PMID-sentid Pub_year Sent_text comp_official_name comp_offset protein_name organism prot_offset 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 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 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. 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 29890087-5 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 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 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 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