PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
17609213-4	2007	Our results demonstrate that hFSHR constitutively activating mutants (CAMs) were not as active as hLHR CAMs containing the comparable mutation.	cams	70-74	follicle stimulating hormone receptor	Homo sapiens	29-34
18207366-1	2008	The present study was designed to determine whether the sarcoplasmic reticulum (SR) could locally produce superoxide (O2-) via NAD(P)H oxidase (NOX) in coronary arterial myocytes (CAMs) and to address whether cADPR-RyR/Ca2+ signaling pathway regulates this local O2- production from the SR.	cams	180-184	ryanodine receptor 2	Homo sapiens	215-218
17609213-6	2007	Our in vitro findings are consistent with in vivo observations of known pathophysiological conditions associated with hLHR CAMs, but not hFSHR CAMs, and with promiscuous activation of hFSHR CAMs, but not hLHR CAMs.	cams	123-127	luteinizing hormone/choriogonadotropin receptor	Homo sapiens	118-122
12149103-9	2002	The beneficial effects of ACE-Is on cAMs may have implications for atherogenesis and the reduction of cardiovascular events, which cannot be fully explained by their antihypertensive effects alone.	cams	36-40	angiotensin I converting enzyme	Homo sapiens	26-29
16682009-4	2006	Indeed, relative energies of the R* state were significantly lower than that of the R state for the rhodopsin mutants G90D/M257Y and E113Q/M257Y (strong CAMs), but not for G90D, E113Q, and M257Y (not CAMs).	cams	153-157	rhodopsin	Homo sapiens	100-109
16682009-4	2006	Indeed, relative energies of the R* state were significantly lower than that of the R state for the rhodopsin mutants G90D/M257Y and E113Q/M257Y (strong CAMs), but not for G90D, E113Q, and M257Y (not CAMs).	cams	200-204	rhodopsin	Homo sapiens	100-109
17420615-3	2007	We report that TRPM4-like cation channels are activated by membrane stretch in rat cerebral artery myocytes (CAMs).	cams	109-113	transient receptor potential cation channel, subfamily M, member 4	Rattus norvegicus	15-20
30012770-9	2018	Altogether, these data demonstrate that some CAMs could interfere with multiple functions of HBc in the viral life cycle.	cams	45-49	keratin 88, pseudogene	Homo sapiens	93-96
31866467-7	2020	Collectively, our results reveal a novel pro-migration mechanism driven by the crosstalk between cisplatin and CAMs, and implicate the CCL20-CCR6 axis as a potential therapeutic target to reduce chemotherapy-induced metastasis in advanced stage ovarian cancer.	cams	111-115	C-C motif chemokine ligand 20	Homo sapiens	135-140
28658262-4	2017	Comparing IL-4 generated in vitro monocyte derived human AAMs to LPS and IFN-gamma generated classically macrophages (CAMs), both infected with mycobacteria (BCG), we demonstrated increased early BCG uptake and increased IL-10 production in AAMs compared to CAMs.	cams	118-122	interleukin 4	Homo sapiens	10-14
28658262-4	2017	Comparing IL-4 generated in vitro monocyte derived human AAMs to LPS and IFN-gamma generated classically macrophages (CAMs), both infected with mycobacteria (BCG), we demonstrated increased early BCG uptake and increased IL-10 production in AAMs compared to CAMs.	cams	118-122	interferon gamma	Homo sapiens	73-82
28658262-4	2017	Comparing IL-4 generated in vitro monocyte derived human AAMs to LPS and IFN-gamma generated classically macrophages (CAMs), both infected with mycobacteria (BCG), we demonstrated increased early BCG uptake and increased IL-10 production in AAMs compared to CAMs.	cams	118-122	interleukin 10	Homo sapiens	221-226
26421717-6	2015	This interaction requires both Ca2+ and a putative CaM-binding segment (CaMS).	cams	72-76	calmodulin 1	Homo sapiens	51-54
28214847-8	2017	Although free ubiquitin content was increased, the colocalization of it to CDK1 was markedly decreased in CD38-/- or baf treated CAMs.	cams	129-133	cyclin-dependent kinase 1	Mus musculus	75-79
28214847-8	2017	Although free ubiquitin content was increased, the colocalization of it to CDK1 was markedly decreased in CD38-/- or baf treated CAMs.	cams	129-133	CD38 antigen	Mus musculus	106-110
26939869-6	2016	miR-181d was upregulated in gastric CAMs.	cams	36-40	microRNA 181d	Homo sapiens	0-8
26939869-8	2016	Examination of a microarray data set then identified Wnt5a as the only consistently upregulated Wnt ligand in gastric CAMs.	cams	118-122	Wnt family member 5A	Homo sapiens	53-58
26939869-8	2016	Examination of a microarray data set then identified Wnt5a as the only consistently upregulated Wnt ligand in gastric CAMs.	cams	118-122	Wnt family member 5A	Homo sapiens	53-56
26939869-12	2016	The data suggest that dysregulation of miRNA expression in gastric CAMs, secondary to Wnt5a signaling, accounts at least in part for the effect of CAMs in promoting cancer cell migration.	cams	67-71	Wnt family member 5A	Homo sapiens	86-91
24445604-7	2014	Further, 7-Ket-induced formation of autophagolysosomes was markedly attenuated in CD38(-/-) CAMs compared with CD38(+/+) CAMs.	cams	92-96	CD38 antigen	Mus musculus	82-86
26315049-10	2015	It was demonstrated that in CD38-/- CAMs, 7-Ket failed to stimulate the production of O2-., while in CD38+/+ CAMs 7-Ket induced marked O2-.	cams	36-40	CD38 antigen	Mus musculus	28-32
24445604-3	2014	Here, we revealed a previously undefined role of CD38, an enzyme that metabolizes NADP(+) into NAADP, in the regulation of autophagic flux in coronary arterial myocytes (CAMs).	cams	170-174	CD38 antigen	Mus musculus	49-53
22100343-8	2012	Further, Nox4 siRNA inhibited OXO-induced intracellular but not extracellular O(2)( -) production, whereas Nox1 siRNA attenuated both intracellular and extracellular O(2)( -) production in CD38(+/+) CAMs.	cams	199-203	CD38 antigen	Mus musculus	189-193
23940720-3	2013	Recent studies have shown that CD38 may sense redox signals and is thereby activated to produce cellular response and that the NADPH oxidase isoform, NOX1, is a major resource to produce superoxide (O2 -)) in coronary arterial myocytes (CAMs) in response to muscarinic receptor agonist, which uses CD38-ADP-ribosylcyclase signaling pathway to exert its action in these CAMs.	cams	237-241	CD38 antigen	Mus musculus	31-35
23940720-3	2013	Recent studies have shown that CD38 may sense redox signals and is thereby activated to produce cellular response and that the NADPH oxidase isoform, NOX1, is a major resource to produce superoxide (O2 -)) in coronary arterial myocytes (CAMs) in response to muscarinic receptor agonist, which uses CD38-ADP-ribosylcyclase signaling pathway to exert its action in these CAMs.	cams	237-241	NADPH oxidase 1	Mus musculus	150-154
23940720-3	2013	Recent studies have shown that CD38 may sense redox signals and is thereby activated to produce cellular response and that the NADPH oxidase isoform, NOX1, is a major resource to produce superoxide (O2 -)) in coronary arterial myocytes (CAMs) in response to muscarinic receptor agonist, which uses CD38-ADP-ribosylcyclase signaling pathway to exert its action in these CAMs.	cams	369-373	CD38 antigen	Mus musculus	31-35
23940720-3	2013	Recent studies have shown that CD38 may sense redox signals and is thereby activated to produce cellular response and that the NADPH oxidase isoform, NOX1, is a major resource to produce superoxide (O2 -)) in coronary arterial myocytes (CAMs) in response to muscarinic receptor agonist, which uses CD38-ADP-ribosylcyclase signaling pathway to exert its action in these CAMs.	cams	369-373	NADPH oxidase 1	Mus musculus	150-154
23940720-7	2013	Correspondingly, NOX1 gene silencing abolished ET-1-induced O2 - production and increased CD38-ADP-ribosylcyclase activity in CAMs, while activation of NOX1 by overexpression of Rac1 or Vav2 or administration of exogenous O2 - significantly increased CD38 internalization in CAMs.	cams	126-130	NADPH oxidase 1	Mus musculus	17-21
23940720-7	2013	Correspondingly, NOX1 gene silencing abolished ET-1-induced O2 - production and increased CD38-ADP-ribosylcyclase activity in CAMs, while activation of NOX1 by overexpression of Rac1 or Vav2 or administration of exogenous O2 - significantly increased CD38 internalization in CAMs.	cams	126-130	endothelin 1	Mus musculus	47-51
23940720-7	2013	Correspondingly, NOX1 gene silencing abolished ET-1-induced O2 - production and increased CD38-ADP-ribosylcyclase activity in CAMs, while activation of NOX1 by overexpression of Rac1 or Vav2 or administration of exogenous O2 - significantly increased CD38 internalization in CAMs.	cams	126-130	CD38 antigen	Mus musculus	90-94
23283937-6	2013	When CAMs were treated with TRP-ML1 siRNA, FasL-induced interactions between the lysosomes and SR were substantially blocked.	cams	5-9	mucolipin 1	Mus musculus	28-35
23283937-6	2013	When CAMs were treated with TRP-ML1 siRNA, FasL-induced interactions between the lysosomes and SR were substantially blocked.	cams	5-9	Fas ligand (TNF superfamily, member 6)	Mus musculus	43-47
23283937-8	2013	These results suggest that TRP-ML1 channel-mediated lysosomal Ca(2+) bursts upon FasL stimulation promote lysosome trafficking and interactions with the SR, leading to apoptosis of CAMs via a Ca(2+)-dependent mechanism.	cams	181-185	mucolipin 1	Mus musculus	27-34
23283937-8	2013	These results suggest that TRP-ML1 channel-mediated lysosomal Ca(2+) bursts upon FasL stimulation promote lysosome trafficking and interactions with the SR, leading to apoptosis of CAMs via a Ca(2+)-dependent mechanism.	cams	181-185	Fas ligand (TNF superfamily, member 6)	Mus musculus	81-85
22100343-9	2012	Direct delivery of exogenous cADPR into CAMs markedly elevated intracellular Ca(2+) and O(2)( -) production in CD38(-/-) CAMs.	cams	40-44	CD38 antigen	Mus musculus	111-115
22100343-11	2012	These results provide direct evidence that the CD38/cADPR pathway is an important controller of Nox4-mediated intracellular O(2)( -) production and that CD38-dependent intracellular O(2)( -) production is augmented in an autocrine manner by CD38-independent Nox1-derived extracellular O(2)( -) production in CAMs.	cams	308-312	CD38 antigen	Mus musculus	47-51
22100343-11	2012	These results provide direct evidence that the CD38/cADPR pathway is an important controller of Nox4-mediated intracellular O(2)( -) production and that CD38-dependent intracellular O(2)( -) production is augmented in an autocrine manner by CD38-independent Nox1-derived extracellular O(2)( -) production in CAMs.	cams	308-312	NADPH oxidase 4	Mus musculus	96-100
22100343-11	2012	These results provide direct evidence that the CD38/cADPR pathway is an important controller of Nox4-mediated intracellular O(2)( -) production and that CD38-dependent intracellular O(2)( -) production is augmented in an autocrine manner by CD38-independent Nox1-derived extracellular O(2)( -) production in CAMs.	cams	308-312	CD38 antigen	Mus musculus	153-157
22100343-11	2012	These results provide direct evidence that the CD38/cADPR pathway is an important controller of Nox4-mediated intracellular O(2)( -) production and that CD38-dependent intracellular O(2)( -) production is augmented in an autocrine manner by CD38-independent Nox1-derived extracellular O(2)( -) production in CAMs.	cams	308-312	CD38 antigen	Mus musculus	153-157
22100343-11	2012	These results provide direct evidence that the CD38/cADPR pathway is an important controller of Nox4-mediated intracellular O(2)( -) production and that CD38-dependent intracellular O(2)( -) production is augmented in an autocrine manner by CD38-independent Nox1-derived extracellular O(2)( -) production in CAMs.	cams	308-312	NADPH oxidase 1	Mus musculus	258-262
20200208-3	2010	The hypothesis being tested is that CD38 signaling pathway mediates FasL-induced intracellular Ca(2+) release through nicotinic acid adenine dinucleotide phosphate (NAADP) in mouse coronary arterial myocytes (CAMs) and thereby produces vasoconstriction in coronary arteries.	cams	209-213	CD38 antigen	Mus musculus	36-40
20200208-3	2010	The hypothesis being tested is that CD38 signaling pathway mediates FasL-induced intracellular Ca(2+) release through nicotinic acid adenine dinucleotide phosphate (NAADP) in mouse coronary arterial myocytes (CAMs) and thereby produces vasoconstriction in coronary arteries.	cams	209-213	Fas ligand (TNF superfamily, member 6)	Mus musculus	68-72
20200208-5	2010	Using fluorescent Ca(2+) imaging analysis, we found that FasL (10 ng/ml) significantly increased Ca(2+) release from 142.5 +/- 22.5 nM at the basal level to 509.4 +/- 64.3 nM in CD38(+/+) CAMs but not in CD38(-/-) CAMs.	cams	188-192	Fas ligand (TNF superfamily, member 6)	Mus musculus	57-61
20200208-5	2010	Using fluorescent Ca(2+) imaging analysis, we found that FasL (10 ng/ml) significantly increased Ca(2+) release from 142.5 +/- 22.5 nM at the basal level to 509.4 +/- 64.3 nM in CD38(+/+) CAMs but not in CD38(-/-) CAMs.	cams	214-218	Fas ligand (TNF superfamily, member 6)	Mus musculus	57-61
20200208-6	2010	However, direct delivery of NAADP, the CD38 metabolite, into CD38(-/-) CAMs still markedly increased Ca(2+) release, which could be significantly attenuated by a lysosomal function inhibitor, bafilomycin A1 (Baf), or a NAADP antagonist, pyridoxalphosphate-6-azophenyl-2-disulfonic acid.	cams	71-75	CD38 antigen	Mus musculus	39-43
20200208-6	2010	However, direct delivery of NAADP, the CD38 metabolite, into CD38(-/-) CAMs still markedly increased Ca(2+) release, which could be significantly attenuated by a lysosomal function inhibitor, bafilomycin A1 (Baf), or a NAADP antagonist, pyridoxalphosphate-6-azophenyl-2-disulfonic acid.	cams	71-75	CD38 antigen	Mus musculus	61-65
20200208-7	2010	Confocal microscopy further demonstrated that FasL produced a typical two-phase Ca(2+) release with a local Ca(2+) burst from lysosomes, followed by a global Ca(2+) response in CD38(+/+) CAMs.	cams	187-191	Fas ligand (TNF superfamily, member 6)	Mus musculus	46-50
20200208-9	2010	These results strongly indicate that the early response of CAMs to FasL is to increase intracellular Ca(2+) levels and enhance the vascular reactivity through stimulation of NAADP production and lysosome-associated two-phase Ca(2+) release in coronary arteries.	cams	59-63	Fas ligand (TNF superfamily, member 6)	Mus musculus	67-71
21036235-5	2010	This chapter describes the experimental methods and strategies underlying studies of hLHR CAMs.	cams	90-94	luteinizing hormone/choriogonadotropin receptor	Homo sapiens	85-89
18723763-7	2008	In floated detergent-resistant membrane fractions, CD38 significantly increased in LR fractions of CAMs treated by Oxo.	cams	99-103	CD38 molecule	Bos taurus	51-55
18723763-10	2008	These results provide the first evidence that the formation of ceramide-enriched lipid macrodomains is crucial for Oxo-induced activation of CD38 to produce cADPR in CAMs, and these lipid macrodomains mediate transmembrane signaling of M(1) receptor activation to produce second messenger cADPR.	cams	166-170	CD38 molecule	Bos taurus	141-145
18754814-2	2009	The present study tested the hypothesis that NAADP induces Ca(2+) release from the lysosomal store via a TRP-ML1 (transient receptor potential-mucolipin 1)-mediated Ca(2+) release channel in coronary arterial myocytes (CAMs).	cams	219-223	mucolipin TRP cation channel 1	Homo sapiens	105-112
18754814-2	2009	The present study tested the hypothesis that NAADP induces Ca(2+) release from the lysosomal store via a TRP-ML1 (transient receptor potential-mucolipin 1)-mediated Ca(2+) release channel in coronary arterial myocytes (CAMs).	cams	219-223	mucolipin TRP cation channel 1	Homo sapiens	114-154
18754814-5	2009	This lysosome-associated Ca(2+) release was significantly inhibited in the TRP-ML1 siRNA pre-treated CAMs by 46.8 +/- 12.6% in the local Ca(2+) burst and 73.3 +/- 14.9% in the global Ca(2+) wave.	cams	101-105	mucolipin TRP cation channel 1	Homo sapiens	75-82
18723763-2	2008	The present study tested a hypothesis that a special lipid-raft (LR) form, ceramide-enriched lipid platform, contributes to CD38 activation to produce cADPR in response to muscarinic type 1 (M(1)) receptor stimulation in bovine coronary arterial myocytes (CAMs).	cams	256-260	CD38 molecule	Bos taurus	124-128