PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
19648473-2	2010	The objective of this study was to determine whether TRPC1 and TRPC3 molecules could be important molecular constituents of native NSCCs controlling the resting membrane potential (Vm) and [Ca(2+)](i) in freshly isolated normal and ovalbumin (OVA)-sensitized/-challenged mouse ASMCs.	asmcs	277-282	transient receptor potential cation channel, subfamily C, member 1	Mus musculus	53-58	
29574924-3	2018	TRPC1 and TRPC3 were upregulated in asthmatic mouse ASMCs and selected for further investigation.	asmcs	52-57	transient receptor potential cation channel, subfamily C, member 1	Mus musculus	0-5	
29574924-5	2018	Furthermore, TRPC1 or TRPC3 overexpression markedly increased Ca2+ concentration and significantly induced the viability of ASMCs; whereas TRPC1 or TRPC3 knockdown exerted the completely conversed effects.	asmcs	124-129	transient receptor potential cation channel, subfamily C, member 1	Mus musculus	13-18	
29574924-7	2018	Finally, we found Ca2+ chelator EGTA or BAPTA-AM significantly diminished the effects of si-TRPC1 and si-TRPC3 on the cell viability, cell cycle, and the protein expression of p-p38, p-JNK, cleaved caspase-3, and Bcl-2 in asthmatic mouse ASMCs.	asmcs	238-243	transient receptor potential cation channel, subfamily C, member 1	Mus musculus	92-97	
29574924-8	2018	Our findings demonstrated that the effects of TRPC1 and TRPC3 on the cell viability and cell cycle of ASMCs were, at least partially, through regulating Ca2+ influx.	asmcs	102-107	transient receptor potential cation channel, subfamily C, member 1	Mus musculus	46-51