PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
31398491-11	2019	Cav1.3 knockout pups exhibited delayed bone mineral accrual, compensatory nifedipine-insensitive Ca2+ absorption in the ileum, and increased expression of renal Ca2+ reabsorption mediators at P14.	Nifedipine	74-84	calcium channel, voltage-dependent, L type, alpha 1D subunit	Mus musculus	0-6	
15331671-2	2004	The block of this current by nifedipine suggests the direct involvement of Ca(v)1.3 Ca(2+) channels in its activation.	Nifedipine	29-39	calcium channel, voltage-dependent, L type, alpha 1D subunit	Mus musculus	75-83	
28801600-6	2017	In SAN cells isolated from mice expressing DHP-insensitive CaV1.2 channels (CaV1.2DHP-/-), I st and CaV1.3-mediated I Ca,L displayed overlapping sensitivity and concentration-response relationships to the DHP blocker nifedipine.	Nifedipine	217-227	calcium channel, voltage-dependent, L type, alpha 1D subunit	Mus musculus	100-106	
20130814-5	2009	A second nifedipine-sensitive isoform, CaV1.3, is present at the mid-spindle zone in telophase, but is also seen at the midbody.	Nifedipine	9-19	calcium channel, voltage-dependent, L type, alpha 1D subunit	Mus musculus	39-45	
28193694-6	2017	Nifedipine-resistant RRP exocytosis was poorly affected by 5 mm intracellular EGTA, suggesting that the Cav1.3 short isoforms are closely associated with the release site at the synaptic ribbons.	Nifedipine	0-10	calcium channel, voltage-dependent, L type, alpha 1D subunit	Mus musculus	104-110	
28193694-7	2017	Conversely, our results suggest that Cav1.3 long isoforms, which carry ~75% of the total IHC Ca2+ current with slow inactivation and confer high sensitivity to nifedipine and to internal EGTA, are essentially involved in recruiting SRP vesicles.	Nifedipine	160-170	calcium channel, voltage-dependent, L type, alpha 1D subunit	Mus musculus	37-43	
28193694-9	2017	We show that this synaptic process involves long and short C-terminal isoforms of the Cav1.3 Ca2+ channel that differ in the kinetics of their Ca2+-dependent inactivation and their relative sensitivity to the l-type Ca2+ channel blocker nifedipine.	Nifedipine	237-247	calcium channel, voltage-dependent, L type, alpha 1D subunit	Mus musculus	86-92	
28185965-5	2017	Similarly, Cav1.3-/- mice showed nicotine-induced place preference which was antagonized by nifedipine.	Nifedipine	92-102	calcium channel, voltage-dependent, L type, alpha 1D subunit	Mus musculus	11-17	
24848473-6	2014	The dihydropyridine (DHP) channel blocker nifedipine reduced single-spike firing in mice expressing DHP-insensitive Cav1.2 channels (Cav1.2DHP(-/-) mice), confirming the significant contribution from the Cav1.3 subtype in basal firing.	Nifedipine	42-52	calcium channel, voltage-dependent, L type, alpha 1D subunit	Mus musculus	204-210	
24848473-8	2014	Nifedipine inhibited burst firing induced by both activators, suggesting that Cav1.3 also serves an essential role in burst firing.	Nifedipine	0-10	calcium channel, voltage-dependent, L type, alpha 1D subunit	Mus musculus	78-84