PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
29407215-1	2018	Hydrogen sulfide (H2S) formed by cystathionine-gamma-lyase (CSE) enhances the activity of Cav3.2 T-type Ca2+ channels, contributing to the bladder pain accompanying hemorrhagic cystitis caused by systemic administration of cyclophosphamide (CPA) in mice.	Cyclophosphamide	223-239	calcium channel, voltage-dependent, T type, alpha 1H subunit	Mus musculus	90-96	
32707767-9	2020	Together, our data suggest that CPA, once metabolized to acrolein, causes urothelial ATP-mediated, redox-dependent HMGB1 release from macrophages, which in turn causes RAGE-mediated CSE upregulation and subsequent H2S-targeted Cav3.2-dependent nociceptor excitation, resulting in bladder pain.	Cyclophosphamide	32-35	calcium channel, voltage-dependent, T type, alpha 1H subunit	Mus musculus	227-233	
32707767-5	2020	The CPA-induced bladder pain was abolished by pharmacological inhibition of T-type Ca2+ channels or CSE, and genetic deletion of Cav3.2.	Cyclophosphamide	4-7	calcium channel, voltage-dependent, T type, alpha 1H subunit	Mus musculus	129-135	
29407215-1	2018	Hydrogen sulfide (H2S) formed by cystathionine-gamma-lyase (CSE) enhances the activity of Cav3.2 T-type Ca2+ channels, contributing to the bladder pain accompanying hemorrhagic cystitis caused by systemic administration of cyclophosphamide (CPA) in mice.	Cyclophosphamide	241-244	calcium channel, voltage-dependent, T type, alpha 1H subunit	Mus musculus	90-96	
29129814-3	2018	The enhanced Cav3.2 activity by H2S formed by the upregulated cystathionine-gamma-lyase (CSE) is involved in the cyclophosphamide (CPA)-induced cystitis-related bladder pain in mice.	Cyclophosphamide	113-129	calcium channel, voltage-dependent, T type, alpha 1H subunit	Mus musculus	13-19	
29129814-3	2018	The enhanced Cav3.2 activity by H2S formed by the upregulated cystathionine-gamma-lyase (CSE) is involved in the cyclophosphamide (CPA)-induced cystitis-related bladder pain in mice.	Cyclophosphamide	131-134	calcium channel, voltage-dependent, T type, alpha 1H subunit	Mus musculus	13-19	
29129814-6	2018	Acute zinc deficiency caused by systemic N,N,N",N"-tetrakis-(2-pyridylmethyl)-ethylendiamine (TPEN), a zinc chelator, mimicked the dietary zinc deficiency-induced Cav3.2-dependent promotion of BP/RH following CPA at 200mg/kg.	Cyclophosphamide	209-212	calcium channel, voltage-dependent, T type, alpha 1H subunit	Mus musculus	163-169	
29129814-7	2018	CPA at 400mg/kg alone or TPEN plus CPA at 200mg/kg caused Cav3.2 overexpression accompanied by upregulation of Egr-1 and USP5, known to promote transcriptional expression and reduce proteasomal degradation of Cav3.2, respectively, in the dorsal root ganglia (DRG).	Cyclophosphamide	0-3	calcium channel, voltage-dependent, T type, alpha 1H subunit	Mus musculus	58-64	
29129814-7	2018	CPA at 400mg/kg alone or TPEN plus CPA at 200mg/kg caused Cav3.2 overexpression accompanied by upregulation of Egr-1 and USP5, known to promote transcriptional expression and reduce proteasomal degradation of Cav3.2, respectively, in the dorsal root ganglia (DRG).	Cyclophosphamide	0-3	calcium channel, voltage-dependent, T type, alpha 1H subunit	Mus musculus	209-215	
29129814-7	2018	CPA at 400mg/kg alone or TPEN plus CPA at 200mg/kg caused Cav3.2 overexpression accompanied by upregulation of Egr-1 and USP5, known to promote transcriptional expression and reduce proteasomal degradation of Cav3.2, respectively, in the dorsal root ganglia (DRG).	Cyclophosphamide	35-38	calcium channel, voltage-dependent, T type, alpha 1H subunit	Mus musculus	58-64	
29129814-7	2018	CPA at 400mg/kg alone or TPEN plus CPA at 200mg/kg caused Cav3.2 overexpression accompanied by upregulation of Egr-1 and USP5, known to promote transcriptional expression and reduce proteasomal degradation of Cav3.2, respectively, in the dorsal root ganglia (DRG).	Cyclophosphamide	35-38	calcium channel, voltage-dependent, T type, alpha 1H subunit	Mus musculus	209-215	
29129814-8	2018	The CSE inhibitor, beta-cyano-l-alanine, prevented the BP/RH and upregulation of Cav3.2, Egr-1 and USP5 in DRG following TPEN plus CPA at 200mg/kg.	Cyclophosphamide	131-134	calcium channel, voltage-dependent, T type, alpha 1H subunit	Mus musculus	81-87	
29129814-9	2018	Together, zinc deficiency promotes bladder pain accompanying CPA-induced cystitis by enhancing function and expression of Cav3.2 in nociceptors, suggesting a novel therapeutic avenue for treatment of bladder pain, such as zinc supplementation.	Cyclophosphamide	61-64	calcium channel, voltage-dependent, T type, alpha 1H subunit	Mus musculus	122-128	
25727961-1	2015	Cav3.2 T-type Ca(2+) channels targeted by H2S, a gasotransmitter, participate in cyclophosphamide-induced cystitis and bladder pain.	Cyclophosphamide	81-97	calcium channel, voltage-dependent, T type, alpha 1H subunit	Mus musculus	0-6	
26162837-5	2015	In mice with cerulein-induced pancreatitis and cyclophosphamide-induced cystitis, visceral pain and/or referred hyperalgesia are inhibited by CSE inhibitors and by pharmacological blockade or genetic silencing of Cav3.2, and CSE protein is upregulated in the pancreas and bladder.	Cyclophosphamide	47-63	calcium channel, voltage-dependent, T type, alpha 1H subunit	Mus musculus	213-219	
22646666-13	2012	CONCLUSION AND IMPLICATIONS: Endogenous H(2) S, generated by up-regulated CSE, caused bladder pain and referred hyperalgesia through the activation of Ca(v) 3.2 channels, one of the T-type Ca(2+) channels, in mice with cyclophosphamide-induced cystitis.	Cyclophosphamide	219-235	calcium channel, voltage-dependent, T type, alpha 1H subunit	Mus musculus	151-160