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 ◽  
...  
2015 ◽  
Vol 221 (4) ◽  
pp. 2061-2074 ◽  
Author(s):  
Stephan Guggenhuber ◽  
Alan Alpar ◽  
Rongqing Chen ◽  
Nina Schmitz ◽  
Melanie Wickert ◽  
...  

2016 ◽  
Vol 91 (2) ◽  
pp. 75-86 ◽  
Author(s):  
Lawrence C. Blume ◽  
Theresa Patten ◽  
Khalil Eldeeb ◽  
Sandra Leone-Kabler ◽  
Alexander A. Ilyasov ◽  
...  

2013 ◽  
Vol 27 (S1) ◽  
Author(s):  
Lawrence C. Blume ◽  
George D. Dalton ◽  
Dana E. Selley ◽  
Allyn C. Howlett

Molecules ◽  
2019 ◽  
Vol 24 (20) ◽  
pp. 3672 ◽  
Author(s):  
William T. Booth ◽  
Noah B. Walker ◽  
W. Todd Lowther ◽  
Allyn C. Howlett

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.


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

2007 ◽  
Vol 19 (4) ◽  
pp. 723-730 ◽  
Author(s):  
Seena K. Ajit ◽  
Suneela Ramineni ◽  
Wade Edris ◽  
Rachel A. Hunt ◽  
Wah-Tung Hum ◽  
...  

2013 ◽  
Vol 52 (4) ◽  
pp. 633-650 ◽  
Author(s):  
Ismael Galve-Roperh ◽  
Valerio Chiurchiù ◽  
Javier Díaz-Alonso ◽  
Monica Bari ◽  
Manuel Guzmán ◽  
...  

2017 ◽  
Vol 313 (2) ◽  
pp. L267-L277 ◽  
Author(s):  
Z. Helyes ◽  
Á. Kemény ◽  
K. Csekő ◽  
É. Szőke ◽  
K. Elekes ◽  
...  

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.


2018 ◽  
Vol 42 (4) ◽  
pp. 718-726 ◽  
Author(s):  
Dal Khatri ◽  
Genevieve Laroche ◽  
Marion L. Grant ◽  
Victoria M. Jones ◽  
Ryan P. Vetreno ◽  
...  

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