Evidence map›Paper›PMID 25657338›Full record

ArticleMolecular pharmacology2015

Cannabinoid receptor-interacting protein 1a modulates CB1 receptor signaling and regulation.

Tricia H Smith, Lawrence C Blume, Alex Straiker, Jordan O Cox, Bethany G David, Julie R Secor McVoy, Katherine W Sayers, Justin L Poklis, Rehab A Abdullah, Michaela Egertová and 5 more

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
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 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
6.2field-weighted citation impact, top 4% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

31 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Mechanisms of cannabinoid tolerance.Biochemical pharmacology · 2023
    Review
  5. Article
  6. Review
  7. Article
  8. Differential Expression of CBCannabis and cannabinoid research · 2022
    Article
  9. Functional Selectivity of a Biased Cannabinoid-1 Receptor (CBACS pharmacology & translational science · 2021
    Article
  10. Review of the Endocannabinoid System.Biological psychiatry. Cognitive neuroscience and neuroimaging · 2021
    Review
  11. Multiple cannabinoid signaling cascades powerfully suppress recurrent excitation in the hippocampus.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Cannabinoids, Endocannabinoids and Sleep.Frontiers in molecular neuroscience · 2020
    Article
  18. Molecular Interaction between Distal C-Terminal Domain of the CBJournal of chemical information and modeling · 2019
    Article
  19. Review
  20. The Endocannabinoid System of Animals.Animals : an open access journal from MDPI · 2019
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

15 authors at 4 institutions in 2 countries.

Tricia H SmithDepartment of Pharmacology and Toxicology and Institute for Drug and Alcohol Studies (T.H.S., J.O.C., B.G.D., J.R.S.M., J.L.P., R.A.A., D.E.S.), Department of Anatomy and Neurobiology (K.W.S.), Department of Biochemistry and Molecular Biology (C.-K.C.), Virginia Commonwealth University School of Medicine, Richmond, Virginia; Department of Physiology and Pharmacology, Wake Forest University Health Sciences, Winston-Salem, North Carolina (L.C.B., A.C.H.); The Gill Center for Biomolecular Science and the Department of Psychological and Brain Sciences, Indiana University, Bloomington, Indiana (A.S., K.M.); and School of Biological and Chemical Sciences, Queen Mary, University of London, London, United Kingdom (M.E., M.R.E.).
Lawrence C BlumeDepartment of Pharmacology and Toxicology and Institute for Drug and Alcohol Studies (T.H.S., J.O.C., B.G.D., J.R.S.M., J.L.P., R.A.A., D.E.S.), Department of Anatomy and Neurobiology (K.W.S.), Department of Biochemistry and Molecular Biology (C.-K.C.), Virginia Commonwealth University School of Medicine, Richmond, Virginia; Department of Physiology and Pharmacology, Wake Forest University Health Sciences, Winston-Salem, North Carolina (L.C.B., A.C.H.); The Gill Center for Biomolecular Science and the Department of Psychological and Brain Sciences, Indiana University, Bloomington, Indiana (A.S., K.M.); and School of Biological and Chemical Sciences, Queen Mary, University of London, London, United Kingdom (M.E., M.R.E.).
Alex StraikerDepartment of Pharmacology and Toxicology and Institute for Drug and Alcohol Studies (T.H.S., J.O.C., B.G.D., J.R.S.M., J.L.P., R.A.A., D.E.S.), Department of Anatomy and Neurobiology (K.W.S.), Department of Biochemistry and Molecular Biology (C.-K.C.), Virginia Commonwealth University School of Medicine, Richmond, Virginia; Department of Physiology and Pharmacology, Wake Forest University Health Sciences, Winston-Salem, North Carolina (L.C.B., A.C.H.); The Gill Center for Biomolecular Science and the Department of Psychological and Brain Sciences, Indiana University, Bloomington, Indiana (A.S., K.M.); and School of Biological and Chemical Sciences, Queen Mary, University of London, London, United Kingdom (M.E., M.R.E.).
Jordan O CoxDepartment of Pharmacology and Toxicology and Institute for Drug and Alcohol Studies (T.H.S., J.O.C., B.G.D., J.R.S.M., J.L.P., R.A.A., D.E.S.), Department of Anatomy and Neurobiology (K.W.S.), Department of Biochemistry and Molecular Biology (C.-K.C.), Virginia Commonwealth University School of Medicine, Richmond, Virginia; Department of Physiology and Pharmacology, Wake Forest University Health Sciences, Winston-Salem, North Carolina (L.C.B., A.C.H.); The Gill Center for Biomolecular Science and the Department of Psychological and Brain Sciences, Indiana University, Bloomington, Indiana (A.S., K.M.); and School of Biological and Chemical Sciences, Queen Mary, University of London, London, United Kingdom (M.E., M.R.E.).
Bethany G DavidDepartment of Pharmacology and Toxicology and Institute for Drug and Alcohol Studies (T.H.S., J.O.C., B.G.D., J.R.S.M., J.L.P., R.A.A., D.E.S.), Department of Anatomy and Neurobiology (K.W.S.), Department of Biochemistry and Molecular Biology (C.-K.C.), Virginia Commonwealth University School of Medicine, Richmond, Virginia; Department of Physiology and Pharmacology, Wake Forest University Health Sciences, Winston-Salem, North Carolina (L.C.B., A.C.H.); The Gill Center for Biomolecular Science and the Department of Psychological and Brain Sciences, Indiana University, Bloomington, Indiana (A.S., K.M.); and School of Biological and Chemical Sciences, Queen Mary, University of London, London, United Kingdom (M.E., M.R.E.).
Julie R Secor McVoyDepartment of Pharmacology and Toxicology and Institute for Drug and Alcohol Studies (T.H.S., J.O.C., B.G.D., J.R.S.M., J.L.P., R.A.A., D.E.S.), Department of Anatomy and Neurobiology (K.W.S.), Department of Biochemistry and Molecular Biology (C.-K.C.), Virginia Commonwealth University School of Medicine, Richmond, Virginia; Department of Physiology and Pharmacology, Wake Forest University Health Sciences, Winston-Salem, North Carolina (L.C.B., A.C.H.); The Gill Center for Biomolecular Science and the Department of Psychological and Brain Sciences, Indiana University, Bloomington, Indiana (A.S., K.M.); and School of Biological and Chemical Sciences, Queen Mary, University of London, London, United Kingdom (M.E., M.R.E.).
Katherine W SayersDepartment of Pharmacology and Toxicology and Institute for Drug and Alcohol Studies (T.H.S., J.O.C., B.G.D., J.R.S.M., J.L.P., R.A.A., D.E.S.), Department of Anatomy and Neurobiology (K.W.S.), Department of Biochemistry and Molecular Biology (C.-K.C.), Virginia Commonwealth University School of Medicine, Richmond, Virginia; Department of Physiology and Pharmacology, Wake Forest University Health Sciences, Winston-Salem, North Carolina (L.C.B., A.C.H.); The Gill Center for Biomolecular Science and the Department of Psychological and Brain Sciences, Indiana University, Bloomington, Indiana (A.S., K.M.); and School of Biological and Chemical Sciences, Queen Mary, University of London, London, United Kingdom (M.E., M.R.E.).
Justin L PoklisDepartment of Pharmacology and Toxicology and Institute for Drug and Alcohol Studies (T.H.S., J.O.C., B.G.D., J.R.S.M., J.L.P., R.A.A., D.E.S.), Department of Anatomy and Neurobiology (K.W.S.), Department of Biochemistry and Molecular Biology (C.-K.C.), Virginia Commonwealth University School of Medicine, Richmond, Virginia; Department of Physiology and Pharmacology, Wake Forest University Health Sciences, Winston-Salem, North Carolina (L.C.B., A.C.H.); The Gill Center for Biomolecular Science and the Department of Psychological and Brain Sciences, Indiana University, Bloomington, Indiana (A.S., K.M.); and School of Biological and Chemical Sciences, Queen Mary, University of London, London, United Kingdom (M.E., M.R.E.).
Rehab A AbdullahDepartment of Pharmacology and Toxicology and Institute for Drug and Alcohol Studies (T.H.S., J.O.C., B.G.D., J.R.S.M., J.L.P., R.A.A., D.E.S.), Department of Anatomy and Neurobiology (K.W.S.), Department of Biochemistry and Molecular Biology (C.-K.C.), Virginia Commonwealth University School of Medicine, Richmond, Virginia; Department of Physiology and Pharmacology, Wake Forest University Health Sciences, Winston-Salem, North Carolina (L.C.B., A.C.H.); The Gill Center for Biomolecular Science and the Department of Psychological and Brain Sciences, Indiana University, Bloomington, Indiana (A.S., K.M.); and School of Biological and Chemical Sciences, Queen Mary, University of London, London, United Kingdom (M.E., M.R.E.).
Michaela EgertováDepartment of Pharmacology and Toxicology and Institute for Drug and Alcohol Studies (T.H.S., J.O.C., B.G.D., J.R.S.M., J.L.P., R.A.A., D.E.S.), Department of Anatomy and Neurobiology (K.W.S.), Department of Biochemistry and Molecular Biology (C.-K.C.), Virginia Commonwealth University School of Medicine, Richmond, Virginia; Department of Physiology and Pharmacology, Wake Forest University Health Sciences, Winston-Salem, North Carolina (L.C.B., A.C.H.); The Gill Center for Biomolecular Science and the Department of Psychological and Brain Sciences, Indiana University, Bloomington, Indiana (A.S., K.M.); and School of Biological and Chemical Sciences, Queen Mary, University of London, London, United Kingdom (M.E., M.R.E.).
Ching-Kang ChenDepartment of Pharmacology and Toxicology and Institute for Drug and Alcohol Studies (T.H.S., J.O.C., B.G.D., J.R.S.M., J.L.P., R.A.A., D.E.S.), Department of Anatomy and Neurobiology (K.W.S.), Department of Biochemistry and Molecular Biology (C.-K.C.), Virginia Commonwealth University School of Medicine, Richmond, Virginia; Department of Physiology and Pharmacology, Wake Forest University Health Sciences, Winston-Salem, North Carolina (L.C.B., A.C.H.); The Gill Center for Biomolecular Science and the Department of Psychological and Brain Sciences, Indiana University, Bloomington, Indiana (A.S., K.M.); and School of Biological and Chemical Sciences, Queen Mary, University of London, London, United Kingdom (M.E., M.R.E.).
Ken MackieDepartment of Pharmacology and Toxicology and Institute for Drug and Alcohol Studies (T.H.S., J.O.C., B.G.D., J.R.S.M., J.L.P., R.A.A., D.E.S.), Department of Anatomy and Neurobiology (K.W.S.), Department of Biochemistry and Molecular Biology (C.-K.C.), Virginia Commonwealth University School of Medicine, Richmond, Virginia; Department of Physiology and Pharmacology, Wake Forest University Health Sciences, Winston-Salem, North Carolina (L.C.B., A.C.H.); The Gill Center for Biomolecular Science and the Department of Psychological and Brain Sciences, Indiana University, Bloomington, Indiana (A.S., K.M.); and School of Biological and Chemical Sciences, Queen Mary, University of London, London, United Kingdom (M.E., M.R.E.).
Maurice R ElphickDepartment of Pharmacology and Toxicology and Institute for Drug and Alcohol Studies (T.H.S., J.O.C., B.G.D., J.R.S.M., J.L.P., R.A.A., D.E.S.), Department of Anatomy and Neurobiology (K.W.S.), Department of Biochemistry and Molecular Biology (C.-K.C.), Virginia Commonwealth University School of Medicine, Richmond, Virginia; Department of Physiology and Pharmacology, Wake Forest University Health Sciences, Winston-Salem, North Carolina (L.C.B., A.C.H.); The Gill Center for Biomolecular Science and the Department of Psychological and Brain Sciences, Indiana University, Bloomington, Indiana (A.S., K.M.); and School of Biological and Chemical Sciences, Queen Mary, University of London, London, United Kingdom (M.E., M.R.E.).
Allyn C HowlettDepartment of Pharmacology and Toxicology and Institute for Drug and Alcohol Studies (T.H.S., J.O.C., B.G.D., J.R.S.M., J.L.P., R.A.A., D.E.S.), Department of Anatomy and Neurobiology (K.W.S.), Department of Biochemistry and Molecular Biology (C.-K.C.), Virginia Commonwealth University School of Medicine, Richmond, Virginia; Department of Physiology and Pharmacology, Wake Forest University Health Sciences, Winston-Salem, North Carolina (L.C.B., A.C.H.); The Gill Center for Biomolecular Science and the Department of Psychological and Brain Sciences, Indiana University, Bloomington, Indiana (A.S., K.M.); and School of Biological and Chemical Sciences, Queen Mary, University of London, London, United Kingdom (M.E., M.R.E.).
Dana E SelleyDepartment of Pharmacology and Toxicology and Institute for Drug and Alcohol Studies (T.H.S., J.O.C., B.G.D., J.R.S.M., J.L.P., R.A.A., D.E.S.), Department of Anatomy and Neurobiology (K.W.S.), Department of Biochemistry and Molecular Biology (C.-K.C.), Virginia Commonwealth University School of Medicine, Richmond, Virginia; Department of Physiology and Pharmacology, Wake Forest University Health Sciences, Winston-Salem, North Carolina (L.C.B., A.C.H.); The Gill Center for Biomolecular Science and the Department of Psychological and Brain Sciences, Indiana University, Bloomington, Indiana (A.S., K.M.); and School of Biological and Chemical Sciences, Queen Mary, University of London, London, United Kingdom (M.E., M.R.E.) deselley@vcu.edu.
Indiana University Bloomington · USQueen Mary University of London · GBVirginia Commonwealth University · USWake Forest University · US

Funding

TRAINING IN THE PHARMACOLOGY OF ABUSED DRUGST32DA007027 · NIDA · VIRGINIA COMMONWEALTH UNIVERSITY · PI William L. Dewey · 1985 to 2026
$14.7M
VCU Center for Drug Addiction ResearchP30DA033934 · NIDA · VIRGINIA COMMONWEALTH UNIVERSITY · PI JOLENE J WINDLE · 2014 to 2026
$13.8M
Center for Clinical and Translational ResearchUL1TR000058 · NCATS · VIRGINIA COMMONWEALTH UNIVERSITY · PI MOELLER, FREDERICK GERARD · 2012 to 2015
$12.5M
VCU Neuroscience Center Core GrantP30NS047463 · NINDS · VIRGINIA COMMONWEALTH UNIVERSITY · PI POVLISHOCK, JOHN T · 2003 to 2013
$5.0M
Neuronal cannabinoidsR01DA011322 · NIDA · UNIVERSITY OF WASHINGTON · PI MACKIE, KENNETH · 1998 to 2014
$3.4M
CANNABINOID RECEPTORS IN NEURONAL CELLS AND BRAINR01DA003690 · NIDA · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI HOWLETT, ALLYN C · 1985 to 2014
$2.8M
THE BRAIN PARENCHYMAL AND VASCULAR RESPONSE TO TRAUMAT32NS007288 · NINDS · VIRGINIA COMMONWEALTH UNIVERSITY · PI POVLISHOCK, JOHN T · 1986 to 2010
$2.0M
Cannabinoid Modulation of Cell FunctionK05DA021696 · NIDA · TRUSTEES OF INDIANA UNIVERSITY · PI MACKIE, KENNETH · 2007 to 2017
$1.3M
GPR119: A novel means to lower intraocular pressure?R21EY021831 · NEI · TRUSTEES OF INDIANA UNIVERSITY · PI STRAIKER, ALEXANDER J · 2011 to 2012
$424k
CB1 Receptor Regulation by Cannabinoid Receptor Interacting Protein CRIP1aR21DA025321 · NIDA · VIRGINIA COMMONWEALTH UNIVERSITY · PI HOWLETT, ALLYN C, SELLEY, DANA E · 2009 to 2010
$420k
Functional studies of cannabinoid receptor-interacting protein 1a in null miceR03DA035424 · NIDA · VIRGINIA COMMONWEALTH UNIVERSITY · PI SELLEY, DANA E · 2014 to 2015
$151k
Cannabinoid Receptor Interacting Protein1a Structure-FunctionF31DA032215 · NIDA · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI BLUME, LAWRENCE CHRISTOPHER · 2012 to 2013
$83k
Biotechnology and Biological Sciences Research Council S19916NCATS NIH HHS UL1 TR000058NCATS NIH HHS UL1-TR000058NEI NIH HHS R21 EY021831NEI NIH HHS R21-EY021831NIDA NIH HHS F31 DA023747NIDA NIH HHS F31-DA023747NIDA NIH HHS F31 DA032215NIDA NIH HHS F31-DA032215NIDA NIH HHS K05 DA021696NIDA NIH HHS K05-DA021696NIDA NIH HHS P30 DA033934NIDA NIH HHS P30-DA033934NIDA NIH HHS R01 DA003690NIDA NIH HHS R01-DA003690NIDA NIH HHS R01 DA011322NIDA NIH HHS R01-DA011322NIDA NIH HHS R03 DA035424NIDA NIH HHS R03-DA035424NIDA NIH HHS R21 DA025321NIDA NIH HHS R21-DA025321NIDA NIH HHS T32 DA007027NINDS NIH HHS P30 NS047463NINDS NIH HHS P30-NS047463NINDS NIH HHS T32 NS007288NINDS NIH HHS T32-NS007288
6 · The paper itself

Abstract

Cannabinoid CB1 receptors (CB1Rs) mediate the presynaptic effects of endocannabinoids in the central nervous system (CNS) and most behavioral effects of exogenous cannabinoids. Cannabinoid receptor-interacting protein 1a (CRIP1a) binds to the CB1R C-terminus and can attenuate constitutive CB1R-mediated inhibition of Ca(2+) channel activity. We now demonstrate cellular colocalization of CRIP1a at neuronal elements in the CNS and show that CRIP1a inhibits both constitutive and agonist-stimulated CB1R-mediated guanine nucleotide-binding regulatory protein (G-protein) activity. Stable overexpression of CRIP1a in human embryonic kidney (HEK)-293 cells stably expressing CB1Rs (CB1-HEK), or in N18TG2 cells endogenously expressing CB1Rs, decreased CB1R-mediated G-protein activation (measured by agonist-stimulated [(35)S]GTPγS (guanylyl-5'-[O-thio]-triphosphate) binding) in both cell lines and attenuated inverse agonism by rimonabant in CB1-HEK cells. Conversely, small-interfering RNA-mediated knockdown of CRIP1a in N18TG2 cells enhanced CB1R-mediated G-protein activation. These effects were not attributable to differences in CB1R expression or endocannabinoid tone because CB1R levels did not differ between cell lines varying in CRIP1a expression, and endocannabinoid levels were undetectable (CB1-HEK) or unchanged (N18TG2) by CRIP1a overexpression. In CB1-HEK cells, 4-hour pretreatment with cannabinoid agonists downregulated CB1Rs and desensitized agonist-stimulated [(35)S]GTPγS binding. CRIP1a overexpression attenuated CB1R downregulation without altering CB1R desensitization. Finally, in cultured autaptic hippocampal neurons, CRIP1a overexpression attenuated both depolarization-induced suppression of excitation and inhibition of excitatory synaptic activity induced by exogenous application of cannabinoid but not by adenosine A1 agonists. These results confirm that CRIP1a inhibits constitutive CB1R activity and demonstrate that CRIP1a can also inhibit agonist-stimulated CB1R signaling and downregulation of CB1Rs. Thus, CRIP1a appears to act as a broad negative regulator of CB1R function.

Indexed as

AnimalsCarrier ProteinsCell LineCerebellumEndocannabinoidsGTP-Binding ProteinsHippocampusHumansMaleMiceNeuronsRadioligand AssayRats, Sprague-DawleyReceptor, Cannabinoid, CB1Signal TransductionCarrier ProteinsCnrip1 protein, ratEndocannabinoidsGTP-Binding ProteinsReceptor, Cannabinoid, CB1

Identifiers

PMID25657338
PMCPMC4366794
OpenAlexW2106342289

What OpenQuestion holds

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Registered trials

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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.