PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
20209143-7	2010	We show that DOP-3 is required for the ability of food and exogenous dopamine to rescue the octanol avoidance defect of rgs-3 mutant animals.	Octanols	92-99	Dopamine receptor 3	Caenorhabditis elegans	13-18	
20209143-8	2010	In addition, otherwise wild-type animals lacking DOP-3 function are hypersensitive to dilute octanol, reminiscent of cat-2 mutants.	Octanols	93-100	Dopamine receptor 3	Caenorhabditis elegans	49-54	
20209143-9	2010	Furthermore, we demonstrate that DOP-3 function in the ASH sensory neurons is sufficient to rescue the hypersensitivity of dop-3 mutant animals, while dop-3 RNAi knockdown in ASH results in octanol hypersensitivity.	Octanols	190-197	Dopamine receptor 3	Caenorhabditis elegans	151-156	
20209143-10	2010	Taken together, our data suggest that dopaminergic signaling through DOP-3 normally acts to dampen ASH signaling and behavioral sensitivity to octanol.	Octanols	143-150	Dopamine receptor 3	Caenorhabditis elegans	69-74