PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
24124190-0	2013	Identification of the SPLUNC1 ENaC-inhibitory domain yields novel strategies to treat sodium hyperabsorption in cystic fibrosis airway epithelial cultures.	Sodium	86-92	BPI fold containing family A member 1	Homo sapiens	22-29
24124190-4	2013	Here we found that an 18 amino acid peptide, S18, which corresponded to residues G22-A39 of the SPLUNC1 NH2 terminus inhibited ENaC activity to a similar degree as full-length SPLUNC1 (~2.5 fold), while SPLUNC1 protein lacking this region was without effect.	Peptides	36-43	BPI fold containing family A member 1	Homo sapiens	96-103
24124190-4	2013	Here we found that an 18 amino acid peptide, S18, which corresponded to residues G22-A39 of the SPLUNC1 NH2 terminus inhibited ENaC activity to a similar degree as full-length SPLUNC1 (~2.5 fold), while SPLUNC1 protein lacking this region was without effect.	Peptides	36-43	BPI fold containing family A member 1	Homo sapiens	176-183
24124190-4	2013	Here we found that an 18 amino acid peptide, S18, which corresponded to residues G22-A39 of the SPLUNC1 NH2 terminus inhibited ENaC activity to a similar degree as full-length SPLUNC1 (~2.5 fold), while SPLUNC1 protein lacking this region was without effect.	Peptides	36-43	BPI fold containing family A member 1	Homo sapiens	176-183
22798424-0	2012	Identification of SPLUNC1"s ENaC-inhibitory domain yields novel strategies to treat sodium hyperabsorption in cystic fibrosis airways.	Sodium	84-90	BPI fold containing family A member 1	Homo sapiens	18-25
23741370-8	2013	We found that: (1) HNE directly increased NTHi load in human airway epithelial cells; (2) HNE degraded human SPLUNC1 protein; (3) Recombinant SPLUNC1 protein reduced NTHi levels in HNE-treated human airway epithelial cells; (4) NTHi levels in lungs of SPLUNC1 knockout mice were increased compared to wild-type mice; and (5) SPLUNC1 was reduced in lungs of COPD patients.	nthi	42-46	BPI fold containing family A member 1	Homo sapiens	142-149
23741370-8	2013	We found that: (1) HNE directly increased NTHi load in human airway epithelial cells; (2) HNE degraded human SPLUNC1 protein; (3) Recombinant SPLUNC1 protein reduced NTHi levels in HNE-treated human airway epithelial cells; (4) NTHi levels in lungs of SPLUNC1 knockout mice were increased compared to wild-type mice; and (5) SPLUNC1 was reduced in lungs of COPD patients.	nthi	42-46	BPI fold containing family A member 1	Homo sapiens	142-149
23741370-8	2013	We found that: (1) HNE directly increased NTHi load in human airway epithelial cells; (2) HNE degraded human SPLUNC1 protein; (3) Recombinant SPLUNC1 protein reduced NTHi levels in HNE-treated human airway epithelial cells; (4) NTHi levels in lungs of SPLUNC1 knockout mice were increased compared to wild-type mice; and (5) SPLUNC1 was reduced in lungs of COPD patients.	nthi	166-170	BPI fold containing family A member 1	Homo sapiens	142-149
23741370-8	2013	We found that: (1) HNE directly increased NTHi load in human airway epithelial cells; (2) HNE degraded human SPLUNC1 protein; (3) Recombinant SPLUNC1 protein reduced NTHi levels in HNE-treated human airway epithelial cells; (4) NTHi levels in lungs of SPLUNC1 knockout mice were increased compared to wild-type mice; and (5) SPLUNC1 was reduced in lungs of COPD patients.	nthi	166-170	BPI fold containing family A member 1	Homo sapiens	142-149
23741370-8	2013	We found that: (1) HNE directly increased NTHi load in human airway epithelial cells; (2) HNE degraded human SPLUNC1 protein; (3) Recombinant SPLUNC1 protein reduced NTHi levels in HNE-treated human airway epithelial cells; (4) NTHi levels in lungs of SPLUNC1 knockout mice were increased compared to wild-type mice; and (5) SPLUNC1 was reduced in lungs of COPD patients.	nthi	166-170	BPI fold containing family A member 1	Homo sapiens	142-149
23741370-8	2013	We found that: (1) HNE directly increased NTHi load in human airway epithelial cells; (2) HNE degraded human SPLUNC1 protein; (3) Recombinant SPLUNC1 protein reduced NTHi levels in HNE-treated human airway epithelial cells; (4) NTHi levels in lungs of SPLUNC1 knockout mice were increased compared to wild-type mice; and (5) SPLUNC1 was reduced in lungs of COPD patients.	nthi	166-170	BPI fold containing family A member 1	Homo sapiens	142-149
17545071-2	2007	METHODS: RT-PCR was used to amplify the CDS sequence of Plunc, which was subsequently cloned into the pEGFP-N1 eukaryotic expression vector.	Cadmium	40-43	BPI fold containing family A member 1	Homo sapiens	56-61
21787332-6	2011	A recent study revealed that OCX-36 originates from a tandem duplication of an ancestral BPI/LBP/PLUNC gene, after the divergence of birds and mammals.	ocx	29-32	BPI fold containing family A member 1	Homo sapiens	97-102
18245229-5	2008	Furthermore, secretion assays demonstrated that PLUNC protein was released by neutrophils upon stimulation with secretogogues, including formyl methionyl leucyl phenylalanine and the calcium ionophore A23187.	N-Formylmethionine Leucyl-Phenylalanine	137-174	BPI fold containing family A member 1	Homo sapiens	48-53
18245229-5	2008	Furthermore, secretion assays demonstrated that PLUNC protein was released by neutrophils upon stimulation with secretogogues, including formyl methionyl leucyl phenylalanine and the calcium ionophore A23187.	Calcium	183-190	BPI fold containing family A member 1	Homo sapiens	48-53
18245229-5	2008	Furthermore, secretion assays demonstrated that PLUNC protein was released by neutrophils upon stimulation with secretogogues, including formyl methionyl leucyl phenylalanine and the calcium ionophore A23187.	Calcimycin	201-207	BPI fold containing family A member 1	Homo sapiens	48-53
16951499-6	2006	Incubating the FITC-LPS with the SPLUNC1 stably transfected or control cells, the intracellular intensity of fluorescence was observed under the fluorescence microscope.	fitc-lps	15-23	BPI fold containing family A member 1	Homo sapiens	33-40
16951499-8	2006	Although the binding efficiency of LPS and SPLUNC1 in vitro was very low, more FITC-LPS entered into the SPLUNC1 stably transfected cells.	fitc-lps	79-87	BPI fold containing family A member 1	Homo sapiens	105-112
32680508-3	2020	We tested the hypothesis that short palate lung and nasal epithelial clone 1 (SPLUNC1)-epithelial sodium channel (ENaC) interactions at the plasma membrane are required to reduce Bcc burden in normal airways.	Sodium	98-104	BPI fold containing family A member 1	Homo sapiens	78-85
15513904-11	2004	Interestingly, ethanol significantly downregulated the plunc expression in GD 15 fetuses.	Ethanol	15-22	BPI fold containing family A member 1	Homo sapiens	55-60
15513904-12	2004	Our results suggest that ethanol-induced FAS is due in part to the downregulation of plunc expression in the fetus, and this gene may be a candidate biological marker for FAS.	Ethanol	25-32	BPI fold containing family A member 1	Homo sapiens	85-90
12920053-6	2004	PLUNC was poorly soluble in water (50 microg/ml) or in 50 mM NaCl but was more soluble in 75% ethanol (> 380 microg/ml).	Water	28-33	BPI fold containing family A member 1	Homo sapiens	0-5
12920053-6	2004	PLUNC was poorly soluble in water (50 microg/ml) or in 50 mM NaCl but was more soluble in 75% ethanol (> 380 microg/ml).	Sodium Chloride	61-65	BPI fold containing family A member 1	Homo sapiens	0-5
12920053-6	2004	PLUNC was poorly soluble in water (50 microg/ml) or in 50 mM NaCl but was more soluble in 75% ethanol (> 380 microg/ml).	Ethanol	94-101	BPI fold containing family A member 1	Homo sapiens	0-5
12409287-2	2003	Using cDNA microarray, we identified a clone, DD4, that contains the cDNA of a novel gene, spurt (secretory protein in upper respiratory tracts) that was significantly induced by all-trans-retinoic acid in primary cultured human tracheobroncheal epithelia.	Tretinoin	179-202	BPI fold containing family A member 1	Homo sapiens	91-96
12409287-3	2003	Two alternatively spliced spurt transcripts of 1090 and 1035 base pairs exist that contain the same open reading frame expressing a 256-amino acid peptide.	amino acid peptide	136-154	BPI fold containing family A member 1	Homo sapiens	26-31
31302339-2	2019	SPX-101 is a novel, investigational small peptide (SPLUNC1 mimetic) that regulates ENaC density with the potential for efficacy without systemic effects.	spx-101	0-7	BPI fold containing family A member 1	Homo sapiens	51-58
31455163-3	2019	Here, we present a minimal mathematical model of ENaC, CFTR and ASL regulation that sheds light on the control of ENaC by the short palate lung and nasal epithelial clone 1 (SPLUNC1) protein and by phosphatidylinositol 4,5-biphosphate (PI(4,5)P2).	pi(4,5)p2	236-245	BPI fold containing family A member 1	Homo sapiens	174-181
29890087-5	2018	We hypothesized that CS alters SPLUNC1 activity, therefore contributing to ASL dehydration.	Cesium	21-23	BPI fold containing family A member 1	Homo sapiens	31-38
30190268-8	2018	Unlike SPLUNC1, the novel SPLUNC1-derived peptide SPX-101 resisted protease degradation, bound apically to HBECs, inhibited ENaC and prevented ASL dehydration following extended pre-incubation with CF sputum.Our data indicate that CF mucosal secretions drive ASL hyperabsorption and that protease-resistant peptides, e.g. SPX-101, can reverse this effect to rehydrate CF ASL.	spx-101	50-57	BPI fold containing family A member 1	Homo sapiens	26-33
29890087-6	2018	CS exposure caused irreversible SPLUNC1 aggregation and prevented SPLUNC1 from internalizing ENaC and maintaining ASL hydration.	Cesium	0-2	BPI fold containing family A member 1	Homo sapiens	32-39
29890087-6	2018	CS exposure caused irreversible SPLUNC1 aggregation and prevented SPLUNC1 from internalizing ENaC and maintaining ASL hydration.	Cesium	0-2	BPI fold containing family A member 1	Homo sapiens	66-73
29890087-7	2018	Proteomic analysis revealed alphabeta-unsaturated aldehyde modifications to SPLUNC1"s cysteine residues.	Aldehydes	50-58	BPI fold containing family A member 1	Homo sapiens	76-83
29890087-7	2018	Proteomic analysis revealed alphabeta-unsaturated aldehyde modifications to SPLUNC1"s cysteine residues.	Cysteine	86-94	BPI fold containing family A member 1	Homo sapiens	76-83
29890087-8	2018	Removal of these cysteines prevented SPLUNC1 from regulating ENaC/ASL volume.	Cysteine	17-26	BPI fold containing family A member 1	Homo sapiens	37-44
29890087-11	2018	These findings suggest that the CS-induced defects in SPLUNC1 can be circumvented, thus making SPX-101 a novel candidate for the treatment of mucus dehydration in COPD.	Cesium	32-34	BPI fold containing family A member 1	Homo sapiens	54-61
29890087-11	2018	These findings suggest that the CS-induced defects in SPLUNC1 can be circumvented, thus making SPX-101 a novel candidate for the treatment of mucus dehydration in COPD.	spx-101	95-102	BPI fold containing family A member 1	Homo sapiens	54-61
30996135-9	2019	BPIFA1 mRNA levels negatively correlated with serum IgE and fractional exhaled nitric oxide.	Nitric Oxide	79-91	BPI fold containing family A member 1	Homo sapiens	0-6
29295861-9	2018	Taken together, our data indicate that SPLUNC1 is an allosteric regulator of ENaC that dissociates alphabetagamma-ENaC to generate a new SPLUNC1-beta-ENaC complex.	alphabetagamma-enac	99-118	BPI fold containing family A member 1	Homo sapiens	39-46
29295861-9	2018	Taken together, our data indicate that SPLUNC1 is an allosteric regulator of ENaC that dissociates alphabetagamma-ENaC to generate a new SPLUNC1-beta-ENaC complex.	alphabetagamma-enac	99-118	BPI fold containing family A member 1	Homo sapiens	137-144
25223608-5	2014	Recombinant SPLUNC1 produced in HEK 293 cells harbored several molecular species of sphingomyelin and phosphatidylcholine as its ligands.	Sphingomyelins	84-97	BPI fold containing family A member 1	Homo sapiens	12-19
27145151-4	2016	Indeed, we find that mutation of just four leucine residues within this helical motif to alanine is sufficient to significantly inhibit the fluid spreading abilities of SPLUNC1, as well as its bacteriostatic actions against Gram-negative pathogens Burkholderia cenocepacia and Pseudomonas aeruginosa.	Leucine	43-50	BPI fold containing family A member 1	Homo sapiens	169-176
27145151-4	2016	Indeed, we find that mutation of just four leucine residues within this helical motif to alanine is sufficient to significantly inhibit the fluid spreading abilities of SPLUNC1, as well as its bacteriostatic actions against Gram-negative pathogens Burkholderia cenocepacia and Pseudomonas aeruginosa.	Alanine	89-96	BPI fold containing family A member 1	Homo sapiens	169-176
27145151-5	2016	Conformational flexibility in the body of SPLUNC1 is also involved in the bacteriostatic, surfactant, and LPS binding functions of the protein as revealed by disulfide mutants introduced into SPLUNC1.	Disulfides	158-167	BPI fold containing family A member 1	Homo sapiens	42-49
25223608-5	2014	Recombinant SPLUNC1 produced in HEK 293 cells harbored several molecular species of sphingomyelin and phosphatidylcholine as its ligands.	Phosphatidylcholines	102-121	BPI fold containing family A member 1	Homo sapiens	12-19
25223608-7	2014	Instead, one of the major and most important pulmonary surfactant phospholipids, dipalmitoylphosphatidylcholine (DPPC), bound to SPLUNC1 with high affinity and specificity.	Phospholipids	66-79	BPI fold containing family A member 1	Homo sapiens	129-136
25223608-7	2014	Instead, one of the major and most important pulmonary surfactant phospholipids, dipalmitoylphosphatidylcholine (DPPC), bound to SPLUNC1 with high affinity and specificity.	1,2-Dipalmitoylphosphatidylcholine	81-111	BPI fold containing family A member 1	Homo sapiens	129-136
25223608-7	2014	Instead, one of the major and most important pulmonary surfactant phospholipids, dipalmitoylphosphatidylcholine (DPPC), bound to SPLUNC1 with high affinity and specificity.	1,2-Dipalmitoylphosphatidylcholine	113-117	BPI fold containing family A member 1	Homo sapiens	129-136
25161098-0	2014	SPLUNC1 is associated with nasopharyngeal carcinoma prognosis and plays an important role in all-trans-retinoic acid-induced growth inhibition and differentiation in nasopharyngeal cancer cells.	2-octenal	97-103	BPI fold containing family A member 1	Homo sapiens	0-7
25161098-0	2014	SPLUNC1 is associated with nasopharyngeal carcinoma prognosis and plays an important role in all-trans-retinoic acid-induced growth inhibition and differentiation in nasopharyngeal cancer cells.	Tretinoin	103-116	BPI fold containing family A member 1	Homo sapiens	0-7
25161098-6	2014	A cDNA micro-array analyzed by significant analysis of micro-array (SAM) and ingenuity pathway analysis (IPA) revealed that an indirect interaction existed between SPLUNC1 and retinoic acid (RA) in the cancer regulatory network.	Tretinoin	176-189	BPI fold containing family A member 1	Homo sapiens	164-171
25161098-6	2014	A cDNA micro-array analyzed by significant analysis of micro-array (SAM) and ingenuity pathway analysis (IPA) revealed that an indirect interaction existed between SPLUNC1 and retinoic acid (RA) in the cancer regulatory network.	Tretinoin	191-193	BPI fold containing family A member 1	Homo sapiens	164-171
25161098-8	2014	The transcriptional activity of the SPLUNC1 promoter was up-regulated significantly by all-trans-retinoic acid (ATRA).	Tretinoin	87-110	BPI fold containing family A member 1	Homo sapiens	36-43
25161098-8	2014	The transcriptional activity of the SPLUNC1 promoter was up-regulated significantly by all-trans-retinoic acid (ATRA).	Tretinoin	112-116	BPI fold containing family A member 1	Homo sapiens	36-43
25161098-12	2014	Under SPLUNC1 knockdown conditions, differentiation was reversed by ATRA treatment.	Tretinoin	68-72	BPI fold containing family A member 1	Homo sapiens	6-13