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