scholarly journals Cannabinoid receptor interacting protein suppresses agonist-driven CB1 receptor internalization and regulates receptor replenishment in an agonist-biased manner

2016 ◽  
Vol 139 (3) ◽  
pp. 396-407 ◽  
Author(s):  
Lawrence C. Blume ◽  
Sandra Leone-Kabler ◽  
Deborah J. Luessen ◽  
Glen S. Marrs ◽  
Erica Lyons ◽  
...  
Keyword(s):  
Cannabinoid Receptor ◽  
Cb1 Receptor ◽  
Receptor Internalization ◽  
Interacting Protein

scholarly journals Cannabinoid Receptor Interacting Protein 1a (CRIP1a): Function and Structure

Molecules ◽  
2019 ◽  
Vol 24 (20) ◽  
pp. 3672 ◽  
Author(s):  
William T. Booth ◽  
Noah B. Walker ◽  
W. Todd Lowther ◽  
Allyn C. Howlett
Keyword(s):  
Metabotropic Glutamate Receptor ◽  
Cannabinoid Receptor ◽  
Cb1 Receptor ◽  
Receptor Internalization ◽  
Receptor Interaction ◽  
Interacting Protein ◽  
Receptor Associated Protein ◽  
Metabotropic Glutamate ◽  
C Terminus

Cannabinoid receptor interacting protein 1a (CRIP1a) is an important CB1 cannabinoid receptor-associated protein, first identified from a yeast two-hybrid screen to modulate CB1-mediated N-type Ca2+ currents. In this paper we review studies of CRIP1a function and structure based upon in vitro experiments and computational chemistry, which elucidate the specific mechanisms for the interaction of CRIP1a with CB1 receptors. N18TG2 neuronal cells overexpressing or silencing CRIP1a highlighted the ability of CRIP1 to regulate cyclic adenosine 3′,5′monophosphate (cAMP) production and extracellular signal-regulated kinase (ERK1/2) phosphorylation. These studies indicated that CRIP1a attenuates the G protein signaling cascade through modulating which Gi/o subtypes interact with the CB1 receptor. CRIP1a also attenuates CB1 receptor internalization via β-arrestin, suggesting that CRIP1a competes for β-arrestin binding to the CB1 receptor. Predictions of CRIP1a secondary structure suggest that residues 34-110 are minimally necessary for association with key amino acids within the distal C-terminus of the CB1 receptor, as well as the mGlu8a metabotropic glutamate receptor. These interactions are disrupted through phosphorylation of serines and threonines in these regions. Through investigations of the function and structure of CRIP1a, new pharmacotherapies based upon the CRIP-CB1 receptor interaction can be designed to treat diseases such as epilepsy, motor dysfunctions and schizophrenia.

scholarly journals Cannabinoid Receptor Interacting Protein 1a Competition with β-Arrestin for CB1 Receptor Binding Sites

2016 ◽  
Vol 91 (2) ◽  
pp. 75-86 ◽  
Author(s):  
Lawrence C. Blume ◽  
Theresa Patten ◽  
Khalil Eldeeb ◽  
Sandra Leone-Kabler ◽  
Alexander A. Ilyasov ◽  
...  
Keyword(s):  
Receptor Binding ◽  
Binding Sites ◽  
Cannabinoid Receptor ◽  
Cb1 Receptor ◽  
Interacting Protein

scholarly journals Cannabinoid Receptor–Interacting Protein 1a Modulates CB1 Receptor Signaling and Regulation

2015 ◽  
Vol 87 (4) ◽  
pp. 747-765 ◽  
Author(s):  
Tricia H. Smith ◽  
Lawrence C. Blume ◽  
Alex Straiker ◽  
Jordan O. Cox ◽  
Bethany G. David ◽  
...  
Keyword(s):  
Cannabinoid Receptor ◽  
Cb1 Receptor ◽  
Receptor Signaling ◽  
Interacting Protein

scholarly journals Cannabinoid Receptor Interacting Protein 1a (CRIP1a) Regulates CB1 Receptor Trafficking

2013 ◽  
Vol 27 (S1) ◽  
Author(s):  
Lawrence C. Blume ◽  
George D. Dalton ◽  
Dana E. Selley ◽  
Allyn C. Howlett
Keyword(s):  
Cannabinoid Receptor ◽  
Cb1 Receptor ◽  
Receptor Trafficking ◽  
Interacting Protein

scholarly journals Cannabinoid receptor-interacting protein Crip1a modulates CB1 receptor signaling in mouse hippocampus

2015 ◽  
Vol 221 (4) ◽  
pp. 2061-2074 ◽  
Author(s):  
Stephan Guggenhuber ◽  
Alan Alpar ◽  
Rongqing Chen ◽  
Nina Schmitz ◽  
Melanie Wickert ◽  
...  
Keyword(s):  
Cannabinoid Receptor ◽  
Cb1 Receptor ◽  
Receptor Signaling ◽  
Interacting Protein ◽  
Mouse Hippocampus

scholarly journals Marijuana smoke induces severe pulmonary hyperresponsiveness, inflammation, and emphysema in a predictive mouse model not via CB1 receptor activation

2017 ◽  
Vol 313 (2) ◽  
pp. L267-L277 ◽  
Author(s):  
Z. Helyes ◽  
Á. Kemény ◽  
K. Csekő ◽  
É. Szőke ◽  
K. Elekes ◽  
...  
Keyword(s):  
Tobacco Smoke ◽  
Airway Hyperresponsiveness ◽  
Inflammatory Cell ◽  
Cannabinoid Receptor ◽  
Receptor Activation ◽  
Cb1 Receptor ◽  
Whole Body ◽  
Myeloperoxidase Activity ◽  
Tissue Destruction ◽  
Cell Hyperplasia

Sporadic clinical reports suggested that marijuana smoking induces spontaneous pneumothorax, but no animal models were available to validate these observations and to study the underlying mechanisms. Therefore, we performed a systematic study in CD1 mice as a predictive animal model and assessed the pathophysiological alterations in response to 4-mo-long whole body marijuana smoke with integrative methodologies in comparison with tobacco smoke. Bronchial responsiveness was measured with unrestrained whole body plethysmography, cell profile in the bronchoalveolar lavage fluid with flow cytometry, myeloperoxidase activity with spectrophotometry, inflammatory cytokines with ELISA, and histopathological alterations with light microscopy. Daily marijuana inhalation evoked severe bronchial hyperreactivity after a week. Characteristic perivascular/peribronchial edema, atelectasis, apical emphysema, and neutrophil and macrophage infiltration developed after 1 mo of marijuana smoking; lymphocyte accumulation after 2 mo; macrophage-like giant cells, irregular or destroyed bronchial mucosa, goblet cell hyperplasia after 3 mo; and severe atelectasis, emphysema, obstructed or damaged bronchioles, and endothelial proliferation at 4 mo. Myeloperoxidase activity, inflammatory cell, and cytokine profile correlated with these changes. Airway hyperresponsiveness and inflammation were not altered in mice lacking the CB1 cannabinoid receptor. In comparison, tobacco smoke induced hyperresponsiveness after 2 mo and significantly later caused inflammatory cell infiltration/activation with only mild emphysema. We provide the first systematic and comparative experimental evidence that marijuana causes severe airway hyperresponsiveness, inflammation, tissue destruction, and emphysema, which are not mediated by the CB1 receptor.

scholarly journals Tat-Cannabinoid Receptor Interacting Protein Reduces Ischemia-Induced Neuronal Damage and Its Possible Relationship with 14-3-3η

Cells ◽  
2020 ◽  
Vol 9 (8) ◽  
pp. 1827 ◽  
Author(s):  
Hyun Jung Kwon ◽  
Duk-Soo Kim ◽  
Woosuk Kim ◽  
Hyo Young Jung ◽  
Yeon Hee Yu ◽  
...  
Keyword(s):  
Cannabinoid Receptor ◽  
Neuronal Damage ◽  
Cell Damage ◽  
Ischemia Reperfusion ◽  
Ischemic Damage ◽  
Dependent Manner ◽  
Ht22 Cells ◽  
Concentration Dependent Manner ◽  
H2o2 Treatment ◽  
Interacting Protein

Cannabinoid receptor-interacting protein 1a (CRIP1a) binds to the C-terminal domain of cannabinoid 1 receptor (CB1R) and regulates CB1R activities. In this study, we made Tat-CRIP1a fusion proteins to enhance CRIP1a penetration into neurons and brain and to evaluate the function of CRIP1a in neuroprotection following oxidative stress in HT22 hippocampal cells and transient forebrain ischemia in gerbils. Purified exogenous Tat-CRIP1a was penetrated into HT22 cells in a time and concentration-dependent manner and prevented H2O2-induced reactive oxygen species formation, DNA fragmentation, and cell damage. Tat-CRIP1a fusion protein also ameliorated the reduction of 14-3-3η expression by H2O2 treatment in HT22 cells. Ischemia–reperfusion damage caused motor hyperactivity in the open field test of gerbils; however, the treatment of Tat-CRIP1a significantly reduced hyperactivity 1 day after ischemia. Four days after ischemia, the administration of Tat-CRIP1a restored the loss of pyramidal neurons and decreased reactive astrocytosis and microgliosis induced by ischemic damage in the hippocampal cornu Ammonis (CA)1 region. Ischemic damage decreased 14-3-3η expression in all hippocampal sub-regions 4 days after ischemia; however, the treatment of Tat-CRIP1 ameliorated the reduction of 14-3-3η expression. These results suggest that Tat-CRIP1a attenuates neuronal damage and hyperactivity induced by ischemic damage, and it restores normal expression levels of 14-3-3η protein in the hippocampus.

scholarly journals 902: CB1 cannabinoid receptor and cannabinoid receptor interacting protein in human myometrium and placenta during labor

2020 ◽  
Vol 222 (1) ◽  
pp. S560-S561
Author(s):  
Melissa L. Kozakiewicz ◽  
Jie Zhang ◽  
Sandra Leone-Kabler ◽  
Liliya M. Yamaleyeva ◽  
Brian C. Brost ◽  
...  
Keyword(s):  
Cannabinoid Receptor ◽  
Human Myometrium ◽  
Interacting Protein ◽  
Cb1 Cannabinoid Receptor
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