ArticleMolecular pharmacology2015
Delineation of a conserved arrestin-biased signaling repertoire in vivo.
Open access · greenAbstract read
In one paragraph
Article in Molecular pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.0field-weighted citation impact, top 8% of its field
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed, 36 citations in OpenAlex.
- GPCR systems coordinate cellular resilience against aging-associated stress.Frontiers in molecular biosciences · 2026Review
- G protein-coupled receptor digital twins for precision and personalized medicine.Computational and structural biotechnology journal · 2025Review
- GPR19 Coordinates Multiple Molecular Aspects of Stress Responses Associated with the Aging Process.International journal of molecular sciences · 2023Article
- Intersection of the Orphan G Protein-Coupled Receptor, GPR19, with the Aging Process.International journal of molecular sciences · 2022Review
- GPCRs Are Optimal Regulators of Complex Biological Systems and Orchestrate the Interface between Health and Disease.International journal of molecular sciences · 2021Review
- A cellular perspective of bias at G protein-coupled receptors.Protein science : a publication of the Protein Society · 2020Review
- The RXFP3 receptor is functionally associated with cellular responses to oxidative stress and DNA damage.Aging · 2019Article
- Multi-functionality of proteins involved in GPCR and G protein signaling: making sense of structure-function continuum with intrinsic disorder-based proteoforms.Cellular and molecular life sciences : CMLS · 2019Review
- G Protein-Coupled Receptor Systems and Their Role in Cellular Senescence.Computational and structural biotechnology journal · 2019Review
- G Protein-Coupled Receptor Systems as Crucial Regulators of DNA Damage Response Processes.International journal of molecular sciences · 2018Review
- Translating in vitro ligand bias into in vivo efficacy.Cellular signalling · 2018Review
- β-Arrestin Based Receptor Signaling Paradigms: Potential Therapeutic Targets for Complex Age-Related Disorders.Frontiers in pharmacology · 2018Review
- Retromer stops beta-arrestin 1-mediated signaling from internalized cannabinoid 2 receptors.Molecular biology of the cell · 2017Article
- The Diverse Roles of Arrestin Scaffolds in G Protein-Coupled Receptor Signaling.Pharmacological reviews · 2017Review
- G Protein-Coupled Receptor Endocytosis Confers Uniformity in Responses to Chemically Distinct Ligands.Molecular pharmacology · 2017Article
- The Multiple Waves of Cannabinoid 1 Receptor Signaling.Molecular pharmacology · 2016Review
- Mechanisms of Biased β-Arrestin-Mediated Signaling Downstream from the Cannabinoid 1 Receptor.Molecular pharmacology · 2016Article
- Human Neuropeptide S Receptor Is Activated via a Gαq Protein-biased Signaling Cascade by a Human Neuropeptide S Analog Lacking the C-terminal 10 Residues.The Journal of biological chemistry · 2016Article
- Informatic deconvolution of biased GPCR signaling mechanisms from in vivo pharmacological experimentation.Methods (San Diego, Calif.) · 2016Article
- Exploring G protein-coupled receptor signaling networks using SILAC-based phosphoproteomics.Methods (San Diego, Calif.) · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 5 institutions in 1 country.
Stuart MaudsleyNational Institutes of Health, National Institute on Aging, Baltimore, Maryland (S.M., B.M., S.P., K.G.B., W.H.W., Y.Z., E.L.); Department of Medicine, Duke University Medical Center, Durham, North Carolina (D.G.-P.); National Institutes of Health, Center for Information Technology, Bethesda, Maryland (H.C., C.J.); Department of Medicine and Department of Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston, South Carolina (L.M.L.); and Ralph H. Johnson Veterans Affairs Medical Center, Charleston, South Carolina (L.M.L.) stuart.maudsley@molgen.vib-ua.be.
Bronwen MartinNational Institutes of Health, National Institute on Aging, Baltimore, Maryland (S.M., B.M., S.P., K.G.B., W.H.W., Y.Z., E.L.); Department of Medicine, Duke University Medical Center, Durham, North Carolina (D.G.-P.); National Institutes of Health, Center for Information Technology, Bethesda, Maryland (H.C., C.J.); Department of Medicine and Department of Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston, South Carolina (L.M.L.); and Ralph H. Johnson Veterans Affairs Medical Center, Charleston, South Carolina (L.M.L.).
Diane Gesty-PalmerNational Institutes of Health, National Institute on Aging, Baltimore, Maryland (S.M., B.M., S.P., K.G.B., W.H.W., Y.Z., E.L.); Department of Medicine, Duke University Medical Center, Durham, North Carolina (D.G.-P.); National Institutes of Health, Center for Information Technology, Bethesda, Maryland (H.C., C.J.); Department of Medicine and Department of Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston, South Carolina (L.M.L.); and Ralph H. Johnson Veterans Affairs Medical Center, Charleston, South Carolina (L.M.L.).
Huey CheungNational Institutes of Health, National Institute on Aging, Baltimore, Maryland (S.M., B.M., S.P., K.G.B., W.H.W., Y.Z., E.L.); Department of Medicine, Duke University Medical Center, Durham, North Carolina (D.G.-P.); National Institutes of Health, Center for Information Technology, Bethesda, Maryland (H.C., C.J.); Department of Medicine and Department of Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston, South Carolina (L.M.L.); and Ralph H. Johnson Veterans Affairs Medical Center, Charleston, South Carolina (L.M.L.).
Calvin JohnsonNational Institutes of Health, National Institute on Aging, Baltimore, Maryland (S.M., B.M., S.P., K.G.B., W.H.W., Y.Z., E.L.); Department of Medicine, Duke University Medical Center, Durham, North Carolina (D.G.-P.); National Institutes of Health, Center for Information Technology, Bethesda, Maryland (H.C., C.J.); Department of Medicine and Department of Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston, South Carolina (L.M.L.); and Ralph H. Johnson Veterans Affairs Medical Center, Charleston, South Carolina (L.M.L.).
Shamit PatelNational Institutes of Health, National Institute on Aging, Baltimore, Maryland (S.M., B.M., S.P., K.G.B., W.H.W., Y.Z., E.L.); Department of Medicine, Duke University Medical Center, Durham, North Carolina (D.G.-P.); National Institutes of Health, Center for Information Technology, Bethesda, Maryland (H.C., C.J.); Department of Medicine and Department of Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston, South Carolina (L.M.L.); and Ralph H. Johnson Veterans Affairs Medical Center, Charleston, South Carolina (L.M.L.).
Kevin G BeckerNational Institutes of Health, National Institute on Aging, Baltimore, Maryland (S.M., B.M., S.P., K.G.B., W.H.W., Y.Z., E.L.); Department of Medicine, Duke University Medical Center, Durham, North Carolina (D.G.-P.); National Institutes of Health, Center for Information Technology, Bethesda, Maryland (H.C., C.J.); Department of Medicine and Department of Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston, South Carolina (L.M.L.); and Ralph H. Johnson Veterans Affairs Medical Center, Charleston, South Carolina (L.M.L.).
William H WoodNational Institutes of Health, National Institute on Aging, Baltimore, Maryland (S.M., B.M., S.P., K.G.B., W.H.W., Y.Z., E.L.); Department of Medicine, Duke University Medical Center, Durham, North Carolina (D.G.-P.); National Institutes of Health, Center for Information Technology, Bethesda, Maryland (H.C., C.J.); Department of Medicine and Department of Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston, South Carolina (L.M.L.); and Ralph H. Johnson Veterans Affairs Medical Center, Charleston, South Carolina (L.M.L.).
Yongqing ZhangNational Institutes of Health, National Institute on Aging, Baltimore, Maryland (S.M., B.M., S.P., K.G.B., W.H.W., Y.Z., E.L.); Department of Medicine, Duke University Medical Center, Durham, North Carolina (D.G.-P.); National Institutes of Health, Center for Information Technology, Bethesda, Maryland (H.C., C.J.); Department of Medicine and Department of Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston, South Carolina (L.M.L.); and Ralph H. Johnson Veterans Affairs Medical Center, Charleston, South Carolina (L.M.L.).
Elin LehrmannNational Institutes of Health, National Institute on Aging, Baltimore, Maryland (S.M., B.M., S.P., K.G.B., W.H.W., Y.Z., E.L.); Department of Medicine, Duke University Medical Center, Durham, North Carolina (D.G.-P.); National Institutes of Health, Center for Information Technology, Bethesda, Maryland (H.C., C.J.); Department of Medicine and Department of Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston, South Carolina (L.M.L.); and Ralph H. Johnson Veterans Affairs Medical Center, Charleston, South Carolina (L.M.L.).
Louis M LuttrellNational Institutes of Health, National Institute on Aging, Baltimore, Maryland (S.M., B.M., S.P., K.G.B., W.H.W., Y.Z., E.L.); Department of Medicine, Duke University Medical Center, Durham, North Carolina (D.G.-P.); National Institutes of Health, Center for Information Technology, Bethesda, Maryland (H.C., C.J.); Department of Medicine and Department of Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston, South Carolina (L.M.L.); and Ralph H. Johnson Veterans Affairs Medical Center, Charleston, South Carolina (L.M.L.).
Medical University of South Carolina · USNational Institute on Aging · USRalph H. Johnson VA Medical Center · USDuke Medical Center · USNational Institutes of Health · US
Funding
Text Analytics, Machine Learning & High Performance ComputingZIHCT000200 · CIT · CENTER FOR INFORMATION TECHNOLOGY · PI JOHNSON, CALVIN A · 2009 to 2019
$25.5MAnalysis of complex biological systems by microarray based gene expressionZICAG000616 · NIA · NATIONAL INSTITUTE ON AGING · PI DE, SUPRIYO · 2009 to 2025
$15.5MInterdisciplinary Research Careers in Women's HealthK12HD043446 · NICHD · DUKE UNIVERSITY · PI AMUNDSEN, CINDY · 2002 to 2023
$9.6MTYROSINE KINASES IN G PROTEIN MEDIATED SIGNALINGR01DK055524 · NIDDK · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI LUTTRELL, LOUIS M · 1998 to 2017
$4.6MPharmacodynamics of Biased G protein-Coupled Receptor AgonismR01GM095497 · NIGMS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI LUTTRELL, LOUIS M · 2013 to 2016
$1.1MNICHD NIH HHS K12 HD043446NICHD NIH HHS T32-HD043446NIDDK NIH HHS R01 DK055524NIDDK NIH HHS R01-DK055524NIGMS NIH HHS R01 GM095497NIGMS NIH HHS R01-GM095497
Abstract
Biased G protein-coupled receptor agonists engender a restricted repertoire of downstream events from their cognate receptors, permitting them to produce mixed agonist-antagonist effects in vivo. While this opens the possibility of novel therapeutics, it complicates rational drug design, since the in vivo response to a biased agonist cannot be reliably predicted from its in cellula efficacy. We have employed novel informatic approaches to characterize the in vivo transcriptomic signature of the arrestin pathway-selective parathyroid hormone analog [d-Trp(12), Tyr(34)]bovine PTH(7-34) in six different murine tissues after chronic drug exposure. We find that [d-Trp(12), Tyr(34)]bovine PTH(7-34) elicits a distinctive arrestin-signaling focused transcriptomic response that is more coherently regulated across tissues than that of the pluripotent agonist, human PTH(1-34). This arrestin-focused network is closely associated with transcriptional control of cell growth and development. Our demonstration of a conserved arrestin-dependent transcriptomic signature suggests a framework within which the in vivo outcomes of arrestin-biased signaling may be generalized.
Indexed as
TranscriptomeAnimalsArrestinsCattleComputational BiologyHumansMaleMice, Inbred C57BLMice, KnockoutOrgan SpecificityParathyroid HormonePeptide FragmentsReceptor, Parathyroid Hormone, Type 1Signal TransductionSpecies SpecificityTranscription, Geneticarrestin3ArrestinsParathyroid Hormoneparathyroid hormone (7-34)Peptide FragmentsReceptor, Parathyroid Hormone, Type 1
Identifiers
What OpenQuestion holds
Textmetadata
Read underepoch 390
Registered trials
None linked
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.