PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
3110270-10	1987	The PLN reaction proved to be antigen-specific, since D-Pen-primed mice exhibited an enhanced reaction when challenged with a suboptimal dose of D-Pen, but not when challenged with an unrelated drug, diphenylhydantoin (DPH).	Phenytoin	219-222	phospholamban	Mus musculus	4-7
32555305-1	2020	Phospholamban (PLN) plays a role in cardiomyocyte calcium handling as primary inhibitor of sarco/endoplasmic reticulum Ca2+-ATPase (SERCA).	Calcium	50-57	phospholamban	Mus musculus	15-18
33278971-2	2021	Here, we aimed to evaluate the structure and bioactivity of PLN-1, an exopolysaccharide derived from the P. liquidambari NJUSTb1 strain.	exopolysaccharide	70-87	phospholamban	Mus musculus	60-63
33463061-11	2021	Mechanistically, these optimized effects were associated with enhanced the adenosine (cAMP)-protein kinase A (PKA) pathway, which upregulated phosphorylate-phospholamban (p-PLN) (Ser16) and promoted sarco/endoplasmic reticulum Ca2+ ATPase (Serca) and Ryanodine Receptor 2 (RyR2) expression in the sarcoplasmic reticulum (SR), and ultimately restored Ca2+ handling in response to sepsis.	Adenosine	75-84	phospholamban	Mus musculus	173-176
33463061-11	2021	Mechanistically, these optimized effects were associated with enhanced the adenosine (cAMP)-protein kinase A (PKA) pathway, which upregulated phosphorylate-phospholamban (p-PLN) (Ser16) and promoted sarco/endoplasmic reticulum Ca2+ ATPase (Serca) and Ryanodine Receptor 2 (RyR2) expression in the sarcoplasmic reticulum (SR), and ultimately restored Ca2+ handling in response to sepsis.	Cyclic AMP	86-90	phospholamban	Mus musculus	173-176
33463061-15	2021	CONCLUSIONS: Our data demonstrated that activation of TLR7 protected against sepsis-induced cardiac dysfunction through promoting cAMP-PKA-PLN pathway, and we revealed that TLR7 might be a novel therapeutic target to block the septic cardiomyopathy and support systolic function during sepsis.	Cyclic AMP	130-134	phospholamban	Mus musculus	139-142
32555305-2	2020	The p.(Arg14del) pathogenic variant in the PLN gene results in a high risk of developing dilated or arrhythmogenic cardiomyopathy with heart failure.	arg14del	7-15	phospholamban	Mus musculus	43-46
31373621-11	2020	The activity of PLB could be inhibited by beta1-AR-cAMP-PKA pathway through PKA-mediated protein phosphorylation.	Cyclic AMP	51-55	phospholamban	Mus musculus	16-19
31626909-14	2020	Moreover, our data shown that stachydrine hydrochloride blocked the hyper-phosphorylation of CaMKII, RyR2, PLN, and prevented the disassociation of FKBP12.6 from RyR2.	indole	30-55	phospholamban	Mus musculus	107-110
32087034-12	2020	In this study, we sought to determine whether feeding mice low-dose lithium, a natural GSK3 inhibitor, would improve left ventricular SERCA function by altering the SERCA2a:PLN ratio.	Lithium	68-75	phospholamban	Mus musculus	173-176
32087034-16	2020	These findings suggest that low-dose lithium supplementation can improve SERCA function by increasing the SERCA2a:PLN ratio.	Lithium	37-44	phospholamban	Mus musculus	114-117
30605506-7	2019	In both 12-mo-old NTG and AC8TG, PLN and GSK3alpha/beta phosphorylation was increased together with main localization of phospho-PKA substrates in Z-line interspaces.	Nitroglycerin	18-21	phospholamban	Mus musculus	33-36
31185731-11	2019	Complexome profiling and Stimulated Emission Depletion imaging revealed that PLN is present in the PPP1R3A-RyR2 interaction, suggesting the existence of a previously unknown SR nanodomain composed of both RyR2 and PLN/sarco/endoplasmic reticulum calcium ATPase-2a macromolecular complexes.	Calcium	246-253	phospholamban	Mus musculus	77-80
31228183-10	2020	Single bolus administration of levosimendan abrogated DXR-induced cardiotoxicity and activated Akt/eNOS and cAMP-PKA/cGMP-PKG/PLN pathways but failed to exert cardioprotection in PLN-/- mice.	Simendan	31-43	phospholamban	Mus musculus	126-129
31228183-10	2020	Single bolus administration of levosimendan abrogated DXR-induced cardiotoxicity and activated Akt/eNOS and cAMP-PKA/cGMP-PKG/PLN pathways but failed to exert cardioprotection in PLN-/- mice.	Simendan	31-43	phospholamban	Mus musculus	179-182
31228183-13	2020	CONCLUSION: Single dose levosimendan prevented doxorubicin cardiotoxicity through a cAMP-PKA-PLN pathway, highlighting the role of inotropy in doxorubicin cardiotoxicity.	Simendan	24-36	phospholamban	Mus musculus	93-96
31228183-13	2020	CONCLUSION: Single dose levosimendan prevented doxorubicin cardiotoxicity through a cAMP-PKA-PLN pathway, highlighting the role of inotropy in doxorubicin cardiotoxicity.	Cyclic AMP	84-88	phospholamban	Mus musculus	93-96
31633177-6	2019	Finally, events leading to abortion following indomethacin administration are effectively prevented by supplementing PGE2 or by PLN removal.	Indomethacin	46-58	phospholamban	Mus musculus	128-131
30280943-4	2019	After oral administration of 2-ME PLN-MP, retention time in mice was evaluated by in vivo imaging technology and the pharmacokinetic parameters in rats were determined by HPLC.	2-Methoxyestradiol	29-33	phospholamban	Mus musculus	34-37
30280943-6	2019	2-ME PLN in the microparticles showed significant pH-sensitive release in the simulated gastrointestinal fluid and controlled release in the intestine.	2-Methoxyestradiol	0-4	phospholamban	Mus musculus	5-8
31507414-8	2019	Significant upregulation of PLN and ANK2 at the mRNA and protein levels was observed in the myocardium of sunitinib-treated mice.	Sunitinib	106-115	phospholamban	Mus musculus	28-31
31507414-10	2019	SiRNA knockdown of PLN or ANK2 prevented sunitinib-induced suppression of contractility in hiPSC-CMs.	Sunitinib	41-50	phospholamban	Mus musculus	19-22
31507414-11	2019	Therefore, our in vivo and in vitro results showed that sunitinib downregulated miR-146a, which contributes to cardiac contractile dysfunction by regulating the downstream targets PLN and ANK2, and that upregulation of miR-146a alleviated the inhibitory effect of SNT on cardiac contractility.	Sunitinib	56-65	phospholamban	Mus musculus	180-183
30806861-10	2018	These results suggest that the abnormal increase in PLN in the ipsilateral fast-twitch fibers may be involved in decreased SERCA activity, SR calcium content, peak calcium transients, and contractile forces of denervated muscles.	sr calcium	139-149	phospholamban	Mus musculus	52-55
30806861-10	2018	These results suggest that the abnormal increase in PLN in the ipsilateral fast-twitch fibers may be involved in decreased SERCA activity, SR calcium content, peak calcium transients, and contractile forces of denervated muscles.	Calcium	142-149	phospholamban	Mus musculus	52-55
29150445-1	2018	The antiapoptotic protein HAX-1 (HS-associated protein X-1) localizes to sarcoplasmic reticulum (SR) in the heart and interacts with the small membrane protein phospholamban (PLN), inhibiting the cardiac sarco/endoplasmic reticulum calcium ATPase 2a (SERCA2a) in the regulation of overall calcium handling and heart muscle contractility.	Calcium	232-239	phospholamban	Mus musculus	175-178
29081219-11	2018	Conclusion: mPLN > 3 in early-stage cervical cancer affects DMFS and DFS.	Adenosine Monophosphate	18-21	phospholamban	Mus musculus	12-16
29081219-9	2018	Multivariate analysis revealed that mPLN > 3, LVI, and non-SqCC were unfavorable index for both DMFS (p < 0.001, p=0.020, and p=0.031, respectively) and DFS (p < 0.001, p=0.017, and p=0.001, respectively).	Adenosine Monophosphate	42-45	phospholamban	Mus musculus	36-40
29081219-9	2018	Multivariate analysis revealed that mPLN > 3, LVI, and non-SqCC were unfavorable index for both DMFS (p < 0.001, p=0.020, and p=0.031, respectively) and DFS (p < 0.001, p=0.017, and p=0.001, respectively).	Adenosine Monophosphate	112-115	phospholamban	Mus musculus	36-40
29277680-3	2018	We sought herein to identify the mechanisms and determine whether PLN-associated immunosuppression and tumor growth can be reversed using alendronate, an immune modulatory drug.	Alendronate	138-149	phospholamban	Mus musculus	66-69
29277680-6	2018	Encapsulating alendronate in PLN reversed these effects on myeloid cells and shifted the profile of multi-cytokine producing T-cells towards an IFNgamma+ perforin+ response, suggesting increased cytotoxic functionality.	Alendronate	14-25	phospholamban	Mus musculus	29-32
29277680-7	2018	Importantly, we also found that PLN-encapsulated alendronate (PLN-alen), but not free alendronate, abrogated PLN-induced tumor growth and increased progression-free survival.	Alendronate	49-60	phospholamban	Mus musculus	32-35
29277680-7	2018	Importantly, we also found that PLN-encapsulated alendronate (PLN-alen), but not free alendronate, abrogated PLN-induced tumor growth and increased progression-free survival.	Alendronate	49-60	phospholamban	Mus musculus	62-65
29277680-7	2018	Importantly, we also found that PLN-encapsulated alendronate (PLN-alen), but not free alendronate, abrogated PLN-induced tumor growth and increased progression-free survival.	Alendronate	49-60	phospholamban	Mus musculus	62-65
29150445-2	2018	However, because global HAX-1 deletion causes early lethality, how much endogenous HAX-1 contributes to PLN"s inhibitory activity on calcium cycling is unknown.	Calcium	133-140	phospholamban	Mus musculus	104-107
29150445-6	2018	The enhanced calcium cycling in the HAX-1-depleted heart was mediated through increases in the calcium affinity of SERCA2a and reduced PLN-SERCA2a binding.	Calcium	13-20	phospholamban	Mus musculus	135-138
29053672-5	2017	Compared to conventional solution forms, such superior efficacy of DMPLN was attributed to the synchronized pharmacokinetics of DOX and MMC and increased intracellular drug bioavailability within tumor cells enabled by the nanocarrier PLN.	Doxorubicin	128-131	phospholamban	Mus musculus	69-72
29053672-5	2017	Compared to conventional solution forms, such superior efficacy of DMPLN was attributed to the synchronized pharmacokinetics of DOX and MMC and increased intracellular drug bioavailability within tumor cells enabled by the nanocarrier PLN.	Mitomycin	136-139	phospholamban	Mus musculus	69-72
27642167-0	2016	Phospholamban is concentrated in the nuclear envelope of cardiomyocytes and involved in perinuclear/nuclear calcium handling.	Calcium	108-115	phospholamban	Mus musculus	0-13
27811197-1	2017	BACKGROUND: Phospholamban (PLN) inhibition enhances calcium cycling and is a potential novel therapy for heart failure (HF).	Calcium	52-59	phospholamban	Mus musculus	27-30
27811197-5	2017	We assessed the therapeutic efficacy of a single-dose LNA-ASO injection targeting PLN in pressure overload-induced cardiac dysfunction.	lna-aso	54-61	phospholamban	Mus musculus	82-85
27811197-7	2017	Subsequently, male C57BL/6 mice were subjected to sham or transverse aortic constriction surgery; after 3 weeks, these were treated with PLN-targeting LNA-ASO (0.3 mg/kg) or scrambled LNA-ASO.	Oligonucleotides, Antisense	155-158	phospholamban	Mus musculus	137-140
27811197-7	2017	Subsequently, male C57BL/6 mice were subjected to sham or transverse aortic constriction surgery; after 3 weeks, these were treated with PLN-targeting LNA-ASO (0.3 mg/kg) or scrambled LNA-ASO.	lna-aso	151-158	phospholamban	Mus musculus	137-140
27811197-10	2017	CONCLUSION: Our study revealed that a single-dose injection of PLN-targeting LNA-ASO improved contractility in pressure overload-induced cardiac dysfunction, suggesting that LNA-ASO is a promising tool for hypertensive HF treatment.	lna-aso	77-84	phospholamban	Mus musculus	63-66
27703301-3	2016	We developed and characterized dexamethasone-loaded lipid nanoemulsions directed towards P-selectin (PLN-Dex) and monitored their anti-inflammatory effects in vitro using cultured EC (EA.hy926 cells) and in vivo using a mouse model of acute inflammation [lipopolysaccharides (LPS) intravenously administered in C57BL/6 mice].	Dexamethasone	31-44	phospholamban	Mus musculus	101-104
26966065-1	2016	Phospholamban (PLN) regulates cardiac type sarco (endo)plasmic reticulum Ca(2+)-ATPase (SERCA2a) via Ser(16)-phosphorylation.	Serine	101-104	phospholamban	Mus musculus	15-18
26966065-4	2016	Cells overexpressing PLN exhibited its degradation post isoproterenol (Iso), forskolin, or 3-isobutyl-1-methylxanthine (IBMX) addition.	Isoproterenol	56-69	phospholamban	Mus musculus	21-24
26966065-4	2016	Cells overexpressing PLN exhibited its degradation post isoproterenol (Iso), forskolin, or 3-isobutyl-1-methylxanthine (IBMX) addition.	Isoproterenol	71-74	phospholamban	Mus musculus	21-24
26966065-4	2016	Cells overexpressing PLN exhibited its degradation post isoproterenol (Iso), forskolin, or 3-isobutyl-1-methylxanthine (IBMX) addition.	Colforsin	77-86	phospholamban	Mus musculus	21-24
26966065-4	2016	Cells overexpressing PLN exhibited its degradation post isoproterenol (Iso), forskolin, or 3-isobutyl-1-methylxanthine (IBMX) addition.	1-Methyl-3-isobutylxanthine	91-118	phospholamban	Mus musculus	21-24
26966065-4	2016	Cells overexpressing PLN exhibited its degradation post isoproterenol (Iso), forskolin, or 3-isobutyl-1-methylxanthine (IBMX) addition.	1-Methyl-3-isobutylxanthine	120-124	phospholamban	Mus musculus	21-24
26966065-10	2016	In another heart failure model, MG132 treatment reversed PLN degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	32-37	phospholamban	Mus musculus	57-60
26966065-11	2016	These data suggest that PLN is, at least partially, oligo-ubiquitinated at Lys(3) and degraded through Ser(16)-phosphorylation-mediated poly-ubiquitination during heart failure.	Lysine	75-78	phospholamban	Mus musculus	24-27
26966065-11	2016	These data suggest that PLN is, at least partially, oligo-ubiquitinated at Lys(3) and degraded through Ser(16)-phosphorylation-mediated poly-ubiquitination during heart failure.	Serine	103-106	phospholamban	Mus musculus	24-27
23919584-4	2013	Here we tested whether HNO alters the inhibitory interaction between phospholamban (PLN) and the sarcoplasmic reticulum Ca(2+)-ATPase (SERCA2a) in a redox-dependent manner, improving Ca(2+) handling in isolated myocytes/hearts.	nitroxyl	23-26	phospholamban	Mus musculus	84-87
25870184-7	2015	NaHS enhanced phosphorylation of phospholamban (PLN), in a PKG-dependent manner.	sodium bisulfide	0-4	phospholamban	Mus musculus	48-51
25870184-11	2015	CONCLUSIONS: Our findings demonstrate (i) that administration of NaHS induces cardioprotection via a cGMP/PKG/PLN pathway and (ii) contribution of nitric oxide to the H2S response is species-specific.	sodium bisulfide	65-69	phospholamban	Mus musculus	110-113
24892712-2	2014	Mice lacking Epac1 (Epac1 KO) exhibited decreased cardiac contractility with reduced phospholamban (PLN) phosphorylation at serine-16, the major PKA-mediated phosphorylation site.	Serine	124-130	phospholamban	Mus musculus	100-103
24892712-4	2014	In contrast, direct activation of EPAC in cardiomyocytes led to increased PLN phosphorylation at serine-16, which was dependent on PLC and PKCepsilon.	Serine	97-103	phospholamban	Mus musculus	74-77
26075818-6	2015	We have provided evidence that thyroid hormone receptor-alpha (TR-alpha), a transcriptional regulator of PLN, interacts with PHD2 and PHD3 and is hydroxylated at 2 proline residues.	Proline	164-171	phospholamban	Mus musculus	105-108
26040000-3	2015	Inhibiting lysosomal and autophagic activities promoted endogenous PLN accumulation, whereas accelerating autophagy with metformin enhanced PLN degradation in CMNCs.	Metformin	121-130	phospholamban	Mus musculus	140-143
26040000-4	2015	This reduction in PLN levels was functionally correlated with an increased rate of SERCA2a activity, accounting for an inotropic effect of metformin.	Metformin	139-148	phospholamban	Mus musculus	18-21
26040000-5	2015	Metabolic labeling reaffirmed that metformin promoted wild-type and R9C PLN degradation.	Metformin	35-44	phospholamban	Mus musculus	72-75
26040000-6	2015	Immunofluorescence showed that PLN and the autophagy marker, microtubule light chain 3, became increasingly colocalized in response to chloroquine and bafilomycin treatments.	Chloroquine	135-146	phospholamban	Mus musculus	31-34
26040000-6	2015	Immunofluorescence showed that PLN and the autophagy marker, microtubule light chain 3, became increasingly colocalized in response to chloroquine and bafilomycin treatments.	bafilomycin	151-162	phospholamban	Mus musculus	31-34
23919584-11	2013	In cardiomyocytes, HNO achieved this effect by stabilizing PLN in an oligomeric disulfide bond-dependent configuration, decreasing the amount of free inhibitory monomeric PLN available.	Disulfides	80-89	phospholamban	Mus musculus	59-62
23624088-6	2013	Concomitantly, relaxation and time constant of [Ca(2+)]i decay (tau) were faster and the phosphorylated fraction of phospholamban (PLN-Ser(16)/PLN) was greater.	Serine	135-138	phospholamban	Mus musculus	131-134
23800848-5	2013	The other model was a gene knockout of phospholamban (PLN KO), a regulator of calcium uptake in the sarcoplasmic reticulum of cardiomyocytes; these hearts exhibit hypercontractility with no pathological abnormalities.	Calcium	78-85	phospholamban	Mus musculus	54-57
23856523-8	2013	Importantly, these effects of PLN-KO were reverted by partially inhibiting sarco(endo)plasmic reticulum Ca2+ ATPase with 2,5-di-tert-butylhydroquinone.	2,5-di-tert-butylhydroquinone	121-150	phospholamban	Mus musculus	30-33
23658728-10	2013	Aerobic exercise trained increased the phosphorylation of PLN at Ser(16) and Thr(17) residues in both KOT and KOCT groups, but carvedilol treatment reduced lipid peroxidation in KOC and KOCT groups compared with KOS group.	Serine	65-68	phospholamban	Mus musculus	58-61
21840315-2	2011	In this study, we sought to permanently alter calcium fluxes via phospholamban (PLN) gene deletion in Tm180 mice in order to sustain long-term improvements in cardiac function and adverse cardiac remodeling/hypertrophy.	Calcium	46-53	phospholamban	Mus musculus	80-83
22484619-9	2012	Conversely, inhibition of cGMP/PKG pathway abolished the Ang II-induced faster relaxation by reducing phospholamban (PLN) Ser(16) phosphorylation.	Cyclic GMP	26-30	phospholamban	Mus musculus	117-120
22484619-9	2012	Conversely, inhibition of cGMP/PKG pathway abolished the Ang II-induced faster relaxation by reducing phospholamban (PLN) Ser(16) phosphorylation.	Serine	122-125	phospholamban	Mus musculus	117-120
21945464-5	2012	Conversely, nNOS-derived NO regulates basal myocardial inotropy and relaxation by inhibiting the sarcolemmal Ca(2+) current (I(Ca)) and promoting protein kinase A-dependent phospholamban (PLN) phosphorylation, independent of cGMP.	Cyclic GMP	225-229	phospholamban	Mus musculus	188-191
18007024-8	2008	Taken together, our findings identify a novel mechanism by which myocardial nNOS promotes left ventricular relaxation by regulating the protein kinase A-mediated phosphorylation of PLN and the rate of sarcoplasmic reticulum Ca2+ reuptake via a cGMP-independent effect on protein phosphatase activity.	Cyclic GMP	244-248	phospholamban	Mus musculus	181-184
20833651-4	2011	The double-knockout (dKO) mice for PLN and SLN showed increased SERCA pump activity, Ca(2+) transients and SR Ca(2+) load, and developed cardiac hypertrophy.	sr ca(2+)	107-116	phospholamban	Mus musculus	35-38
20942811-5	2011	Western blots were carried out on myocyte extracts with antibodies against total phospholamban (PLN) and PLN phosphorylated at serine-16.	Serine	127-133	phospholamban	Mus musculus	105-108
20942811-8	2011	Urocortin 2 also increased PLN phosphorylation at serine-16.	Serine	50-56	phospholamban	Mus musculus	27-30
19696029-7	2009	We found that when activated, Akt interacts with and phosphorylates PLN at Thr(17), the Ca(2+)-calmodulin-dependent kinase IIdelta site, whereas silencing Akt signaling, through the knock-out of phosphatidylinositol-dependent kinase-1, resulted in reduced phosphorylation of PLN at Thr(17).	Threonine	75-78	phospholamban	Mus musculus	68-71
19696029-7	2009	We found that when activated, Akt interacts with and phosphorylates PLN at Thr(17), the Ca(2+)-calmodulin-dependent kinase IIdelta site, whereas silencing Akt signaling, through the knock-out of phosphatidylinositol-dependent kinase-1, resulted in reduced phosphorylation of PLN at Thr(17).	Threonine	282-285	phospholamban	Mus musculus	68-71
18400986-9	2008	Acute inhibition of NOS1 with SMLT in WT myocytes also decreased basal PLB serine16 phosphorylation.	serine16	75-83	phospholamban	Mus musculus	71-74
18400986-14	2008	Thus NOS1 signaling modulates PLB serine16 phosphorylation, in part, via peroxynitrite.	serine16	34-42	phospholamban	Mus musculus	30-33
18400986-14	2008	Thus NOS1 signaling modulates PLB serine16 phosphorylation, in part, via peroxynitrite.	Peroxynitrous Acid	73-86	phospholamban	Mus musculus	30-33
18045856-5	2008	Bethanecol increased the amplitudes of phasic contractions in antrum smooth muscles from both control and PLB-KO mice.	Bethanechol	0-10	phospholamban	Mus musculus	106-109
18045856-6	2008	Caffeine decreased and cyclopiazonic acid (CPA) increased the basal tone of antrum smooth muscle strips from PLB-KO mice, but the effects were less pronounced compared with control strips.	cyclopiazonic acid	23-41	phospholamban	Mus musculus	109-112
18045856-6	2008	Caffeine decreased and cyclopiazonic acid (CPA) increased the basal tone of antrum smooth muscle strips from PLB-KO mice, but the effects were less pronounced compared with control strips.	cyclopiazonic acid	43-46	phospholamban	Mus musculus	109-112
18045856-7	2008	The CaM kinase II inhibitor KN-93 was less effective at inhibiting caffeine-induced relaxation in antrum smooth muscle strips from PLB-KO mice.	KN 93	28-33	phospholamban	Mus musculus	131-134
21903937-7	2011	Rolipram increased PLN phosphorylation in WT cardiomyocytes to levels indistinguishable from those in PDE4D(-/-) cardiomyocytes.	Rolipram	0-8	phospholamban	Mus musculus	19-22
21903937-9	2011	CONCLUSIONS: PDE4D regulates basal cAMP levels in SR microdomains containing SERCA2a-PLN, but not L-type Ca2+ channels or ryanodine receptor.	Cyclic AMP	35-39	phospholamban	Mus musculus	85-88
20392835-5	2010	Interestingly, a PLB reporter gene containing only the core promoter sequences -156 to +64 displayed robust T(3)-dependent silencing in HL-1 cells, thus suggesting that transcriptional repression is facilitated by TRalpha1 via the PLB core promoter, a regulatory region highly conserved in mammals.	Triiodothyronine	108-112	phospholamban	Mus musculus	17-20
20392835-5	2010	Interestingly, a PLB reporter gene containing only the core promoter sequences -156 to +64 displayed robust T(3)-dependent silencing in HL-1 cells, thus suggesting that transcriptional repression is facilitated by TRalpha1 via the PLB core promoter, a regulatory region highly conserved in mammals.	Triiodothyronine	108-112	phospholamban	Mus musculus	231-234
20392835-7	2010	Furthermore, addition of T(3) triggered alterations in covalent histone modifications at the PLB promoter that are associated with gene silencing, namely a pronounced decrease in both histone H3 acetylation and histone H3 lysine 4 methylation.	Triiodothyronine	25-29	phospholamban	Mus musculus	93-96
20392835-7	2010	Furthermore, addition of T(3) triggered alterations in covalent histone modifications at the PLB promoter that are associated with gene silencing, namely a pronounced decrease in both histone H3 acetylation and histone H3 lysine 4 methylation.	Lysine	222-228	phospholamban	Mus musculus	93-96
20392835-8	2010	Taken together, our data reveal that T(3)-dependent repression of PLB in cardiac myocytes is directly facilitated by TRalpha1 and involves the hormone-dependent recruitment of histone-modifying enzymes associated with transcriptional silencing.	Triiodothyronine	37-41	phospholamban	Mus musculus	66-69
19959778-2	2010	We hypothesized that phospholamban (PLN) ablation would restore SR Ca(2+) load and prevent the decreased ventricular contractility, dilation and mortality seen in CaMKII-TG.	Thioguanine	170-172	phospholamban	Mus musculus	36-39
16516179-1	2006	OBJECTIVE: To investigate the importance of the phosphorylation of Ser16 and Thr17 sites of phospholamban (PLN) on intracellular Ca2+ (Cai2+) handling and contractile recovery of the stunned myocardium.	cai2+	135-140	phospholamban	Mus musculus	107-110
16861697-8	2006	Verapamil pretreatment prevented Iso-induced apoptosis in PLN(-/-) mice, indicating the involvement of a Ca(2+)-dependent pathway.	Verapamil	0-9	phospholamban	Mus musculus	58-61
16861697-8	2006	Verapamil pretreatment prevented Iso-induced apoptosis in PLN(-/-) mice, indicating the involvement of a Ca(2+)-dependent pathway.	Isoproterenol	33-36	phospholamban	Mus musculus	58-61
18064719-11	2008	Down-regulation of PLN led to enhanced cell shortening and relaxation and to a decrease in the time constant of calcium decay, signs of improved contractility and calcium handling.	Calcium	112-119	phospholamban	Mus musculus	19-22
18064719-11	2008	Down-regulation of PLN led to enhanced cell shortening and relaxation and to a decrease in the time constant of calcium decay, signs of improved contractility and calcium handling.	Calcium	163-170	phospholamban	Mus musculus	19-22
17950750-19	2007	This most likely was due to higher PLB Thr-17 phosphorylation in CaMKIIdelta(C) myocytes.	Threonine	39-42	phospholamban	Mus musculus	35-38
16849635-7	2006	PLN(-/-) mice had a markedly reduced constrictive response to methacholine.	Methacholine Chloride	62-74	phospholamban	Mus musculus	0-3
16516179-8	2006	CONCLUSIONS: PLN phosphorylation appears to be crucial for the mechanical and Cai2+ recovery during stunning and protective against the mechanical abnormalities typical of Cai2+ overload.	cai2+	78-83	phospholamban	Mus musculus	13-16
16516179-8	2006	CONCLUSIONS: PLN phosphorylation appears to be crucial for the mechanical and Cai2+ recovery during stunning and protective against the mechanical abnormalities typical of Cai2+ overload.	cai2+	172-177	phospholamban	Mus musculus	13-16
15059971-7	2004	However, isoproterenol stimulation reversed the inhibitory effects of PLN on the transgenic soleus twitch kinetics.	Isoproterenol	9-22	phospholamban	Mus musculus	70-73
16461894-5	2006	In these cardiomyocytes, isoproterenol restored calcium dynamics to the levels seen in PLN KO.	Isoproterenol	25-38	phospholamban	Mus musculus	87-90
16461894-5	2006	In these cardiomyocytes, isoproterenol restored calcium dynamics to the levels seen in PLN KO.	Calcium	48-55	phospholamban	Mus musculus	87-90
15358683-11	2004	Our findings suggest that numerous alterations in protein expression and phosphorylation state occurred upon ablation of PLN and that a complex functional relationship among proteins involved in calcium handling, myofibrils, and energy production may exist to coordinately maintain the hyperdynamic cardiac contractile performance of the PLN-KO mouse in the long term.	Calcium	195-202	phospholamban	Mus musculus	121-124
16436691-2	2006	We determined the MICs of miltefosine against key fungal pathogens, correlated antifungal activity with inhibition of the PLB1 activities (PLB, lysophospholipase [LPL], and lysophospholipase-transacylase [LPTA]), and investigated its efficacy in a mouse model of disseminated cryptococcosis.	miltefosine	26-37	phospholamban	Mus musculus	122-125
15276030-3	2004	Phosphorylation of PLN occurs on residues: serine-16 (Ser(16)) and threonine-17 (Thr(17)) in vivo.	Serine	43-49	phospholamban	Mus musculus	19-22
15276030-3	2004	Phosphorylation of PLN occurs on residues: serine-16 (Ser(16)) and threonine-17 (Thr(17)) in vivo.	Serine	54-57	phospholamban	Mus musculus	19-22
15276030-3	2004	Phosphorylation of PLN occurs on residues: serine-16 (Ser(16)) and threonine-17 (Thr(17)) in vivo.	Threonine	67-76	phospholamban	Mus musculus	19-22
15276030-3	2004	Phosphorylation of PLN occurs on residues: serine-16 (Ser(16)) and threonine-17 (Thr(17)) in vivo.	Threonine	81-84	phospholamban	Mus musculus	19-22
15276030-4	2004	In isolated wild-type cardiomyocytes, we found that increases of stimulation frequency from 0.5 to 5 Hz were associated with increased Thr(17) phosphorylation of PLN and cardiac contractility.	Threonine	135-138	phospholamban	Mus musculus	162-165
15276030-10	2004	These results indicate that Thr(17) phosphorylation of PLN is the major contributor to frequency-dependent increases of contractile and relaxation parameters in mouse cardiomyocytes, although some increases in these parameters occur even in the absence of PLN phosphorylation.	Threonine	28-31	phospholamban	Mus musculus	55-58
11854448-7	2002	The association was inhibited by cAMP-dependent phosphorylation of the PLN fusion protein and by usage of anti-PLN monoclonal antibody.	Cyclic AMP	33-37	phospholamban	Mus musculus	71-74
14985072-6	2004	At the two highest doses of ISO, the rate of relaxation (-dP/dt) was significantly smaller in PLB/ssTnI than in PLB/cTnI hearts.	dp	58-60	phospholamban	Mus musculus	94-97
14985072-6	2004	At the two highest doses of ISO, the rate of relaxation (-dP/dt) was significantly smaller in PLB/ssTnI than in PLB/cTnI hearts.	dp	58-60	phospholamban	Mus musculus	112-115
14985072-6	2004	At the two highest doses of ISO, the rate of relaxation (-dP/dt) was significantly smaller in PLB/ssTnI than in PLB/cTnI hearts.	Thymidine	61-63	phospholamban	Mus musculus	94-97
11992736-4	2002	In BALB/c mice, diclofenac caused dose-dependent increases in PLN weight and PLN cellularity in the direct PLNA; 0.25 mg was non-immunostimulating whereas 0.50-1.00 mg caused a significant PLN reaction.	Diclofenac	16-26	phospholamban	Mus musculus	62-65
11992736-4	2002	In BALB/c mice, diclofenac caused dose-dependent increases in PLN weight and PLN cellularity in the direct PLNA; 0.25 mg was non-immunostimulating whereas 0.50-1.00 mg caused a significant PLN reaction.	Diclofenac	16-26	phospholamban	Mus musculus	77-80
11992736-4	2002	In BALB/c mice, diclofenac caused dose-dependent increases in PLN weight and PLN cellularity in the direct PLNA; 0.25 mg was non-immunostimulating whereas 0.50-1.00 mg caused a significant PLN reaction.	Diclofenac	16-26	phospholamban	Mus musculus	77-80
11992736-5	2002	In the direct PLNA, diclofenac also increased the percent of T cells in the PLN with activated phenotypes (CD44(high)CD62L(low) and CD44(high)CD62L(high)).	Diclofenac	20-30	phospholamban	Mus musculus	14-17
11992736-6	2002	Finally, the magnitude of the diclofenac-induced direct PLN reaction was significantly reduced when the assay was conducted in T-cell-deficient mice.	Diclofenac	30-40	phospholamban	Mus musculus	56-59
11992736-7	2002	When co-injected with the reporter antigen TNP-Ficoll (trinitrophenyl Ficoll), 0.50 mg diclofenac caused significant increases in PLN weight, PLN cellularity, and induced IgM and IgG(1) anti-TNP antibody forming cells (AFCs) in the PLN.	Diclofenac	87-97	phospholamban	Mus musculus	130-133
11992736-7	2002	When co-injected with the reporter antigen TNP-Ficoll (trinitrophenyl Ficoll), 0.50 mg diclofenac caused significant increases in PLN weight, PLN cellularity, and induced IgM and IgG(1) anti-TNP antibody forming cells (AFCs) in the PLN.	Diclofenac	87-97	phospholamban	Mus musculus	142-145
11992736-7	2002	When co-injected with the reporter antigen TNP-Ficoll (trinitrophenyl Ficoll), 0.50 mg diclofenac caused significant increases in PLN weight, PLN cellularity, and induced IgM and IgG(1) anti-TNP antibody forming cells (AFCs) in the PLN.	Diclofenac	87-97	phospholamban	Mus musculus	142-145
11992736-10	2002	Streptozotocin (1.00 mg) caused significant increases in PLN cellularity, IgM AFCs, and selectively induced IgG(2a) and IgG(2b) AFCs against TNP-OVA.	Streptozocin	0-14	phospholamban	Mus musculus	57-60
11992736-11	2002	Likewise, diclofenac caused dose-dependent increases (0.25-1.00 mg) in PLN cellularity and IgM AFCs.	Diclofenac	10-20	phospholamban	Mus musculus	71-74
11992736-13	2002	Finally, an increase in the intracellular level of IL-4, but not INFgamma, was detected in CD4(+) PLN cells following the injection of diclofenac mixed with TNP-OVA.	Diclofenac	135-145	phospholamban	Mus musculus	98-101
11992736-14	2002	Collectively, these data suggest that diclofenac: (i) induces a T-cell-dependent direct PLN reaction that; (ii) provides non-cognate help for IgG AFC production when co-injected with TNP-Ficoll, possibly through the formation of neo-antigens; and (iii) possesses intrinsic adjuvant activity that selectively induces IL-4 mediated production of IgG(1) and IgE against co-injected TNP-OVA.	Diclofenac	38-48	phospholamban	Mus musculus	88-91
12781630-2	2003	We hypothesized that the contact sensitizer oxazolone (OX) would cause a strong PLN reaction in naive mice and that the PLN reaction would be attenuated in mice orally pretreated with OX due to the induction of oral tolerance.	Oxazolone	44-53	phospholamban	Mus musculus	80-83
12781630-2	2003	We hypothesized that the contact sensitizer oxazolone (OX) would cause a strong PLN reaction in naive mice and that the PLN reaction would be attenuated in mice orally pretreated with OX due to the induction of oral tolerance.	Oxazolone	55-57	phospholamban	Mus musculus	80-83
12781630-11	2003	Furthermore, like OX, the diclofenac-induced PLN reaction was attenuated in mice that had been orally pretreated three times with DF.	Diclofenac	26-36	phospholamban	Mus musculus	45-48
11854448-7	2002	The association was inhibited by cAMP-dependent phosphorylation of the PLN fusion protein and by usage of anti-PLN monoclonal antibody.	Cyclic AMP	33-37	phospholamban	Mus musculus	111-114
11502581-2	2001	The role of PLB in regulating Ca(2+) release through ryanodine-sensitive Ca(2+) release channels, measured as Ca(2+) sparks, was examined using smooth muscle cells of cerebral arteries from PLB-deficient ("knockout") mice (PLB-KO).	Ryanodine	53-62	phospholamban	Mus musculus	12-15
11559781-7	2001	Inhibition of SERCA with cyclopiazonic acid (CPA) abolished these differences between WT and PLB-KO bladder, localizing the effects to the SR. 3.	cyclopiazonic acid	25-43	phospholamban	Mus musculus	93-96
11559781-7	2001	Inhibition of SERCA with cyclopiazonic acid (CPA) abolished these differences between WT and PLB-KO bladder, localizing the effects to the SR. 3.	cyclopiazonic acid	45-48	phospholamban	Mus musculus	93-96
11559781-11	2001	In PLB-SMOE bladders, in contrast, the response of [Ca2+]i and force to CCh was significantly increased and the EC50 values were decreased.	Carbachol	72-75	phospholamban	Mus musculus	3-6
11502581-7	2001	Forskolin or PLB-KO increased SR Ca(2+) load, as measured by caffeine-induced Ca(2+) transients.	Caffeine	61-69	phospholamban	Mus musculus	13-16
10809743-7	2000	The use of antibodies specific against Ser(16)- and Thr(17)-PLN peptides showed that phosphorylation of both pentameric and monomeric PLN were increased between 1.2- and 2.4-fold in both the L37A and I40A lines but not in the wtOE line.	Serine	39-42	phospholamban	Mus musculus	134-137
11087739-2	2001	The time course of thapsigargin-sensitive ATP-dependent (45)Ca influx into and efflux out of cardiac SR vesicles from PLB-KO and wild-type (WT) mice was measured at 100 nm free [Ca].	Thapsigargin	19-31	phospholamban	Mus musculus	118-121
11087739-2	2001	The time course of thapsigargin-sensitive ATP-dependent (45)Ca influx into and efflux out of cardiac SR vesicles from PLB-KO and wild-type (WT) mice was measured at 100 nm free [Ca].	Adenosine Triphosphate	42-45	phospholamban	Mus musculus	118-121
10809743-7	2000	The use of antibodies specific against Ser(16)- and Thr(17)-PLN peptides showed that phosphorylation of both pentameric and monomeric PLN were increased between 1.2- and 2.4-fold in both the L37A and I40A lines but not in the wtOE line.	Threonine	52-55	phospholamban	Mus musculus	134-137
10024311-6	1999	Endothelium-dependent relaxation to acetylcholine was attenuated in aorta of PLB-deficient (PLB-KO) mice compared with wild-type (WT) controls.	Acetylcholine	36-49	phospholamban	Mus musculus	77-80
10484417-6	1999	Upon removal of the stimulus (either PE or KCl), the decrease in [Ca2+]i was two times as fast in the PLB- as in the wild-type aorta.	Phenylephrine	37-39	phospholamban	Mus musculus	102-105
10484417-6	1999	Upon removal of the stimulus (either PE or KCl), the decrease in [Ca2+]i was two times as fast in the PLB- as in the wild-type aorta.	Potassium Chloride	43-46	phospholamban	Mus musculus	102-105
10484417-8	1999	Interestingly, stimulation of the cAMP pathway before cGMP pathway activation resulted in a significant increase in sensitivity and a difference in relaxation parameters between PLB- and wild-type aortas.	Cyclic AMP	34-38	phospholamban	Mus musculus	178-181
10845191-10	2000	On the other hand, after first injection of SDS, primary response reached maximal PLN cellularity index (2.8) on day 10, but neither secondary response nor increase in the B cell proportion were observed.	Sodium Dodecyl Sulfate	44-47	phospholamban	Mus musculus	82-85
9922946-5	1998	The examinations using mice and guinea pigs showed that mouse PLN responses to TNBS, penicillin G and cephalothin correlated with the allergenicity responses obtained in the GP-PCA reaction to three compounds.	Trinitrobenzenesulfonic Acid	79-83	phospholamban	Mus musculus	62-65
9922946-5	1998	The examinations using mice and guinea pigs showed that mouse PLN responses to TNBS, penicillin G and cephalothin correlated with the allergenicity responses obtained in the GP-PCA reaction to three compounds.	Penicillin G	85-97	phospholamban	Mus musculus	62-65
9922946-5	1998	The examinations using mice and guinea pigs showed that mouse PLN responses to TNBS, penicillin G and cephalothin correlated with the allergenicity responses obtained in the GP-PCA reaction to three compounds.	Cephalothin	102-113	phospholamban	Mus musculus	62-65
9435620-7	1997	Baseline values for positive and negative dP/dt were linearly correlated with PLB levels.	dp	42-44	phospholamban	Mus musculus	78-81
10603985-1	1998	Accumulating evidence points to the critical role of phospholamban (PLB) regulation of the cardiac sarcoplasmic reticulum (SR) calcium ATPase in influencing the kinetics of calcium handling within the cardiac myocyte under normal and pathological conditions.	Calcium	127-134	phospholamban	Mus musculus	68-71
10603985-3	1998	Experiments measuring tension transients in saponin-permeabilized cardiac muscles from genetically engineered mice under a variety of SR calcium loading conditions provide evidence of the functional alterations that can be achieved by manipulation of the degree of PLB inhibition of the calcium pump.	Saponins	44-51	phospholamban	Mus musculus	265-268
10603985-3	1998	Experiments measuring tension transients in saponin-permeabilized cardiac muscles from genetically engineered mice under a variety of SR calcium loading conditions provide evidence of the functional alterations that can be achieved by manipulation of the degree of PLB inhibition of the calcium pump.	sr calcium	134-144	phospholamban	Mus musculus	265-268
9575939-11	1998	Furthermore, the CaMKII inhibitor KN-93 (1 microM) abolished the stimulation-dependent acceleration of twitch [Ca]i decline in PLB-KO.	KN 93	34-39	phospholamban	Mus musculus	127-130
9435620-7	1997	Baseline values for positive and negative dP/dt were linearly correlated with PLB levels.	Thymidine	45-47	phospholamban	Mus musculus	78-81
9435620-8	1997	In PLB heterozygotes, contractile response to isoproterenol (Iso) was blunted compared with WT, but maximum rates of contraction were similar between the two groups.	Isoproterenol	46-59	phospholamban	Mus musculus	3-6
9435620-8	1997	In PLB heterozygotes, contractile response to isoproterenol (Iso) was blunted compared with WT, but maximum rates of contraction were similar between the two groups.	Isoproterenol	61-64	phospholamban	Mus musculus	3-6
9435620-10	1997	The effects of Iso on negative dP/dt were also blunted in both PLB heterozygous and PLB homozygous animals.	dp	31-33	phospholamban	Mus musculus	63-66
9435620-10	1997	The effects of Iso on negative dP/dt were also blunted in both PLB heterozygous and PLB homozygous animals.	dp	31-33	phospholamban	Mus musculus	84-87
9435620-10	1997	The effects of Iso on negative dP/dt were also blunted in both PLB heterozygous and PLB homozygous animals.	Thymidine	34-36	phospholamban	Mus musculus	63-66
9435620-10	1997	The effects of Iso on negative dP/dt were also blunted in both PLB heterozygous and PLB homozygous animals.	Thymidine	34-36	phospholamban	Mus musculus	84-87
9314829-4	1997	Quantitative immunoblotting indicated a 2-fold increase in the cardiac phospholamban protein levels compared with wild-type controls, with approximately equal to 50% of phospholamban migrating as monomers and approximately 50% as pentamers upon SDS-PAGE.	Sodium Dodecyl Sulfate	245-248	phospholamban	Mus musculus	71-84
9314829-6	1997	SR Ca(2+)-uptake assays revealed that the EC50 values for Ca2+ were as follows: 0.32 +/- 0.01 mumol/L in hearts overexpressing monomeric phospholamban, 0.49 +/- 0.05 mumol/L in hearts overexpressing wild-type phospholamban, and 0.26 +/- 0.01 mumol/L in wild-type control mouse hearts.	sr ca(2+)	0-9	phospholamban	Mus musculus	137-150
9314829-8	1997	The differences in basal cardiac, myocyte mechanics and Ca2+ transients among the animal groups overexpressing monomeric or wild-type phospholamban and wild-type control mice were abolished upon isoproterenol stimulation.	Isoproterenol	195-208	phospholamban	Mus musculus	134-147
1346732-3	1992	Supplementation of a nucleotide-free (NF) diet with yeast RNA (NFR) or uracil (NFU) significantly enhanced the host PLN immune response as compared with NF and NF supplemented with adenine (NFA) diets.	Uracil	71-77	phospholamban	Mus musculus	116-119
9252436-8	1997	These results suggest that PLB is a key determinant of relaxation in slow-twitch skeletal muscle under basal conditions and during isoproterenol stimulation.	Isoproterenol	131-144	phospholamban	Mus musculus	27-30
8764561-3	1996	Here, using the direct popliteal lymph node assay (PLNA) in mice we found that PTU-SO3-, indeed, induced a T-cell-dependent primary PLN response, whereas the parent compound PTU failed to do so.	ptu-so3	79-86	phospholamban	Mus musculus	51-54
8764561-3	1996	Here, using the direct popliteal lymph node assay (PLNA) in mice we found that PTU-SO3-, indeed, induced a T-cell-dependent primary PLN response, whereas the parent compound PTU failed to do so.	Propylthiouracil	79-82	phospholamban	Mus musculus	51-54
8760070-3	1996	PLB-deficient myocytes also demonstrated significant increases in the peak amplitude of the fura 2 fluorescence ratio and the rates of rising and falling phases of the Ca2+ transient.	Fura-2	92-98	phospholamban	Mus musculus	0-3
8760070-5	1996	In PLB-deficient myocytes, 0.05 microM isoproterenol induced an increase in the twitch amplitude by 152 +/- 11% (n = 6) compared with 290 +/- 31% (n = 6) in wild-type cells.	Isoproterenol	39-52	phospholamban	Mus musculus	3-6
8760070-7	1996	The isoproterenol-induced increase in maximum relengthening velocity was increased by 168 +/- 8% (n = 6) in PLB-deficient cells compared with 445 +/- 71% (n = 6) in wild-type myocytes.	Isoproterenol	4-17	phospholamban	Mus musculus	108-111
9118481-6	1997	The time course of force development with phenylephrine stimulation was faster in the PLB- aorta, suggesting changes in SR Ca2+ release.	Phenylephrine	42-55	phospholamban	Mus musculus	86-90
9118481-8	1997	The cumulative concentration-isometric force relations for the PLB- aorta were to the right of the wild-type for both KCl and phenylephrine stimulation, indicating a less sensitive tissue.	Potassium Chloride	118-121	phospholamban	Mus musculus	63-67
9118481-8	1997	The cumulative concentration-isometric force relations for the PLB- aorta were to the right of the wild-type for both KCl and phenylephrine stimulation, indicating a less sensitive tissue.	Phenylephrine	126-139	phospholamban	Mus musculus	63-67
9118481-12	1997	Our results suggest that PLB is a regulator of the SR Ca2+ pump in mouse aorta and plays a regulatory role in both KCl-induced and receptor-mediated contractility in vascular smooth muscle.	Potassium Chloride	115-118	phospholamban	Mus musculus	25-28
7612820-7	1995	Phosphorylation of PLB in ventricular SR decreased the population of large-scale Ca-ATPase aggregates to a level similar to that of atrial tumor SR. Lipid chain mobility (fluidity), detected by electron paramagnetic resonance of stearic acid spin labels, was very similar in the two preparations, indicating that the higher protein mobility in atrial tumor SR is not due to higher lipid fluidity.	stearic acid	229-241	phospholamban	Mus musculus	19-22
35468773-9	2022	Our data also demonstrate that TCA blocked the hyperphosphorylation of ryanodine receptor type 2 (RyR2) and phospholamban (PLN) and restored Ca2+ handling and sarcomere shortening in AMCMs.	cinnamaldehyde	31-34	phospholamban	Mus musculus	123-126
1363474-3	1992	Changes in lymphocyte subsets during an acute GVH reaction were compared to STZ-induced PLN response in mice.	Streptozocin	76-79	phospholamban	Mus musculus	88-91
34462437-4	2021	Here, we study antisense oligonucleotides (ASOs) as a therapeutic modality, interfering with the PLN/SERCA2a interaction by targeting Pln mRNA for downregulation in the heart of murine HF models.	Oligonucleotides	25-41	phospholamban	Mus musculus	97-100
34462437-4	2021	Here, we study antisense oligonucleotides (ASOs) as a therapeutic modality, interfering with the PLN/SERCA2a interaction by targeting Pln mRNA for downregulation in the heart of murine HF models.	Oligonucleotides	25-41	phospholamban	Mus musculus	134-137
34462437-4	2021	Here, we study antisense oligonucleotides (ASOs) as a therapeutic modality, interfering with the PLN/SERCA2a interaction by targeting Pln mRNA for downregulation in the heart of murine HF models.	Oligonucleotides, Antisense	43-47	phospholamban	Mus musculus	97-100
34462437-4	2021	Here, we study antisense oligonucleotides (ASOs) as a therapeutic modality, interfering with the PLN/SERCA2a interaction by targeting Pln mRNA for downregulation in the heart of murine HF models.	Oligonucleotides, Antisense	43-47	phospholamban	Mus musculus	134-137
34138844-10	2021	After ISO withdrawal, phosphorylation of phospholamban (PLN) at the protein kinase A (PKA) phosphorylation site Ser-16 dropped down to 20% as compared to only 50% at the Ca2+/Calmodulin-dependent kinase II (CaMKII) phosphorylation site Thr-17 in "ISO off" mice.	Serine	112-115	phospholamban	Mus musculus	56-59
1688560-4	1990	In addition, this antibody also blocked the binding to the HR of PPME, a polyphosphomannan carbohydrate known to inhibit lymphocyte-pln endothelium interactions, suggesting that Mel 14 may recognize the lectin domain of the pln HR.	polyphosphomannan carbohydrate	73-103	phospholamban	Mus musculus	132-135
1688560-4	1990	In addition, this antibody also blocked the binding to the HR of PPME, a polyphosphomannan carbohydrate known to inhibit lymphocyte-pln endothelium interactions, suggesting that Mel 14 may recognize the lectin domain of the pln HR.	polyphosphomannan carbohydrate	73-103	phospholamban	Mus musculus	224-227
1688560-8	1990	Since Mel 14 efficiently blocks lymphocyte-endothelial interactions, these results support the hypothesis that the pln HR lectin domain may be directly involved with binding of lymphocytes to a carbohydrate ligand on the pln postcapillary venule endothelium.	Carbohydrates	194-206	phospholamban	Mus musculus	115-118
1688560-8	1990	Since Mel 14 efficiently blocks lymphocyte-endothelial interactions, these results support the hypothesis that the pln HR lectin domain may be directly involved with binding of lymphocytes to a carbohydrate ligand on the pln postcapillary venule endothelium.	Carbohydrates	194-206	phospholamban	Mus musculus	221-224
35297759-2	2022	PLN interacts with sarco/endoplasmic reticulum Ca2+-ATPase (SERCA) and regulates calcium uptake, which is modulated by the protein kinase A (PKA)-dependent phosphorylation of PLN during the fight-or-flight response.	Calcium	81-88	phospholamban	Mus musculus	0-3
35297759-2	2022	PLN interacts with sarco/endoplasmic reticulum Ca2+-ATPase (SERCA) and regulates calcium uptake, which is modulated by the protein kinase A (PKA)-dependent phosphorylation of PLN during the fight-or-flight response.	Calcium	81-88	phospholamban	Mus musculus	175-178
35063742-2	2022	Herein, upper intestinal absorptive polymer-lipid hybrid nanoparticles (PLN) was designed by exploiting the lipidic core for drug encapsulation and the decanoic acid conjugated rapeseed protein as the biopolymeric shell for gastrointestinal stability, retention and permeability.	Polymers	36-43	phospholamban	Mus musculus	72-75
35063742-2	2022	Herein, upper intestinal absorptive polymer-lipid hybrid nanoparticles (PLN) was designed by exploiting the lipidic core for drug encapsulation and the decanoic acid conjugated rapeseed protein as the biopolymeric shell for gastrointestinal stability, retention and permeability.	decanoic acid	152-165	phospholamban	Mus musculus	72-75
35063742-3	2022	Polyphenol ellagic acid loaded core-shell PLN (EA-PLN(C/S)) was characterized of favorable physicochemical properties in simulated gastric- and intestinal fluids, including high drug loading capacity, slow drug release and prolonged stability.	Polyphenols	0-10	phospholamban	Mus musculus	42-45
35063742-3	2022	Polyphenol ellagic acid loaded core-shell PLN (EA-PLN(C/S)) was characterized of favorable physicochemical properties in simulated gastric- and intestinal fluids, including high drug loading capacity, slow drug release and prolonged stability.	Ellagic Acid	11-23	phospholamban	Mus musculus	42-45
3262595-12	1988	The weight increase of the draining PLN after HgCl2 injection was preceded in time by an increased 3H thymidine uptake by the PLN.	Mercuric Chloride	46-51	phospholamban	Mus musculus	36-39
3262595-12	1988	The weight increase of the draining PLN after HgCl2 injection was preceded in time by an increased 3H thymidine uptake by the PLN.	Mercuric Chloride	46-51	phospholamban	Mus musculus	126-129
3262595-12	1988	The weight increase of the draining PLN after HgCl2 injection was preceded in time by an increased 3H thymidine uptake by the PLN.	3h thymidine	99-111	phospholamban	Mus musculus	36-39
3262595-12	1988	The weight increase of the draining PLN after HgCl2 injection was preceded in time by an increased 3H thymidine uptake by the PLN.	3h thymidine	99-111	phospholamban	Mus musculus	126-129
3262595-14	1988	When CH3HgCl, instead of HgCl2, was injected all three strains tested, including DBA/2, responded by PLN enlargement.	methylmercuric chloride	5-12	phospholamban	Mus musculus	101-104