PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
30687088-10	2018	HU-210-evoked activation of CB1 receptors was unable to further activate mTORC1 signaling, whereas CB1 receptor blockade with rimonabant attenuated mTORC1 overactivation.	HU 211	0-6	cannabinoid receptor 1	Homo sapiens	28-31	
29314831-5	2018	We coupled the cannabinoid agonist HU210 to the fluorescent tag Alexa Fluor 488, generating a fluorescent probe with high affinity for CB1 and selectivity over CB2.	HU 211	35-40	cannabinoid receptor 1	Homo sapiens	135-138	
29314831-6	2018	We validate HU210-Alexa488 for the rapid, simultaneous, and reproducible identification of CB1 in human monocytes, T cells, and B cells by multiplexed flow cytometry.	HU 211	12-17	cannabinoid receptor 1	Homo sapiens	91-94	
28445587-3	2017	Adopting a combined pharmacological and genetic approach to study the molecular mechanisms of CB1R-induced silencing, we found that adenylyl cyclase inhibition decreases cAMP levels while it increases the number of silent synaptic boutons and occludes the induction of further silencing by the cannabinoid agonist HU-210.	HU 211	314-320	cannabinoid receptor 1	Homo sapiens	94-98	
20590572-6	2010	The AEA- or HU210-induced cell death and MAPK activation were attenuated by CB(1) antagonists [SR141716 (rimonabant) and AM281], inhibitors of p38 and JNK-MAPKs or the antioxidant N-acetylcysteine.	HU 211	12-17	cannabinoid receptor 1	Homo sapiens	76-81	
23332708-4	2013	In the present study, an active state model for the CB1 receptor, guided by the X-ray structure of the active state for beta2AR, was constructed with HU210 bound as a ligand.	HU 211	150-155	cannabinoid receptor 1	Homo sapiens	52-55	
21795705-1	2011	The classical cannabinoid agonist HU210, a structural analog of (-)-Delta(9)-tetrahydrocannabinol, binds to brain cannabinoid (CB1) receptors and activates signal transduction pathways.	HU 211	34-39	cannabinoid receptor 1	Homo sapiens	127-130	
21795705-3	2011	Utilizing the minor binding pocket of the CB1 receptor as the primary ligand interaction site, we explored HU210 binding using lipid bilayer molecular dynamics (MD) simulations.	HU 211	107-112	cannabinoid receptor 1	Homo sapiens	42-45	
17484889-10	2007	Antagonists at CB1- and CB2-receptors were effective in reversing HU210-induced antinociception, whereas a combination of CB1- and CB2-antagonists was required to block the anti-inflammatory effects of HU210 in pancreatitis.	HU 211	202-207	cannabinoid receptor 1	Homo sapiens	122-125	
19942623-6	2010	The DOX-induced MAPK activation and cell death were significantly enhanced when DOX was co-administered with CB1 agonists AEA or HU210.	HU 211	129-134	cannabinoid receptor 1	Homo sapiens	109-112	
19942623-7	2010	Remarkably, cell death and MAPK activation induced by AEA, HU210, and DOX +/- AEA/HU210 were largely attenuated by either CB1 antagonists (rimonabant and AM281) or by inhibitors of p38 and JNK MAPKs.	HU 211	59-64	cannabinoid receptor 1	Homo sapiens	122-125	
20081235-2	2009	When given at a dose of 0.1 mg/kg, the CB1 receptor agonist, 3-(1,1-dimethylheptyl)-11-hydroxy-Delta(8)-tetrahydrocannabinol (HU-210), increased the levels of the phosphorylated forms of ERK (pERK1 and pERK2) in the hippocampus when measured 30 min after injection.	HU 211	126-132	cannabinoid receptor 1	Homo sapiens	39-42	
18565191-11	2008	Incubation with the cannabinoid agonist HU-210 (100 nmol/L) resulted in rapid CB1 internalization, reaching a maximum within 20 min.	HU 211	40-46	cannabinoid receptor 1	Homo sapiens	78-81	
17369778-8	2007	Drugs acting as agonists of CB1 receptors (Dronabinol, Dexanabinol) are currently proposed for evaluation as drugs to treat neurodegenerative disorders (Alzheimer"s and Parkinson"s diseases), epilepsy, anxiety, and stroke.	HU 211	55-66	cannabinoid receptor 1	Homo sapiens	28-31	
14758634-1	2003	It was found that CB1- and CB2-receptor activation by intravenous administration of the selective CB-agonist HU-210 at a dose 0.1 mg/kg prompts an increase of myocardial resistance to the pathogenic action of ischemia and reperfusion in vitro.	HU 211	109-115	cannabinoid receptor 1	Homo sapiens	18-21	
10974429-10	2000	Furthermore, the cannabinoid antagonist SR141716A completely prevented the HU210-induced excitation whilst having no effect on its own, thus indicating a CB1-receptor mediated mechanism for the observed increase in firing.	HU 211	75-80	cannabinoid receptor 1	Homo sapiens	154-157	
10698714-3	2000	In ECV304 cells, both the highly potent synthetic cannabinoid agonist HU-210 and the endogenous ligand anandamide induce activation of mitogen-activated protein (MAP) kinase, and the effect of HU-210 was completely blocked, whereas the effect of anandamide was partially inhibited by SR141716A, a selective CB1 receptor antagonist.	HU 211	70-76	cannabinoid receptor 1	Homo sapiens	307-310	
10698714-3	2000	In ECV304 cells, both the highly potent synthetic cannabinoid agonist HU-210 and the endogenous ligand anandamide induce activation of mitogen-activated protein (MAP) kinase, and the effect of HU-210 was completely blocked, whereas the effect of anandamide was partially inhibited by SR141716A, a selective CB1 receptor antagonist.	HU 211	193-199	cannabinoid receptor 1	Homo sapiens	307-310	
10494885-2	1999	The cannabinoid CB1 receptor agonists CP55,940, HU210 and anandamide inhibited evoked [3H]noradrenaline release.	HU 211	48-53	cannabinoid receptor 1	Homo sapiens	16-19	
35550070-6	2022	RESULTS: We found that acute activation of cannabinoid receptor type 1 (CB1R) by the synthetic cannabinoid HU210 induced dose-dependent impairment of association learning, which could be alleviated by intra-dorsomedial striatum (DMS) injection of CB1R antagonist.	HU 211	107-112	cannabinoid receptor 1	Homo sapiens	72-76	
9204917-4	1997	In striatal neurons in primary culture, both the CB1 receptor agonist [3-(1, 1-dimethylheptyl)-11-hydroxy-Delta8tetrahydrocannabinol] (HU210) and the D2 receptor agonist quinpirole inhibited forskolin-stimulated cAMP accumulation when applied separately.	HU 211	135-140	cannabinoid receptor 1	Homo sapiens	49-52	
35550070-6	2022	RESULTS: We found that acute activation of cannabinoid receptor type 1 (CB1R) by the synthetic cannabinoid HU210 induced dose-dependent impairment of association learning, which could be alleviated by intra-dorsomedial striatum (DMS) injection of CB1R antagonist.	HU 211	107-112	cannabinoid receptor 1	Homo sapiens	247-251