PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
19077057-7	2009	Together, these results suggest that NMDA receptor-dependent Kv2.1 membrane translocation is regulated by a soluble N-ethylmaleimide-sensitive factor attachment protein receptor-dependent vesicular trafficking mechanism and is responsible for neuronal cell death induced by chronic loss of K(+).	Ethylmaleimide	116-132	potassium voltage-gated channel subfamily B member 1	Homo sapiens	61-66	
24928958-3	2014	We showed previously that the observed increase in K(+) currents is a soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE)-mediated process, and that the SNARE protein syntaxin binds directly to Kv2.1 channels.	Ethylmaleimide	78-94	potassium voltage-gated channel subfamily B member 1	Homo sapiens	220-225	
15518587-1	2005	We have shown that SNARE (soluble N-ethylmaleimide-sensitive fusion protein attachment protein receptor) proteins not only participate directly in exocytosis, but also regulate the dominant membrane-repolarizing Kv channels (voltage-gated K+ channels), such as Kv2.1, in pancreatic beta-cells.	Ethylmaleimide	36-50	potassium voltage-gated channel subfamily B member 1	Homo sapiens	261-266	
16754785-0	2006	Target soluble N-ethylmaleimide-sensitive factor attachment protein receptors (t-SNAREs) differently regulate activation and inactivation gating of Kv2.2 and Kv2.1: Implications on pancreatic islet cell Kv channels.	Ethylmaleimide	17-31	potassium voltage-gated channel subfamily B member 1	Homo sapiens	158-163