semantic proximity Read ↗

β2 -Adrenoceptor agonist profiling reveals biased signalling phenotypes for the β2 -adrenoceptor with possible implications for the treatment of asthma.Semantic proximity Read ↗

Metformin suppresses epithelial sodium channel hyperactivation and its associated phenotypes in a mouse model of obstructive lung diseases.Semantic proximity Read ↗

Development of Mutant M3 Muscarinic Receptors Biased for G Protein Activation or Recruitment of β-Arrestins.Semantic proximity Read ↗

AMPK-driven Macrophage Responses Are Autophagy Dependent in Experimental Bronchopulmonary DysplasiaSemantic proximity Read ↗

AMP-activated protein kinase phosphorylation of the R domain inhibits PKA stimulation of CFTR.Semantic proximity Read ↗

Targeted transgenesis reveals discrete attenuator functions of GRK and PKA in airway beta2-adrenergic receptor physiologic signaling.Semantic proximity Read ↗

Physiological modulation of CFTR activity by AMP-activated protein kinase in polarized T84 cells.Semantic proximity Read ↗

Phophatidylinositol-3 kinase/mammalian target of rapamycin/p70S6K regulates contractile protein accumulation in airway myocyte differentiation.Semantic proximity Read ↗

Muscarinic M(3) receptor-dependent regulation of airway smooth muscle contractile phenotype.Semantic proximity Read ↗

Calpastatin overexpression in the skeletal muscle of mice prevents clenbuterol-induced muscle hypertrophy and phenotypic shift.Semantic proximity Read ↗

Glucocorticosteroids and β₂-adrenoceptor agonists synergize to inhibit airway smooth muscle remodeling.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.