PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
32187825-3	2020	Using smooth muscle cells (VSMCs) from mouse mesenteric arteries, we found that both Cav 3.2 channel inhibition by Ni2+ (50 microM) and caveolae disruption by methyl-ss-cyclodextrin or genetic abolition of Eps15 homology domain-containing protein (EHD2) inhibited Ca2+ sparks in cells from young (4 months) but not old (12 months) mice.	Nickel(2+)	115-119	calcium channel, voltage-dependent, T type, alpha 1H subunit	Mus musculus	85-92	
30354206-5	2018	These observations indicate a mistargeting of CaV3.2 in caveolin 1-/- mice, a view supported by a loss of Ni2+-sensitive Ca2+ spark generation and colocalization signal (CaV3.2-RyR) from the proximity ligation assay.	Nickel(2+)	106-110	calcium channel, voltage-dependent, T type, alpha 1H subunit	Mus musculus	46-52	
30354206-5	2018	These observations indicate a mistargeting of CaV3.2 in caveolin 1-/- mice, a view supported by a loss of Ni2+-sensitive Ca2+ spark generation and colocalization signal (CaV3.2-RyR) from the proximity ligation assay.	Nickel(2+)	106-110	calcium channel, voltage-dependent, T type, alpha 1H subunit	Mus musculus	170-176	
30146760-10	2018	Ni2+ , Cd2+ and methyl-beta-cyclodextrin were used to inhibit Cav 3.2 channels, Cav 1.2 channels and caveolae, respectively.	Nickel(2+)	0-4	calcium channel, voltage-dependent, T type, alpha 1H subunit	Mus musculus	62-69	
26752249-12	2016	Ni2+ had both CaV 3.2-dependent and independent effects.	Nickel(2+)	0-4	calcium channel, voltage-dependent, T type, alpha 1H subunit	Mus musculus	14-21	
16195632-4	2005	CONCLUSION: The results indicate that the mechanism of change of Ni(2+)-sensitivity is partly, if not completely, the subtype switch of T-type Ca(2+) channel from Cav3.2 to Cav3.1 at the transcriptional level, and that the expression of the L-type Ca(2+) channel might have an attenuating effect on Ni(2+)-sensitivity to automaticity in the late stage of differentiation.	Nickel(2+)	65-71	calcium channel, voltage-dependent, T type, alpha 1H subunit	Mus musculus	163-169	
16195632-4	2005	CONCLUSION: The results indicate that the mechanism of change of Ni(2+)-sensitivity is partly, if not completely, the subtype switch of T-type Ca(2+) channel from Cav3.2 to Cav3.1 at the transcriptional level, and that the expression of the L-type Ca(2+) channel might have an attenuating effect on Ni(2+)-sensitivity to automaticity in the late stage of differentiation.	Nickel(2+)	299-305	calcium channel, voltage-dependent, T type, alpha 1H subunit	Mus musculus	163-169