PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
2627938-0	1989	The interaction of a lung surfactant protein (SP-A) with macrophages is mannose dependent.	Mannose	72-79	surfactant protein A1	Homo sapiens	46-50
2627938-6	1989	Two mannose-dependent recognition mechanisms might mediate SP-A uptake by macrophages.	Mannose	4-11	surfactant protein A1	Homo sapiens	59-63
2627938-7	1989	First, as SP-A is a glycoprotein with N-glycosylated glycans it could act as a ligand for the mannose-specific receptor on macrophages.	Polysaccharides	53-60	surfactant protein A1	Homo sapiens	10-14
2627938-8	1989	Second, as SP-A is a mannose-specific lectin itself it could bind to mannose residues on the macrophage"s cell surface.	Mannose	21-28	surfactant protein A1	Homo sapiens	11-15
2627938-8	1989	Second, as SP-A is a mannose-specific lectin itself it could bind to mannose residues on the macrophage"s cell surface.	Mannose	69-76	surfactant protein A1	Homo sapiens	11-15
2788165-3	1989	Because SP-A enhances the endocytosis of phospholipids by alveolar type II cells and alveolar macrophages, we examined whether these two molecules were functionally interchangeable.	Phospholipids	41-54	surfactant protein A1	Homo sapiens	8-12
15493255-5	1989	These results suggest a similar binding site on human IgG for SPA and the HSV-1 Fc receptor with involvement of the amino acid residues Tyr and His but not Lys.	Tyrosine	136-139	surfactant protein A1	Homo sapiens	62-65
2544593-2	1989	We previously observed that dexamethasone had a biphasic effect on the levels of mRNA encoding the major surfactant protein (SP-A) in human fetal lung in vitro; at concentrations of 10(-10) and 10(-9) M, dexamethasone caused an increase in the levels of SP-A mRNA, whereas at concentrations of greater than 10(-8) M, the steroid had a pronounced inhibitory effect on SP-A mRNA levels.	Dexamethasone	28-41	surfactant protein A1	Homo sapiens	125-129
2544593-2	1989	We previously observed that dexamethasone had a biphasic effect on the levels of mRNA encoding the major surfactant protein (SP-A) in human fetal lung in vitro; at concentrations of 10(-10) and 10(-9) M, dexamethasone caused an increase in the levels of SP-A mRNA, whereas at concentrations of greater than 10(-8) M, the steroid had a pronounced inhibitory effect on SP-A mRNA levels.	Dexamethasone	28-41	surfactant protein A1	Homo sapiens	254-258
2544593-2	1989	We previously observed that dexamethasone had a biphasic effect on the levels of mRNA encoding the major surfactant protein (SP-A) in human fetal lung in vitro; at concentrations of 10(-10) and 10(-9) M, dexamethasone caused an increase in the levels of SP-A mRNA, whereas at concentrations of greater than 10(-8) M, the steroid had a pronounced inhibitory effect on SP-A mRNA levels.	Dexamethasone	28-41	surfactant protein A1	Homo sapiens	254-258
2544593-2	1989	We previously observed that dexamethasone had a biphasic effect on the levels of mRNA encoding the major surfactant protein (SP-A) in human fetal lung in vitro; at concentrations of 10(-10) and 10(-9) M, dexamethasone caused an increase in the levels of SP-A mRNA, whereas at concentrations of greater than 10(-8) M, the steroid had a pronounced inhibitory effect on SP-A mRNA levels.	Dexamethasone	204-217	surfactant protein A1	Homo sapiens	125-129
2544593-2	1989	We previously observed that dexamethasone had a biphasic effect on the levels of mRNA encoding the major surfactant protein (SP-A) in human fetal lung in vitro; at concentrations of 10(-10) and 10(-9) M, dexamethasone caused an increase in the levels of SP-A mRNA, whereas at concentrations of greater than 10(-8) M, the steroid had a pronounced inhibitory effect on SP-A mRNA levels.	Steroids	321-328	surfactant protein A1	Homo sapiens	125-129
2544593-3	1989	It was also found that dexamethasone antagonized the stimulatory effect of dibutyryl cyclic AMP (Bt2cAMP) on SP-A mRNA levels in human fetal lung in vitro.	Dexamethasone	23-36	surfactant protein A1	Homo sapiens	109-113
2544593-3	1989	It was also found that dexamethasone antagonized the stimulatory effect of dibutyryl cyclic AMP (Bt2cAMP) on SP-A mRNA levels in human fetal lung in vitro.	Bucladesine	75-95	surfactant protein A1	Homo sapiens	109-113
2544593-3	1989	It was also found that dexamethasone antagonized the stimulatory effect of dibutyryl cyclic AMP (Bt2cAMP) on SP-A mRNA levels in human fetal lung in vitro.	Bucladesine	97-104	surfactant protein A1	Homo sapiens	109-113
2544593-4	1989	It was our objective, in the present study, to characterize further the effects of dexamethasone and Bt2cAMP on SP-A mRNA levels in human fetal lung tissue and to determine whether such effects are associated with comparable changes in the transcriptional activity of the SP-A gene.	Dexamethasone	83-96	surfactant protein A1	Homo sapiens	112-116
2544593-5	1989	We found that the action of dexamethasone (10(-7) M) to reduce the levels of SP-A mRNA in control and Bt2cAMP-treated fetal lung explants was evident within 2 h of its addition to the culture medium; SP-A mRNA was reduced to barely detectable levels in control and in Bt2cAMP-treated tissues after 24 h of dexamethasone treatment.	Dexamethasone	28-41	surfactant protein A1	Homo sapiens	77-81
2544593-5	1989	We found that the action of dexamethasone (10(-7) M) to reduce the levels of SP-A mRNA in control and Bt2cAMP-treated fetal lung explants was evident within 2 h of its addition to the culture medium; SP-A mRNA was reduced to barely detectable levels in control and in Bt2cAMP-treated tissues after 24 h of dexamethasone treatment.	Dexamethasone	28-41	surfactant protein A1	Homo sapiens	200-204
2544593-5	1989	We found that the action of dexamethasone (10(-7) M) to reduce the levels of SP-A mRNA in control and Bt2cAMP-treated fetal lung explants was evident within 2 h of its addition to the culture medium; SP-A mRNA was reduced to barely detectable levels in control and in Bt2cAMP-treated tissues after 24 h of dexamethasone treatment.	Dexamethasone	306-319	surfactant protein A1	Homo sapiens	77-81
2544593-6	1989	The action of dexamethasone to reduce SP-A mRNA levels was not prevented by co-incubation with either actinomycin D or cycloheximide.	Dexamethasone	14-27	surfactant protein A1	Homo sapiens	38-42
2544593-7	1989	In contrast to its dose-related biphasic effects on the levels of SP-A mRNA, we found that dexamethasone caused a dose-dependent stimulation of SP-A gene transcription.	Dexamethasone	91-104	surfactant protein A1	Homo sapiens	144-148
2495325-6	1989	Similarly, polyclonal IgM fractionated on a SPA-Sepharose CL4B column showed nearly complete partition of VHIII molecules into the SPA-binding fraction, and VHI and VHII subgroup proteins into the fall-through.	Sepharose CL 4B	48-62	surfactant protein A1	Homo sapiens	44-47
15493255-5	1989	These results suggest a similar binding site on human IgG for SPA and the HSV-1 Fc receptor with involvement of the amino acid residues Tyr and His but not Lys.	Histidine	144-147	surfactant protein A1	Homo sapiens	62-65
3382698-2	1988	SP-A was detected by immunoblot analysis, ELISA assay and by [35S]methionine labelling of the cells.	Sulfur-35	62-65	surfactant protein A1	Homo sapiens	0-4
3194412-4	1988	The time course of response to dexamethasone was biphasic, with early stimulation and later inhibition of SP-A accumulation.	Dexamethasone	31-44	surfactant protein A1	Homo sapiens	106-110
3194412-5	1988	Maximal induction of SP-A occurred with 3-10 nM dexamethasone and approximately 300 nM cortisol for 72 hr, and stimulation diminished at higher concentrations.	Dexamethasone	48-61	surfactant protein A1	Homo sapiens	21-25
3194412-6	1988	SP-A mRNA accumulation was maximally stimulated at 24-48 hr of exposure to dexamethasone (10 nM) and was generally inhibited by 4-6 days.	Dexamethasone	75-88	surfactant protein A1	Homo sapiens	0-4
3194412-9	1988	The content of SP-A and its mRNA was also increased by dibromo-cAMP, terbutaline, and forskolin, and effects were approximately additive with those of dexamethasone.	dibromo-camp	55-67	surfactant protein A1	Homo sapiens	15-19
3194412-9	1988	The content of SP-A and its mRNA was also increased by dibromo-cAMP, terbutaline, and forskolin, and effects were approximately additive with those of dexamethasone.	Terbutaline	69-80	surfactant protein A1	Homo sapiens	15-19
3194412-9	1988	The content of SP-A and its mRNA was also increased by dibromo-cAMP, terbutaline, and forskolin, and effects were approximately additive with those of dexamethasone.	Colforsin	86-95	surfactant protein A1	Homo sapiens	15-19
3194412-9	1988	The content of SP-A and its mRNA was also increased by dibromo-cAMP, terbutaline, and forskolin, and effects were approximately additive with those of dexamethasone.	Dexamethasone	151-164	surfactant protein A1	Homo sapiens	15-19
2464382-11	1988	The substance P analogue, [D-Pro4,D-Trp7,9,10] SP4-11 (SPA), not only reduced substance P-induced histamine release in a concentration-related manner but also inhibited that induced by VIP, somatostatin, compound 48/80, poly-L-lysine and morphine but not anti-IgE.	[d-pro4,d-trp7,9,10] sp4-11	26-53	surfactant protein A1	Homo sapiens	55-58
2464382-11	1988	The substance P analogue, [D-Pro4,D-Trp7,9,10] SP4-11 (SPA), not only reduced substance P-induced histamine release in a concentration-related manner but also inhibited that induced by VIP, somatostatin, compound 48/80, poly-L-lysine and morphine but not anti-IgE.	Histamine	98-107	surfactant protein A1	Homo sapiens	55-58
2464382-11	1988	The substance P analogue, [D-Pro4,D-Trp7,9,10] SP4-11 (SPA), not only reduced substance P-induced histamine release in a concentration-related manner but also inhibited that induced by VIP, somatostatin, compound 48/80, poly-L-lysine and morphine but not anti-IgE.	Lysine	220-233	surfactant protein A1	Homo sapiens	55-58
2464382-11	1988	The substance P analogue, [D-Pro4,D-Trp7,9,10] SP4-11 (SPA), not only reduced substance P-induced histamine release in a concentration-related manner but also inhibited that induced by VIP, somatostatin, compound 48/80, poly-L-lysine and morphine but not anti-IgE.	Morphine	238-246	surfactant protein A1	Homo sapiens	55-58
3382694-8	1988	Synthesis of SP-A, as measured by [35S]methionine labeling and immunoprecipitation, was detectable on day 1 but not thereafter.	Sulfur-35	35-38	surfactant protein A1	Homo sapiens	13-17
3382694-8	1988	Synthesis of SP-A, as measured by [35S]methionine labeling and immunoprecipitation, was detectable on day 1 but not thereafter.	Methionine	39-49	surfactant protein A1	Homo sapiens	13-17
3382694-9	1988	Levels of mRNAs for SP-A and for the two lipophilic surfactant proteins SP-B (18 kDa) and SP-C (5 kDa) fell with half-times of maximally 24 h. In contrast, total protein synthesis measured by [35S]methionine incorporation increased and then plateaued.	Methionine	197-207	surfactant protein A1	Homo sapiens	20-24
3205630-3	1988	Amniotic fluid SP-A concentrations increased as a function of gestational age, from less than 3 micrograms/ml at 30-31 wk to 24 micrograms/ml at 40-41 wk, and were positively correlated with the lecithin to sphingomyelin ratio (p less than 0.01).	Lecithins	195-203	surfactant protein A1	Homo sapiens	15-19
3205630-3	1988	Amniotic fluid SP-A concentrations increased as a function of gestational age, from less than 3 micrograms/ml at 30-31 wk to 24 micrograms/ml at 40-41 wk, and were positively correlated with the lecithin to sphingomyelin ratio (p less than 0.01).	Sphingomyelins	207-220	surfactant protein A1	Homo sapiens	15-19
3382698-2	1988	SP-A was detected by immunoblot analysis, ELISA assay and by [35S]methionine labelling of the cells.	Methionine	66-76	surfactant protein A1	Homo sapiens	0-4
3382698-3	1988	SP-A was secreted into the media as an endoglycosidase F sensitive glycoprotein which co-migrated with the isoforms of SP-A identified in human lavage fluid by 2D-IEF-SDS-PAGE.	Sodium Dodecyl Sulfate	167-170	surfactant protein A1	Homo sapiens	0-4
3382698-3	1988	SP-A was secreted into the media as an endoglycosidase F sensitive glycoprotein which co-migrated with the isoforms of SP-A identified in human lavage fluid by 2D-IEF-SDS-PAGE.	Sodium Dodecyl Sulfate	167-170	surfactant protein A1	Homo sapiens	119-123
3382698-5	1988	SP-A RNA and protein content were markedly inhibited by dexamethasone in a dose-dependent fashion.	Dexamethasone	56-69	surfactant protein A1	Homo sapiens	0-4
3732535-7	1986	Exposure to DMSO but not VS1 reduced hSPA values.	Dimethyl Sulfoxide	12-16	surfactant protein A1	Homo sapiens	37-41
3024480-7	1986	Thus, when fluorescein isothiocyanate conjugated (FITC) SPA was used as conjugate instead of FITC antibody to human IgG, true HSV-1 antibody-containing sera remained positive, but the false positives identified in the commercial IFA kits did not.	Fluorescein-5-isothiocyanate	11-37	surfactant protein A1	Homo sapiens	56-59
3024480-7	1986	Thus, when fluorescein isothiocyanate conjugated (FITC) SPA was used as conjugate instead of FITC antibody to human IgG, true HSV-1 antibody-containing sera remained positive, but the false positives identified in the commercial IFA kits did not.	Fluorescein-5-isothiocyanate	50-54	surfactant protein A1	Homo sapiens	56-59
2419771-2	1985	The release of histamine induced by these neuropeptides was inhibited by preincubation of the cells with the SP analogue [D-Pro4,D-Trp7,9,10]-SP4-11 (SP-A) (10 microM), and also by benzalkonium chloride (10 microM).	d-trp7,9,10]-sp4-11	129-148	surfactant protein A1	Homo sapiens	150-154
3520164-3	1986	In 4 patients with acute leukemia, a plasma volume of 1500 cm3 was passed in an ex-vivo system over immobilized SpA-Sepharose and then reinfused.	Sepharose	116-125	surfactant protein A1	Homo sapiens	112-115
2419771-2	1985	The release of histamine induced by these neuropeptides was inhibited by preincubation of the cells with the SP analogue [D-Pro4,D-Trp7,9,10]-SP4-11 (SP-A) (10 microM), and also by benzalkonium chloride (10 microM).	Benzalkonium Compounds	181-202	surfactant protein A1	Homo sapiens	150-154
2419771-2	1985	The release of histamine induced by these neuropeptides was inhibited by preincubation of the cells with the SP analogue [D-Pro4,D-Trp7,9,10]-SP4-11 (SP-A) (10 microM), and also by benzalkonium chloride (10 microM).	Histamine	15-24	surfactant protein A1	Homo sapiens	150-154
2419771-2	1985	The release of histamine induced by these neuropeptides was inhibited by preincubation of the cells with the SP analogue [D-Pro4,D-Trp7,9,10]-SP4-11 (SP-A) (10 microM), and also by benzalkonium chloride (10 microM).	d-pro4	122-128	surfactant protein A1	Homo sapiens	150-154
2419771-3	1985	In addition, SP-A inhibited histamine release induced by compound 48/80, whilst that induced by goat anti-(rat-IgE) was unaffected.	Histamine	28-37	surfactant protein A1	Homo sapiens	13-17
6333685-3	1984	In response to SpA, the [3H]thymidine uptake of PBM-E+ was reduced by 80% compared to PBM.	Tritium	25-27	surfactant protein A1	Homo sapiens	15-18
6333685-3	1984	In response to SpA, the [3H]thymidine uptake of PBM-E+ was reduced by 80% compared to PBM.	Thymidine	28-37	surfactant protein A1	Homo sapiens	15-18
6333685-3	1984	In response to SpA, the [3H]thymidine uptake of PBM-E+ was reduced by 80% compared to PBM.	pbm-e+	48-54	surfactant protein A1	Homo sapiens	15-18
6333685-3	1984	In response to SpA, the [3H]thymidine uptake of PBM-E+ was reduced by 80% compared to PBM.	pbm	48-51	surfactant protein A1	Homo sapiens	15-18
6440856-1	1984	The protein A-binding site of human IgM was studied by affinity chromatography on SpA-Sepharose using fragments derived from a human monoclonal SpA-reactive IgM, Iz.	Sepharose	86-95	surfactant protein A1	Homo sapiens	82-85
6440856-6	1984	Thus, the principal requirement for SpA reactivity with IgM Iz seems to be related to the presence of Fabmu regions in a polymeric state resembling native IgM.	fabmu	102-107	surfactant protein A1	Homo sapiens	36-39
6868334-4	1983	The cells are then washed and incubated with 125Iodine-labeled SpA (125I-SpA).	Iodine-125	45-54	surfactant protein A1	Homo sapiens	63-66
6604091-4	1983	The inhibition occurred if monocytes were treated with ammonium chloride and chloroquine for 1.5 hr, starting only 30 min after exposure to the stimulants, whereas only minimal inhibition occurred when monocytes were treated with the two lysosomotropic compounds 2 hr after pulsing with SLO or SpA.	Ammonium Chloride	55-72	surfactant protein A1	Homo sapiens	294-297
6604091-4	1983	The inhibition occurred if monocytes were treated with ammonium chloride and chloroquine for 1.5 hr, starting only 30 min after exposure to the stimulants, whereas only minimal inhibition occurred when monocytes were treated with the two lysosomotropic compounds 2 hr after pulsing with SLO or SpA.	Chloroquine	77-88	surfactant protein A1	Homo sapiens	294-297
6602061-5	1983	Two-mercaptoethanol significantly enhanced the number of T-cell colonies when PWM, Con A, or SPA, but not PHA, were added as mitogens.	two-mercaptoethanol	0-19	surfactant protein A1	Homo sapiens	93-96
6603411-3	1983	Passage of SPA255-26 placental cells in medium containing retinoic acid induced a stable altered phenotype characterized by elevated levels of HCG and PS beta G and a reduced level of HCG alpha.	Tretinoin	58-71	surfactant protein A1	Homo sapiens	11-14
6868334-4	1983	The cells are then washed and incubated with 125Iodine-labeled SpA (125I-SpA).	Iodine-125	45-54	surfactant protein A1	Homo sapiens	73-76
6757889-7	1982	SPA adsorption greatly increased the specificity of routine RHI and TFA tests in the diagnosis of congenital rubella and toxoplasmosis.	Trifluoroacetic Acid	68-71	surfactant protein A1	Homo sapiens	0-3
18962558-0	1979	Metal chelates of phosphonate-containing ligands-II: stability constants of some beta-styrylphosphonic acid metal chelates.	Metals	0-5	surfactant protein A1	Homo sapiens	81-107
6972936-4	1981	Methylprednisolone (MP) at concentrations as low as 10-7 M inhibited NIF-T activity from peripheral blood lymphocytes (PBL) in response to staphylococcal protein A (SPA) and concanavalin A (Con A).	Methylprednisolone	0-18	surfactant protein A1	Homo sapiens	139-163
6972936-4	1981	Methylprednisolone (MP) at concentrations as low as 10-7 M inhibited NIF-T activity from peripheral blood lymphocytes (PBL) in response to staphylococcal protein A (SPA) and concanavalin A (Con A).	Methylprednisolone	0-18	surfactant protein A1	Homo sapiens	165-168
6972936-4	1981	Methylprednisolone (MP) at concentrations as low as 10-7 M inhibited NIF-T activity from peripheral blood lymphocytes (PBL) in response to staphylococcal protein A (SPA) and concanavalin A (Con A).	Methylprednisolone	20-22	surfactant protein A1	Homo sapiens	139-163
6972936-4	1981	Methylprednisolone (MP) at concentrations as low as 10-7 M inhibited NIF-T activity from peripheral blood lymphocytes (PBL) in response to staphylococcal protein A (SPA) and concanavalin A (Con A).	Methylprednisolone	20-22	surfactant protein A1	Homo sapiens	165-168
6252344-11	1980	When dexamethasone-treated and untreated GR cells were compared, measurements of gp52-specific SPA binding indicated that dexamethasone stimulation leads to a 12.2-fold increase in the amount of cell surface gp52 detected.	Dexamethasone	122-135	surfactant protein A1	Homo sapiens	95-98
15612263-2	1980	In the present study, SpA coupled to either fluorescein isothiocyanate (FITC) or peroxidase was used in place of antisera to IgG for the fluorescent antibody (FA) techniques and the enzyme linked immunoassay (ELISA).	Fluorescein-5-isothiocyanate	44-70	surfactant protein A1	Homo sapiens	22-25
15612263-2	1980	In the present study, SpA coupled to either fluorescein isothiocyanate (FITC) or peroxidase was used in place of antisera to IgG for the fluorescent antibody (FA) techniques and the enzyme linked immunoassay (ELISA).	Fluorescein-5-isothiocyanate	72-76	surfactant protein A1	Homo sapiens	22-25
389311-4	1979	Fluorescein-labeled SPA, in turn is useful in monitoring the functional consequences of antibody attachment to the surface of polymorphonuclear leukocytes (PMN).	Fluorescein	0-11	surfactant protein A1	Homo sapiens	20-23
6967091-6	1980	STA, treated to prevent the leakage of soluble SpA during culture, exclusively stimulated non-T cells: the responding cell population was characterized to be E-rosette negative but positive for C3 receptors, surface Ia, a receptor for STA itself, and likely carried surface immunoglobulin.	sta	0-3	surfactant protein A1	Homo sapiens	47-50
18962558-0	1979	Metal chelates of phosphonate-containing ligands-II: stability constants of some beta-styrylphosphonic acid metal chelates.	Organophosphonates	18-29	surfactant protein A1	Homo sapiens	81-107
18962558-5	1979	The stability constants of the complexes formed between SPA and the bivalent Mg, Ca, Ba, Co, Ni and Pd ions at 25 degrees and ionic strength of 0.12M KNO(3) were also determined.	Magnesium	77-79	surfactant protein A1	Homo sapiens	56-59
18962558-5	1979	The stability constants of the complexes formed between SPA and the bivalent Mg, Ca, Ba, Co, Ni and Pd ions at 25 degrees and ionic strength of 0.12M KNO(3) were also determined.	Barium	85-87	surfactant protein A1	Homo sapiens	56-59
18962558-5	1979	The stability constants of the complexes formed between SPA and the bivalent Mg, Ca, Ba, Co, Ni and Pd ions at 25 degrees and ionic strength of 0.12M KNO(3) were also determined.	Cobalt	89-91	surfactant protein A1	Homo sapiens	56-59
18962558-5	1979	The stability constants of the complexes formed between SPA and the bivalent Mg, Ca, Ba, Co, Ni and Pd ions at 25 degrees and ionic strength of 0.12M KNO(3) were also determined.	Palladium	100-102	surfactant protein A1	Homo sapiens	56-59
308929-6	1978	The low response of highly purified peripheral blood T lymphocytes to soluble SPA could be potentiated by the addition of autologous mitomycin-treated B cells, whereas the unresponsiveness of purified T lymphocytes to StaCw was not affected.	Mitomycin	133-142	surfactant protein A1	Homo sapiens	78-81
756721-2	1978	The efficacy and tolerance of mepartricin sodium lauryl sulphate (SPA-S-222) was evaluated in patients with vaginal trichomoniasis and/or moniliasis.	mepartricin sodium lauryl sulphate	30-64	surfactant protein A1	Homo sapiens	66-69
110884-4	1979	The amount of antibody specifically bound to the cells is quantitated by the addition of 125I-labeled SpA.	Iodine-125	89-93	surfactant protein A1	Homo sapiens	102-105
308929-7	1978	Mitogenic activity of SPA coupled to Sepharose beads was different from that of soluble SPA and paralleled that of StaCw.	Sepharose	37-46	surfactant protein A1	Homo sapiens	22-25
62807-1	1976	Fluorescein-conjugated staphylococcal protein A (SPA) was complexed with either: 1) heat-aggregated IgG, 2) B cell specific antibody, or 3) T cell specific antibody and then used for an immunofluorescent analysis of mononuclear cell surfaces.	Fluorescein	0-11	surfactant protein A1	Homo sapiens	23-47
62807-1	1976	Fluorescein-conjugated staphylococcal protein A (SPA) was complexed with either: 1) heat-aggregated IgG, 2) B cell specific antibody, or 3) T cell specific antibody and then used for an immunofluorescent analysis of mononuclear cell surfaces.	Fluorescein	0-11	surfactant protein A1	Homo sapiens	49-52
1090679-0	1975	Demonstration and assaying of IgG antibodies in tissues and on cells by labeled staphylococcal protein A. Staphylococcal protein  A (SpA) labeled with FITC was used to detect IgG antibodies to tissue and cell surface antigens.	Fluorescein-5-isothiocyanate	151-155	surfactant protein A1	Homo sapiens	133-136
32736039-5	2020	Among the total 446 ST and 82 SPA isolates, fluoroquinolone (FQ) resistance was very common in both serovars.	Fluoroquinolones	44-59	surfactant protein A1	Homo sapiens	30-33
4826374-0	1974	[Sesquiterpene lactones of Vernonia sp.--a new group of biologically active compounds (author"s transl)].	sesquiterpene lactones	1-23	surfactant protein A1	Homo sapiens	36-42
33159796-1	2021	OBJECTIVES: To evaluate the efficacy and safety of a step-down regimen of oral prednisolone over 24 weeks in patients of axial SpA (axSpA).	Prednisolone	79-91	surfactant protein A1	Homo sapiens	127-130
33572664-2	2021	This work discusses the experimental and computational evaluation of chloranilic acid (CLA) as a universal chromogenic reagent for developing a novel 96-microwell spectrophotometric assay (MW-SPA) for TKIs.	chloranilic acid	69-85	surfactant protein A1	Homo sapiens	192-195
33572664-2	2021	This work discusses the experimental and computational evaluation of chloranilic acid (CLA) as a universal chromogenic reagent for developing a novel 96-microwell spectrophotometric assay (MW-SPA) for TKIs.	chloranilic acid	87-90	surfactant protein A1	Homo sapiens	192-195
33453722-3	2021	The aim of this study was to investigate the role of LMR in axial SpA diagnosis, disease activity classification and sacroiliitis staging.	lmr	53-56	surfactant protein A1	Homo sapiens	66-69
33419485-11	2021	A statistically significant linear relationship was noted between SP-A1 and DA ratio in all three groups.	amsonic acid	76-78	surfactant protein A1	Homo sapiens	66-71
32780286-13	2021	Moreover, novel non-ROS-related proteins were part of these forming functional hybrids, such as the NOX5/sGC, NOX1,2/NOS2, NRF2/ENC-1 and MPO/SP-A modules.	Reactive Oxygen Species	20-23	surfactant protein A1	Homo sapiens	142-146
33256760-10	2020	Pirfenidone treatment reduced the decline in VC with statistical significance in the low SP-D and low SP-A subgroups over most of the treatment period, and also prolonged PFS in the low SP-D and low KL-6 subgroups.	pirfenidone	0-11	surfactant protein A1	Homo sapiens	102-106
33378911-4	2020	The Six-Sigma-based quality-level and its connection with the process yield are introduced in the capability zone of Spa-PCAC to check if the process capabilities can meet the requirements.	pcac	121-125	surfactant protein A1	Homo sapiens	117-120
33955239-5	2021	Results: The study included 60 RA and 269 ax-SpA patients.	Amoxicillin	42-44	surfactant protein A1	Homo sapiens	45-48
33955239-6	2021	At month 24, the retention rates were 67.2 and 57.1% (biologic-naive and biologic-experienced RA) and 74.8 and 80.4% (anti-TNF-naive and -experienced ax-SpA).	Amoxicillin	150-152	surfactant protein A1	Homo sapiens	153-156
33119787-6	2021	Dexmedetomidine was prescribed by 70% of the respondents (ESPA 53%; SPANZA 69%; APAGBI 34% and SPA 96%), mostly for procedural sedation (68%), premedication (46%) and/or ICU sedation (46%).	Dexmedetomidine	0-15	surfactant protein A1	Homo sapiens	59-62
33119787-8	2021	The main difference in dexmedetomidine use concerned the age of patients (SPA primarily < 1 year, others primarily > 1 year).	Dexmedetomidine	23-38	surfactant protein A1	Homo sapiens	74-77
33706528-4	2021	Furthermore, the unique characteristics of cs-IgG such as passive toward SpA adsorption and exposure of the multivalence state at nonspecific binding conditions was revealed spectroscopically.	Cesium	37-39	surfactant protein A1	Homo sapiens	73-76
33428425-7	2021	Using these parameters, IS-SPA accounts for asymmetry of charge solvation and reproduces the explicit solvent potential of mean force of dimerization of two oppositely charged Lennard-Jones spheres in chloroform with high fidelity.	Chloroform	201-211	surfactant protein A1	Homo sapiens	27-30
33343935-9	2020	The negative association between SP-A1 and Ks was found in mild, moderate, and severe keratoconus eyes (r mild = -0.171, r moderate = -0.317, r severe = -0.288, all P < 0.05).	Potassium	43-45	surfactant protein A1	Homo sapiens	33-38
33245936-13	2021	Furthermore, a higher SP-A1 was associated with a greater risk of visual field progression (P=0.002), synergistic with thinner CCT (P=0.010).	cct	127-130	surfactant protein A1	Homo sapiens	22-27
32933785-0	2020	Corrigendum to "Adverse impact of ambient PM2.5 on expression and trafficking of surfactant protein A through reactive oxygen species damage to lamellar bodies" [Toxicology Letters 315 (2019) 47-54].	Reactive Oxygen Species	110-133	surfactant protein A1	Homo sapiens	81-101
32736039-5	2020	Among the total 446 ST and 82 SPA isolates, fluoroquinolone (FQ) resistance was very common in both serovars.	Fluoroquinolones	61-63	surfactant protein A1	Homo sapiens	30-33
32736039-6	2020	Ciprofloxacin resistance of 24.9% and 9.8% & ofloxacin resistance of 20.9% and 87.8% were found in ST and SPA respectively.	Ciprofloxacin	0-13	surfactant protein A1	Homo sapiens	106-109
32736039-6	2020	Ciprofloxacin resistance of 24.9% and 9.8% & ofloxacin resistance of 20.9% and 87.8% were found in ST and SPA respectively.	Ofloxacin	4-13	surfactant protein A1	Homo sapiens	106-109
32736039-8	2020	A single point mutation in gyrA gene (S83F) was responsible for causing DCS in 37.5% (n = 42/112) ST and 63% (n = 46/73) SPA isolates.	gyra	27-31	surfactant protein A1	Homo sapiens	121-124
32747360-10	2020	Chlorhexidine MICs decreased (P < 0.001 for trend) in association with a decline in frequency of the qacA/B gene that was related to reductions in specific spa types.Conclusions: The incidence of MRSAB in ICUs has decreased dramatically over time, but most of the microbiological and genotypic characteristics of MRSA isolates have not changed.	Chlorhexidine	0-13	surfactant protein A1	Homo sapiens	156-159
32428691-4	2020	Data to be collected at the initial systematic review comprised 5 patient"s self-administered questionnaires, 3 variables of the physician"s interview, 2 variables of the physical examination, 2 variables of the specific ax-SpA imaging and 2 other investigations.	Amoxicillin	221-223	surfactant protein A1	Homo sapiens	224-227
32428691-6	2020	CONCLUSIONS: Using an evidence-based and an expert consensus approaches, this initiative defined a core set of variables to be collected and reported right after the diagnosis and during follow-up of patients with ax-SpA in daily practice.	Amoxicillin	214-216	surfactant protein A1	Homo sapiens	217-220
32126674-0	2020	Antibacterial Effect of Silver Nanomaterials on Staphylococcal Protein A by Molecular Dynamics Simulation.	Silver	24-30	surfactant protein A1	Homo sapiens	48-72
32639871-3	2020	SP-A is involved in phospholipid absorption.	Phospholipids	20-32	surfactant protein A1	Homo sapiens	0-4
32861238-7	2020	ASA-positive seminal fluid exhibited significant increases in the mean migration distance (2.6 +- 1.4 cm vs. 1.54 +- 1.1 cm, respectively; p< 0.001) and sperm concentration (174 +- 121.0 x 103/mL vs. 101 +- 93.7 x 103/mL, respectively; p= 0.033) after treatment with SPA compared to pre-treated samples.	Aspirin	0-3	surfactant protein A1	Homo sapiens	267-270
32856796-9	2020	In addition, SP-A was also increased by Phe and Flu, while it was decreased by their mixture at 600 muM.	phenanthrene	40-43	surfactant protein A1	Homo sapiens	13-17
32856796-9	2020	In addition, SP-A was also increased by Phe and Flu, while it was decreased by their mixture at 600 muM.	fluorene	48-51	surfactant protein A1	Homo sapiens	13-17
32126674-8	2020	Finally, it was found that the average amount of hydrogen bond in SPA was reduced in the presence of Ag which was origin of antimicrobial activity of Ag.	Hydrogen	49-57	surfactant protein A1	Homo sapiens	66-69
33029079-1	2020	1"-(2-Acryloxyethyl)-3,3"-dimethyl-6-nitrospiro[2 H-1-benzopyran-2,2"-indoline] (SPA) was synthesized and grafted onto a water-soluble carboxymethyl chitin (CMCH) macromolecule to prepare a photochromic copolymer (CMCH-g-SPA).	1"-(2-acryloxyethyl)-3,3"-dimethyl-6-nitrospiro[2 h-1-benzopyran-2,2"-indoline]	0-79	surfactant protein A1	Homo sapiens	81-84
33029079-1	2020	1"-(2-Acryloxyethyl)-3,3"-dimethyl-6-nitrospiro[2 H-1-benzopyran-2,2"-indoline] (SPA) was synthesized and grafted onto a water-soluble carboxymethyl chitin (CMCH) macromolecule to prepare a photochromic copolymer (CMCH-g-SPA).	1"-(2-acryloxyethyl)-3,3"-dimethyl-6-nitrospiro[2 h-1-benzopyran-2,2"-indoline]	0-79	surfactant protein A1	Homo sapiens	221-224
32001339-6	2020	Here it is demonstrated that non-SpA binding Nbs can be mutagenized for purification by SpA affinity chromatography and that these Nb variants retain their thermostability and antigen affinity, while biodistribution remains unaffected.	Niobium	45-47	surfactant protein A1	Homo sapiens	33-36
32001339-6	2020	Here it is demonstrated that non-SpA binding Nbs can be mutagenized for purification by SpA affinity chromatography and that these Nb variants retain their thermostability and antigen affinity, while biodistribution remains unaffected.	Niobium	45-47	surfactant protein A1	Homo sapiens	88-91
33029079-1	2020	1"-(2-Acryloxyethyl)-3,3"-dimethyl-6-nitrospiro[2 H-1-benzopyran-2,2"-indoline] (SPA) was synthesized and grafted onto a water-soluble carboxymethyl chitin (CMCH) macromolecule to prepare a photochromic copolymer (CMCH-g-SPA).	Water	121-126	surfactant protein A1	Homo sapiens	81-84
33029079-1	2020	1"-(2-Acryloxyethyl)-3,3"-dimethyl-6-nitrospiro[2 H-1-benzopyran-2,2"-indoline] (SPA) was synthesized and grafted onto a water-soluble carboxymethyl chitin (CMCH) macromolecule to prepare a photochromic copolymer (CMCH-g-SPA).	O-(carboxymethyl)chitin	135-155	surfactant protein A1	Homo sapiens	81-84
33029079-1	2020	1"-(2-Acryloxyethyl)-3,3"-dimethyl-6-nitrospiro[2 H-1-benzopyran-2,2"-indoline] (SPA) was synthesized and grafted onto a water-soluble carboxymethyl chitin (CMCH) macromolecule to prepare a photochromic copolymer (CMCH-g-SPA).	O-(carboxymethyl)chitin	157-161	surfactant protein A1	Homo sapiens	81-84
33029079-1	2020	1"-(2-Acryloxyethyl)-3,3"-dimethyl-6-nitrospiro[2 H-1-benzopyran-2,2"-indoline] (SPA) was synthesized and grafted onto a water-soluble carboxymethyl chitin (CMCH) macromolecule to prepare a photochromic copolymer (CMCH-g-SPA).	copolymer	203-212	surfactant protein A1	Homo sapiens	81-84
33029079-2	2020	The structure of CMCH-g-SPA was characterized by Fourier-transform infrared (FT-IR) spectroscopy, thermogravimetric (TG) analysis, X-ray diffraction (XRD) analysis, water-solubility evaluation, and UV-vis spectroscopy.	Water	165-170	surfactant protein A1	Homo sapiens	24-27
33029079-3	2020	XRD patterns of CMCH-g-SPA revealed that grafting copolymerization disrupts the CMCH semicrystalline structure, thus improving water solubility.	Water	127-132	surfactant protein A1	Homo sapiens	23-26
33029079-4	2020	UV-vis spectroscopy results supported the negative photochromic behavior of the merocyanine (MC) form of CMCH-g-SPA (CMCH-g-MCA) present in a water solution of the target copolymer.	merocyanine	80-91	surfactant protein A1	Homo sapiens	112-115
33029079-4	2020	UV-vis spectroscopy results supported the negative photochromic behavior of the merocyanine (MC) form of CMCH-g-SPA (CMCH-g-MCA) present in a water solution of the target copolymer.	merocyanine	93-95	surfactant protein A1	Homo sapiens	112-115
33029079-4	2020	UV-vis spectroscopy results supported the negative photochromic behavior of the merocyanine (MC) form of CMCH-g-SPA (CMCH-g-MCA) present in a water solution of the target copolymer.	Water	142-147	surfactant protein A1	Homo sapiens	112-115
32774419-0	2020	Assessment of Changes in the Hemoglobin Level under the Influence of Comprehensive Spa Therapy Using Therapeutic Radon-Sulfur Waters and Its Correlation with Free Radical Reactions.	radon-sulfur	113-125	surfactant protein A1	Homo sapiens	83-86
32661962-1	2021	Due to excessive application of essential oils and scented products in spa salons during aromatherapy and massage sessions, the elevated concentration of total volatile organic compounds (TVOCs), particularly terpenes, which are known as secondary organic aerosol (SOA) precursors, is expected there.	Oils, Volatile	32-46	surfactant protein A1	Homo sapiens	71-74
32661962-1	2021	Due to excessive application of essential oils and scented products in spa salons during aromatherapy and massage sessions, the elevated concentration of total volatile organic compounds (TVOCs), particularly terpenes, which are known as secondary organic aerosol (SOA) precursors, is expected there.	Terpenes	209-217	surfactant protein A1	Homo sapiens	71-74
32661962-5	2021	Obtained results allowed to characterize chemical composition of indoor air of spa salons and also to relate the dependence between applied essential oil and indoor air chemical composition.	Oils, Volatile	140-153	surfactant protein A1	Homo sapiens	79-82
32661962-7	2021	On the basis of obtained results, it may be stated that extensive application of essential oils rich in terpenes can significantly alter indoor air chemistry of spa salons, thereby influencing health and well-being of employees working there.	Oils, Volatile	81-95	surfactant protein A1	Homo sapiens	161-164
32661962-7	2021	On the basis of obtained results, it may be stated that extensive application of essential oils rich in terpenes can significantly alter indoor air chemistry of spa salons, thereby influencing health and well-being of employees working there.	Terpenes	104-112	surfactant protein A1	Homo sapiens	161-164
32033337-6	2020	The DEX treatment decreased the mRNA levels of SFTPA1 and SFTPB but increased the mRNA levels of SFTPC and SFTPD.	Dexamethasone	4-7	surfactant protein A1	Homo sapiens	47-53
32373171-0	2020	Assessment of Changes in Concentration of Total Antioxidant Status, Acute-Phase Protein, and Prolactin in Patients with Osteoarthritis Subjected to a Complex Spa Treatment with Radon Water: Preliminary Results.	Water	183-188	surfactant protein A1	Homo sapiens	158-161
31927192-8	2020	Alterations in inflammatory biomarkers (CC16, SP-A, MMP-9, and MMP-9/TIMP-1) were significantly associated with As-induced lung function impairment.	Arsenic	112-114	surfactant protein A1	Homo sapiens	46-50
32555254-4	2020	SiO2NPs, which primary particle size was 12 nm, caused the accumulation of intracellular Si, the decrease in cell viability, and the decrease in mRNAs expression of surfactant, including surfactant protein (SP)-A, SP-B, SP-C, and SP-D.	sio2nps	0-7	surfactant protein A1	Homo sapiens	187-212
32005219-5	2020	We aim to clarify whether serum SP-A, SP-D, and KL-6 reflect therapeutic outcomes of pirfenidone and nintedanib administration in patients with IPF.	pirfenidone	85-96	surfactant protein A1	Homo sapiens	32-36
31358361-8	2020	bDMARD naive compared with non-naive ax-SpA patients had better 3-month ASDAS/BASDAI/MHAQ responses (p <= 0.02).	Amoxicillin	37-39	surfactant protein A1	Homo sapiens	40-43
31358361-8	2020	bDMARD naive compared with non-naive ax-SpA patients had better 3-month ASDAS/BASDAI/MHAQ responses (p <= 0.02).	1-hydroxy-5,8-bis(2-((2-hydroxyethyl)amino)ethylamino)-9,10-anthracenedione	85-89	surfactant protein A1	Homo sapiens	40-43
31358361-12	2020	Treatment responses were significantly better for bDMARD naive than non-naive ax-SpA patients.	Amoxicillin	78-80	surfactant protein A1	Homo sapiens	81-84
31358361-13	2020	Identified predictors of golimumab discontinuation were patient"s global and female gender in patients overall and in subgroups of PsA and ax-SpA patients, and patient"s global and CRP in RA.	Amoxicillin	139-141	surfactant protein A1	Homo sapiens	142-145
31669698-4	2020	We developed four synthetic approaches to generate RBC-Staphylococcal protein A (RBC-SpA) complexes: amino group targeting through N-hydrosuccinidyl ester-functionalized homobifunctional poly(ethylene glycol) (NHS-PEG-NHS), direct thiol group targeting using heterobifunctional NHS-PEG-maleimide (NHS-PEG-MAL), converted thiol targeting using heterobifunctional NHS-PEG-MAL, and click chemistry using a heterobifunctional NHS-PEG-azido (NHS-PEG-N3) and NHS-PEG-alkyne (NHS-PEG-alk).	Amino Acids	101-106	surfactant protein A1	Homo sapiens	85-88
31969151-16	2020	Although no MRSA was found from dairy cows the existence of the human and animal adapted and globally spread strain, MRSA SCCmec IVa spa t064, warrants for a coordinated action to tackle AMR in both human and veterinary in the country.	amrubicin	187-190	surfactant protein A1	Homo sapiens	133-136
31669698-4	2020	We developed four synthetic approaches to generate RBC-Staphylococcal protein A (RBC-SpA) complexes: amino group targeting through N-hydrosuccinidyl ester-functionalized homobifunctional poly(ethylene glycol) (NHS-PEG-NHS), direct thiol group targeting using heterobifunctional NHS-PEG-maleimide (NHS-PEG-MAL), converted thiol targeting using heterobifunctional NHS-PEG-MAL, and click chemistry using a heterobifunctional NHS-PEG-azido (NHS-PEG-N3) and NHS-PEG-alkyne (NHS-PEG-alk).	Esters	131-154	surfactant protein A1	Homo sapiens	85-88
31669698-4	2020	We developed four synthetic approaches to generate RBC-Staphylococcal protein A (RBC-SpA) complexes: amino group targeting through N-hydrosuccinidyl ester-functionalized homobifunctional poly(ethylene glycol) (NHS-PEG-NHS), direct thiol group targeting using heterobifunctional NHS-PEG-maleimide (NHS-PEG-MAL), converted thiol targeting using heterobifunctional NHS-PEG-MAL, and click chemistry using a heterobifunctional NHS-PEG-azido (NHS-PEG-N3) and NHS-PEG-alkyne (NHS-PEG-alk).	poly(ethylene glycol)-poly(caprolactone)-poly(ethylene glycol)	187-208	surfactant protein A1	Homo sapiens	85-88
31669698-4	2020	We developed four synthetic approaches to generate RBC-Staphylococcal protein A (RBC-SpA) complexes: amino group targeting through N-hydrosuccinidyl ester-functionalized homobifunctional poly(ethylene glycol) (NHS-PEG-NHS), direct thiol group targeting using heterobifunctional NHS-PEG-maleimide (NHS-PEG-MAL), converted thiol targeting using heterobifunctional NHS-PEG-MAL, and click chemistry using a heterobifunctional NHS-PEG-azido (NHS-PEG-N3) and NHS-PEG-alkyne (NHS-PEG-alk).	hydroxysuccinimidyl-poly(ethylene glycol)-biotin	210-221	surfactant protein A1	Homo sapiens	85-88
31669698-4	2020	We developed four synthetic approaches to generate RBC-Staphylococcal protein A (RBC-SpA) complexes: amino group targeting through N-hydrosuccinidyl ester-functionalized homobifunctional poly(ethylene glycol) (NHS-PEG-NHS), direct thiol group targeting using heterobifunctional NHS-PEG-maleimide (NHS-PEG-MAL), converted thiol targeting using heterobifunctional NHS-PEG-MAL, and click chemistry using a heterobifunctional NHS-PEG-azido (NHS-PEG-N3) and NHS-PEG-alkyne (NHS-PEG-alk).	Sulfhydryl Compounds	231-236	surfactant protein A1	Homo sapiens	85-88
31669698-4	2020	We developed four synthetic approaches to generate RBC-Staphylococcal protein A (RBC-SpA) complexes: amino group targeting through N-hydrosuccinidyl ester-functionalized homobifunctional poly(ethylene glycol) (NHS-PEG-NHS), direct thiol group targeting using heterobifunctional NHS-PEG-maleimide (NHS-PEG-MAL), converted thiol targeting using heterobifunctional NHS-PEG-MAL, and click chemistry using a heterobifunctional NHS-PEG-azido (NHS-PEG-N3) and NHS-PEG-alkyne (NHS-PEG-alk).	hydroxysuccinimidyl-poly(ethylene glycol)-biotin	278-295	surfactant protein A1	Homo sapiens	85-88
31669698-4	2020	We developed four synthetic approaches to generate RBC-Staphylococcal protein A (RBC-SpA) complexes: amino group targeting through N-hydrosuccinidyl ester-functionalized homobifunctional poly(ethylene glycol) (NHS-PEG-NHS), direct thiol group targeting using heterobifunctional NHS-PEG-maleimide (NHS-PEG-MAL), converted thiol targeting using heterobifunctional NHS-PEG-MAL, and click chemistry using a heterobifunctional NHS-PEG-azido (NHS-PEG-N3) and NHS-PEG-alkyne (NHS-PEG-alk).	hydroxysuccinimidyl-poly(ethylene glycol)-biotin	297-308	surfactant protein A1	Homo sapiens	85-88
31669698-4	2020	We developed four synthetic approaches to generate RBC-Staphylococcal protein A (RBC-SpA) complexes: amino group targeting through N-hydrosuccinidyl ester-functionalized homobifunctional poly(ethylene glycol) (NHS-PEG-NHS), direct thiol group targeting using heterobifunctional NHS-PEG-maleimide (NHS-PEG-MAL), converted thiol targeting using heterobifunctional NHS-PEG-MAL, and click chemistry using a heterobifunctional NHS-PEG-azido (NHS-PEG-N3) and NHS-PEG-alkyne (NHS-PEG-alk).	Sulfhydryl Compounds	321-326	surfactant protein A1	Homo sapiens	85-88
31669698-4	2020	We developed four synthetic approaches to generate RBC-Staphylococcal protein A (RBC-SpA) complexes: amino group targeting through N-hydrosuccinidyl ester-functionalized homobifunctional poly(ethylene glycol) (NHS-PEG-NHS), direct thiol group targeting using heterobifunctional NHS-PEG-maleimide (NHS-PEG-MAL), converted thiol targeting using heterobifunctional NHS-PEG-MAL, and click chemistry using a heterobifunctional NHS-PEG-azido (NHS-PEG-N3) and NHS-PEG-alkyne (NHS-PEG-alk).	hydroxysuccinimidyl-poly(ethylene glycol)-biotin	210-217	surfactant protein A1	Homo sapiens	85-88
31669698-4	2020	We developed four synthetic approaches to generate RBC-Staphylococcal protein A (RBC-SpA) complexes: amino group targeting through N-hydrosuccinidyl ester-functionalized homobifunctional poly(ethylene glycol) (NHS-PEG-NHS), direct thiol group targeting using heterobifunctional NHS-PEG-maleimide (NHS-PEG-MAL), converted thiol targeting using heterobifunctional NHS-PEG-MAL, and click chemistry using a heterobifunctional NHS-PEG-azido (NHS-PEG-N3) and NHS-PEG-alkyne (NHS-PEG-alk).	4-azido-2-nitrophenyl polyethylene glycol	426-435	surfactant protein A1	Homo sapiens	85-88
31669698-4	2020	We developed four synthetic approaches to generate RBC-Staphylococcal protein A (RBC-SpA) complexes: amino group targeting through N-hydrosuccinidyl ester-functionalized homobifunctional poly(ethylene glycol) (NHS-PEG-NHS), direct thiol group targeting using heterobifunctional NHS-PEG-maleimide (NHS-PEG-MAL), converted thiol targeting using heterobifunctional NHS-PEG-MAL, and click chemistry using a heterobifunctional NHS-PEG-azido (NHS-PEG-N3) and NHS-PEG-alkyne (NHS-PEG-alk).	hydroxysuccinimidyl-poly(ethylene glycol)-biotin	437-447	surfactant protein A1	Homo sapiens	85-88
31669698-4	2020	We developed four synthetic approaches to generate RBC-Staphylococcal protein A (RBC-SpA) complexes: amino group targeting through N-hydrosuccinidyl ester-functionalized homobifunctional poly(ethylene glycol) (NHS-PEG-NHS), direct thiol group targeting using heterobifunctional NHS-PEG-maleimide (NHS-PEG-MAL), converted thiol targeting using heterobifunctional NHS-PEG-MAL, and click chemistry using a heterobifunctional NHS-PEG-azido (NHS-PEG-N3) and NHS-PEG-alkyne (NHS-PEG-alk).	Alkynes	453-467	surfactant protein A1	Homo sapiens	85-88
31669698-4	2020	We developed four synthetic approaches to generate RBC-Staphylococcal protein A (RBC-SpA) complexes: amino group targeting through N-hydrosuccinidyl ester-functionalized homobifunctional poly(ethylene glycol) (NHS-PEG-NHS), direct thiol group targeting using heterobifunctional NHS-PEG-maleimide (NHS-PEG-MAL), converted thiol targeting using heterobifunctional NHS-PEG-MAL, and click chemistry using a heterobifunctional NHS-PEG-azido (NHS-PEG-N3) and NHS-PEG-alkyne (NHS-PEG-alk).	hydroxysuccinimidyl-poly(ethylene glycol)-biotin	278-285	surfactant protein A1	Homo sapiens	85-88
31669698-5	2020	The RBC-PEG-SpA complexes were formed within minutes, followed by the attachment of over 105 antibodies per RBC to the accessible RBCs-bound SpA via Fc-Protein A coupling.	pentaerythritol poly(ethylene glycol) ether tetrasuccinimidyl glutarate	8-11	surfactant protein A1	Homo sapiens	12-15
31669698-5	2020	The RBC-PEG-SpA complexes were formed within minutes, followed by the attachment of over 105 antibodies per RBC to the accessible RBCs-bound SpA via Fc-Protein A coupling.	pentaerythritol poly(ethylene glycol) ether tetrasuccinimidyl glutarate	8-11	surfactant protein A1	Homo sapiens	141-144
31669698-6	2020	The RBC-PEG-SpA-antibody arrays were shown to be stable for more than 60 days in PBS and for more than 7 days in whole serum.	pentaerythritol poly(ethylene glycol) ether tetrasuccinimidyl glutarate	8-11	surfactant protein A1	Homo sapiens	12-15
31669698-7	2020	RBC-PEG-SpA-antibody complexes were shown to remove TNFalpha from physiological buffer and had similar mechanical properties to unmodified RBCs.	pentaerythritol poly(ethylene glycol) ether tetrasuccinimidyl glutarate	4-7	surfactant protein A1	Homo sapiens	8-11
32112323-4	2020	Using detergent-purified GlyT1 protein and a tritium-labeled glycine uptake inhibitor small molecule, we find sybody candidates that increase the apparent melting temperature in SPA-TS by several degrees.	Tritium	45-52	surfactant protein A1	Homo sapiens	178-181
32468745-10	2020	However, SP-A levels were directly correlated with cotinine levels (r= 0.503, p=0.001).	Cotinine	51-59	surfactant protein A1	Homo sapiens	9-13
32468745-13	2020	Plasma cotinine levels (an indication of the tobacco use) were positively correlated with plasma SP-A levels in study subjects.	Cotinine	7-15	surfactant protein A1	Homo sapiens	97-101
32112323-4	2020	Using detergent-purified GlyT1 protein and a tritium-labeled glycine uptake inhibitor small molecule, we find sybody candidates that increase the apparent melting temperature in SPA-TS by several degrees.	Glycine	61-68	surfactant protein A1	Homo sapiens	178-181
30954271-3	2019	SP-A, being a carbohydrate pattern recognition molecule, has a wide range of innate immune functions against respiratory pathogens, including influenza A virus (IAV).	Carbohydrates	14-26	surfactant protein A1	Homo sapiens	0-4
31585191-7	2019	Placebo and SA3Ag groups had similar persistence of colonization, with 19.6-30.7% due to single spa types.	sa3ag	12-17	surfactant protein A1	Homo sapiens	96-99
31329997-2	2019	The investigated balneotherapeutic facility and its natural hot spa water are used for treatments and rehabilitations of rheumatic patients.	Water	68-73	surfactant protein A1	Homo sapiens	64-67
31278555-0	2019	Oriented assembly of surface plasmon resonance biosensor through staphylococcal protein A for the chlorpyrifos detection.	Chlorpyrifos	98-110	surfactant protein A1	Homo sapiens	65-89
31278555-2	2019	In this covalent-orientated strategy, staphylococcal protein A (SPA) was first covalently bound to the surface for monitoring chlorpyrifos residue, with subsequent binding of the antibody in an orientated fashion via its fragment crystallizable (Fc) region.	Chlorpyrifos	126-138	surfactant protein A1	Homo sapiens	38-62
31278555-2	2019	In this covalent-orientated strategy, staphylococcal protein A (SPA) was first covalently bound to the surface for monitoring chlorpyrifos residue, with subsequent binding of the antibody in an orientated fashion via its fragment crystallizable (Fc) region.	Chlorpyrifos	126-138	surfactant protein A1	Homo sapiens	64-67
31278555-3	2019	Consequently, the SPA-modified biosensor exhibited a satisfactory specificity and a low detection limit of 0.056 ng mL-1 for chlorpyrifos, with a linear detection range of 0.25-50.0 ng mL-1.	Chlorpyrifos	125-137	surfactant protein A1	Homo sapiens	18-21
30317939-4	2019	Our aim was to clarify whether progesterone can affect dexamethasone (DXM)-regulated expression of surfactant protein A (SP-A), SP-B, and SP-D in lung epithelial cells.	Dexamethasone	55-68	surfactant protein A1	Homo sapiens	99-119
30317939-4	2019	Our aim was to clarify whether progesterone can affect dexamethasone (DXM)-regulated expression of surfactant protein A (SP-A), SP-B, and SP-D in lung epithelial cells.	Dexamethasone	55-68	surfactant protein A1	Homo sapiens	121-125
30317939-4	2019	Our aim was to clarify whether progesterone can affect dexamethasone (DXM)-regulated expression of surfactant protein A (SP-A), SP-B, and SP-D in lung epithelial cells.	Dexamethasone	70-73	surfactant protein A1	Homo sapiens	99-119
30317939-4	2019	Our aim was to clarify whether progesterone can affect dexamethasone (DXM)-regulated expression of surfactant protein A (SP-A), SP-B, and SP-D in lung epithelial cells.	Dexamethasone	70-73	surfactant protein A1	Homo sapiens	121-125
30317939-10	2019	The effect of progesterone on DXM-regulated genes was not specific for SP-B, as expression of SP-A and SP-D mRNAs was also antagonized.	Dexamethasone	30-33	surfactant protein A1	Homo sapiens	94-98
32687301-6	2020	CONCLUSION: The implementation of the proposed measures will restore the world-recognized achievements of domestic balneology and increase the effectiveness and accessibility of sanatorium-and-spa treatment, as well as achieve the targets specified in the Development Strategy of the spa complex of the Russian Federation.	sanatorium	178-188	surfactant protein A1	Homo sapiens	284-287
31781112-4	2019	Binding assays using recombinant rSP-A expressed in insect cells showed that lack of proline hydroxylation, truncations of amino-terminal oligomerization domains, and site-directed serine (S) or alanine (A) mutagenesis of cysteine 6 (C6S), glutamate 195 (E195A), and glutamate 171 (E171A) in the carbohydrate recognition domain (CRD) all impaired SP-A binding.	Serine	181-187	surfactant protein A1	Homo sapiens	34-38
31781112-5	2019	Replacement of arginine 197 with alanine found in hSP-A (R197A), however, restored the binding of hydroxyproline-deficient rSP-A to the SP-A receptor SP-R210 similar to native rat and human SP-A.	Hydroxyproline	98-112	surfactant protein A1	Homo sapiens	124-128
31781112-9	2019	Furthermore, our data indicate that the auxiliary ion coordination loop encompassing the conserved E171 residue may comprise a conserved site of interaction with macrophages, and SP-R210 specifically, that merits further investigation to discern conserved and divergent SP-A functions between species.	titanium dioxide	99-103	surfactant protein A1	Homo sapiens	270-274
31624912-0	2019	Assessment of spa mineral water quality from Vrnjacka Banja, Serbia: geochemical, bacteriological, and health risk aspects.	Water	26-31	surfactant protein A1	Homo sapiens	14-17
31449845-0	2019	Adverse impact of ambient PM2.5 on expression and trafficking of surfactant protein A through reactive oxygen species damage to lamellar bodies.	Reactive Oxygen Species	94-117	surfactant protein A1	Homo sapiens	65-85
31449845-5	2019	The results showed that the low and medium concentration of PM2.5 gradually enhanced SP-A protein and mRNA expression, whereas the high concentration of PM2.5 conspicuously decreased SP-A protein but not its mRNA compared with the control.	[4-(3-AMINOMETHYL-PHENYL)-PIPERIDIN-1-YL]-(5-PHENETHYL- PYRIDIN-3-YL)-METHANONE	60-63	surfactant protein A1	Homo sapiens	85-89
31449845-6	2019	The trafficking of SP-A to LBs was gradually disturbed, and concomitantly, the lesions of LBs responsible for the transport and storage of SP-A protein were exacerbated with increased PM2.5 concentration.	Levanbiose	27-30	surfactant protein A1	Homo sapiens	19-23
31449845-8	2019	Subsequently, the injured LBs and the decrease in SP-A expression under exposure to the high concentration of PM2.5 were well rescued.	[4-(3-AMINOMETHYL-PHENYL)-PIPERIDIN-1-YL]-(5-PHENETHYL- PYRIDIN-3-YL)-METHANONE	110-113	surfactant protein A1	Homo sapiens	50-54
30954271-4	2019	Some pandemic pH1N1 strains resist neutralization by SP-A due to differences in the N-glycosylation of viral hemagglutinin (HA).	Nitrogen	17-18	surfactant protein A1	Homo sapiens	53-57
30954271-5	2019	Here, we provide evidence, for the first time, that a recombinant form of human SP-A (rfhSP-A), composed of alpha-helical neck and carbohydrate recognition domains, can actually promote the IAV replication, as observed by an upregulation of M1 expression in lung epithelial cell line, A549, when challenged with pH1N1 and H3N2 IAV subtypes.	Carbohydrates	131-143	surfactant protein A1	Homo sapiens	80-84
30827536-3	2019	In this study, surfactant protein A and D expression responses were investigated during pharmacogenetics upon methylprednisolone treatment as observed during lung transplantation.	Methylprednisolone	110-128	surfactant protein A1	Homo sapiens	15-41
30827536-6	2019	RESULTS: In NCI-H441 cells, methylprednisolone treatment at 10-5 M and 10-6 M reduced surfactant protein A1 and surfactant protein A2 messenger RNA and surfactant protein A protein expression (P < .05).	Methylprednisolone	28-46	surfactant protein A1	Homo sapiens	86-107
30827536-6	2019	RESULTS: In NCI-H441 cells, methylprednisolone treatment at 10-5 M and 10-6 M reduced surfactant protein A1 and surfactant protein A2 messenger RNA and surfactant protein A protein expression (P < .05).	Methylprednisolone	28-46	surfactant protein A1	Homo sapiens	86-106
30827536-8	2019	CONCLUSIONS: The surfactant protein A genotype and methylprednisolone stimuli influence donor lung surfactant protein A and D expression.	Methylprednisolone	51-69	surfactant protein A1	Homo sapiens	99-119
30827536-9	2019	Lungs carrying the surfactant protein A2 variant 1A0 have a greater expression of surfactant protein A when treated with methylprednisolone.	Methylprednisolone	121-139	surfactant protein A1	Homo sapiens	19-39
30724601-7	2019	"Spa pool of medicinal water" treatment was the most common care in each year which incidence showed a downward trend during the past years: 2 544  617 treatments were performed in 2009 but 2016 showed only 1 898  338 treatments.	Water	23-28	surfactant protein A1	Homo sapiens	1-4
30854216-5	2019	This variant encodes the substitution p.(Val178Met), localized within the carbohydrate recognition domain of surfactant protein A and segregates with the genes causing idiopathic interstitial pneumonia.	Carbohydrates	74-86	surfactant protein A1	Homo sapiens	109-129
30563057-5	2018	We now identify the minimal effective sequences of rat/mouse and human SP-A as 9-aa sequences that we have called PLA2-inhibitory peptide (PIP).These sequences are PIP-1, rat/mouse; PIP-2, human; and PIP-3, a hybrid of PIPs 1&amp;amp;2.	pip	139-142	surfactant protein A1	Homo sapiens	71-75
30651822-8	2019	Compared with the control group, SP-A treatment significantly increased the ROS production, type I collagen secretion and cell apoptosis, which was partially inhibited by addition of anti-CRT.	Reactive Oxygen Species	76-79	surfactant protein A1	Homo sapiens	33-37
30563057-5	2018	We now identify the minimal effective sequences of rat/mouse and human SP-A as 9-aa sequences that we have called PLA2-inhibitory peptide (PIP).These sequences are PIP-1, rat/mouse; PIP-2, human; and PIP-3, a hybrid of PIPs 1&amp;amp;2.	piperidine	219-223	surfactant protein A1	Homo sapiens	71-75
30563057-5	2018	We now identify the minimal effective sequences of rat/mouse and human SP-A as 9-aa sequences that we have called PLA2-inhibitory peptide (PIP).These sequences are PIP-1, rat/mouse; PIP-2, human; and PIP-3, a hybrid of PIPs 1&amp;amp;2.	Adenosine Monophosphate	226-229	surfactant protein A1	Homo sapiens	71-75
30563057-5	2018	We now identify the minimal effective sequences of rat/mouse and human SP-A as 9-aa sequences that we have called PLA2-inhibitory peptide (PIP).These sequences are PIP-1, rat/mouse; PIP-2, human; and PIP-3, a hybrid of PIPs 1&amp;amp;2.	Adenosine Monophosphate	230-233	surfactant protein A1	Homo sapiens	71-75
30076539-9	2018	The mean concentration of 3-SPA in patients with AD treated with tramiprosate was 135 +- 51 nM.	tramiprosate	65-77	surfactant protein A1	Homo sapiens	28-31
29923965-7	2018	RESULTS: Fluorescence double staining with 4,6-diamidino 2-pheynlindole and SPs showed strong immunostaining for SP-A, SP-B, SP-C, SP-D, and SP-H/SFTA3.	4,6-diamidino 2-pheynlindole	43-71	surfactant protein A1	Homo sapiens	113-117
29923965-7	2018	RESULTS: Fluorescence double staining with 4,6-diamidino 2-pheynlindole and SPs showed strong immunostaining for SP-A, SP-B, SP-C, SP-D, and SP-H/SFTA3.	Sodium phenolsulfonate	76-79	surfactant protein A1	Homo sapiens	113-117
30076539-3	2018	During clinical studies, we discovered that the primary metabolite of tramiprosate and its prodrug ALZ-801, 3-sulfopropanoic acid (3-SPA), is an endogenous molecule in the human brain and present in the cerebrospinal fluid (CSF) of patients with AD and other neurodegenerative brain diseases.	tramiprosate	70-82	surfactant protein A1	Homo sapiens	133-136
30076539-3	2018	During clinical studies, we discovered that the primary metabolite of tramiprosate and its prodrug ALZ-801, 3-sulfopropanoic acid (3-SPA), is an endogenous molecule in the human brain and present in the cerebrospinal fluid (CSF) of patients with AD and other neurodegenerative brain diseases.	3-Sulfopropanoic acid	108-129	surfactant protein A1	Homo sapiens	133-136
30393427-2	2018	There are four subtypes of SPs: SP-A, SP-B, SP-C, and SP-D.	Sodium phenolsulfonate	27-30	surfactant protein A1	Homo sapiens	32-36
30076539-13	2018	CONCLUSIONS: We confirmed the endogenous presence of 3-SPA, the major metabolite of tramiprosate, in the CSF of drug-naive elderly patients with memory deficits due to AD and a variety of other neurodegenerative disorders.	tramiprosate	84-96	surfactant protein A1	Homo sapiens	55-58
30076539-14	2018	The levels of 3-SPA were up to 12.6-fold greater in patients with AD receiving tramiprosate than in drug-naive patients.	tramiprosate	79-91	surfactant protein A1	Homo sapiens	16-19
30076539-16	2018	3-SPA displays excellent oral availability and brain penetration in rats, suggesting that the higher CSF concentrations of 3-SPA in the human brain after oral administration of ALZ-801 or tramiprosate (and subsequent conversion to 3-SPA) result from the penetration of the metabolite into the central nervous system.	tramiprosate	188-200	surfactant protein A1	Homo sapiens	2-5
30076539-16	2018	3-SPA displays excellent oral availability and brain penetration in rats, suggesting that the higher CSF concentrations of 3-SPA in the human brain after oral administration of ALZ-801 or tramiprosate (and subsequent conversion to 3-SPA) result from the penetration of the metabolite into the central nervous system.	tramiprosate	188-200	surfactant protein A1	Homo sapiens	125-128
28209032-1	2017	The developed surface plasmon resonance (SPR) biosensor based on the recombinant Staphylococcal protein A with an additional cysteine residue (SPA-Cys) used as a biorecognition component showed a good selectivity and sensitivity for the immunoglobulin detection.	Cysteine	125-133	surfactant protein A1	Homo sapiens	143-146
29716959-5	2018	Activity is inhibited by a serine "protease" inhibitor (diethyl p-nitrophenyl phosphate), an analog of the PLA2 transition state [1-hexadecyl-3-(trifluoroethyl)-sn-glycero-2-phosphomethanol (MJ33)], and by two naturally occurring proteins (surfactant protein A and p67phox), but not by bromoenol lactone.	Paraoxon	56-87	surfactant protein A1	Homo sapiens	240-260
29632404-0	2018	Formation of trihalomethanes as disinfection byproducts in herbal spa pools.	Trihalomethanes	13-28	surfactant protein A1	Homo sapiens	66-69
29632404-4	2018	Although there have been many studies on DBP formation in swimming pools, the role of organic matter derived from herbal medicines applied in herbal spa water has been largely neglected.	Water	153-158	surfactant protein A1	Homo sapiens	149-152
29632404-5	2018	Accordingly, the present study investigated the effect of herbal medicines on the formation of trihalomethanes (THMs) in simulated herbal spa water.	Trihalomethanes	95-110	surfactant protein A1	Homo sapiens	138-141
29632404-5	2018	Accordingly, the present study investigated the effect of herbal medicines on the formation of trihalomethanes (THMs) in simulated herbal spa water.	Trihalomethanes	112-116	surfactant protein A1	Homo sapiens	138-141
29632404-5	2018	Accordingly, the present study investigated the effect of herbal medicines on the formation of trihalomethanes (THMs) in simulated herbal spa water.	Water	142-147	surfactant protein A1	Homo sapiens	138-141
29632404-7	2018	The results showed that the organic molecules introduced by the herbal medicines are significant precursors to the formation of THMs in spa pool water.	Trihalomethanes	128-132	surfactant protein A1	Homo sapiens	136-139
29927374-9	2018	Nucleotide sequences of CDR showed high identity (90-100 %) within the same PspA clade, although the CDR identity among different PspA families ranged from 53 to 69 %.	cdr	24-27	surfactant protein A1	Homo sapiens	76-80
29282698-8	2018	CSF-SP concentrations (mean +- standard deviation) of the overall collective were as follows: SP-A = 0.73 +- 0.58 ng/ml, SP-B = 0.17 +- 0.93 ng/ml, SP-C = 0.95 +- 0.75 ng/ml, and SP-D = 7.43 +- 5.17 ng/ml.	-sp	3-6	surfactant protein A1	Homo sapiens	94-98
29544026-10	2018	Two pairs of SP-A 18-mers with carbohydrate recognition domains pointing inwardly and outwardly, stacked vertically as a column of four molecules, then repeated side by side in rows, approximated the size and layering patterns observed in these granules.	Carbohydrates	31-43	surfactant protein A1	Homo sapiens	13-17
29875071-4	2018	Studies, primarily using the Salmonella mutagenicity assay, have continued to show that chlorination or chloramination of source waters results in finished, tap, or swimming pool/spa water that is more mutagenic than the original source water.	Water	129-134	surfactant protein A1	Homo sapiens	179-182
29875071-4	2018	Studies, primarily using the Salmonella mutagenicity assay, have continued to show that chlorination or chloramination of source waters results in finished, tap, or swimming pool/spa water that is more mutagenic than the original source water.	Water	183-188	surfactant protein A1	Homo sapiens	179-182
29951070-9	2018	In contrast, surfactant protein A, ficolins, and other inhibitors present sialic acid rich ligands to which the HA can bind.	N-Acetylneuraminic Acid	74-85	surfactant protein A1	Homo sapiens	13-33
30701855-5	2018	MATERIALS AND METHODS:  RESULTS: A significant increase in SP-A and SP-D (p&amp;lt;0.05) was observed in patients compared with patients in the control group, a direct correlation was found with signs of activity: SP-A with alveolitis (p&amp;lt;0.05), SP- D with progressive fibrosis (p&amp;lt;0.05), inverse correlation of surfactant proteins with respiratory function indices (p&amp;lt;0.05).	Adenosine Monophosphate	76-79	surfactant protein A1	Homo sapiens	59-63
30701855-5	2018	MATERIALS AND METHODS:  RESULTS: A significant increase in SP-A and SP-D (p&amp;lt;0.05) was observed in patients compared with patients in the control group, a direct correlation was found with signs of activity: SP-A with alveolitis (p&amp;lt;0.05), SP- D with progressive fibrosis (p&amp;lt;0.05), inverse correlation of surfactant proteins with respiratory function indices (p&amp;lt;0.05).	Adenosine Monophosphate	238-241	surfactant protein A1	Homo sapiens	59-63
30701855-5	2018	MATERIALS AND METHODS:  RESULTS: A significant increase in SP-A and SP-D (p&amp;lt;0.05) was observed in patients compared with patients in the control group, a direct correlation was found with signs of activity: SP-A with alveolitis (p&amp;lt;0.05), SP- D with progressive fibrosis (p&amp;lt;0.05), inverse correlation of surfactant proteins with respiratory function indices (p&amp;lt;0.05).	Adenosine Monophosphate	238-241	surfactant protein A1	Homo sapiens	59-63
29632404-7	2018	The results showed that the organic molecules introduced by the herbal medicines are significant precursors to the formation of THMs in spa pool water.	Water	145-150	surfactant protein A1	Homo sapiens	136-139
29632404-8	2018	Since at least 50% of THMs were produced within the first six hours of the reaction time, the presence of herbal medicines in spa water could present a parallel route for THM exposure.	Trihalomethanes	22-26	surfactant protein A1	Homo sapiens	126-129
29632404-8	2018	Since at least 50% of THMs were produced within the first six hours of the reaction time, the presence of herbal medicines in spa water could present a parallel route for THM exposure.	Water	130-135	surfactant protein A1	Homo sapiens	126-129
29632404-8	2018	Since at least 50% of THMs were produced within the first six hours of the reaction time, the presence of herbal medicines in spa water could present a parallel route for THM exposure.	Trihalomethanes	22-25	surfactant protein A1	Homo sapiens	126-129
28972165-4	2017	We also found that SP-A directly binds the recombinant extracellular domain of EGFR (soluble EGFR or sEGFR), and this binding, unlike that of SP-D, was not blocked by EDTA, excess mannose, or peptide:N-glycosidase F treatment.	Mannose	180-187	surfactant protein A1	Homo sapiens	19-23
28814727-3	2017	In this study, we hypothesised that cigarette smoke (CS) and its component acrolein might influence pulmonary innate immunity by affecting the function of SP-A.	Cesium	53-55	surfactant protein A1	Homo sapiens	155-159
28791362-4	2017	The levels of SP-A and SP-D were detected in the exhaled breath condensate (EBC) using ELISA analysis.	NSC638702	76-79	surfactant protein A1	Homo sapiens	14-18
28791362-12	2017	The results of the present study indicated that the SP-A and SP-D levels in EBC were correlated with lung function, which contributed to COPD diagnosis.	NSC638702	76-79	surfactant protein A1	Homo sapiens	52-56
26648443-5	2017	We hypothesized that birch pollen-induced inflammation could change the concentrations of surfactant protein A and albumin in the respiratory tract lining fluid of the small airways and influence the amount of exhaled particles.	birch pollen	21-33	surfactant protein A1	Homo sapiens	90-110
28814727-5	2017	To further confirm this finding, recombinant human SP-A (hSP-A) was incubated with CS extract (CSE) or acrolein and then analysed by western blotting and nanoscale liquid chromatography-matrix-assisted laser desorption/ionisation time-of-flight tandem mass spectrometry.	Cesium	83-85	surfactant protein A1	Homo sapiens	51-55
28814727-5	2017	To further confirm this finding, recombinant human SP-A (hSP-A) was incubated with CS extract (CSE) or acrolein and then analysed by western blotting and nanoscale liquid chromatography-matrix-assisted laser desorption/ionisation time-of-flight tandem mass spectrometry.	Cesium	83-85	surfactant protein A1	Homo sapiens	57-62
28814727-5	2017	To further confirm this finding, recombinant human SP-A (hSP-A) was incubated with CS extract (CSE) or acrolein and then analysed by western blotting and nanoscale liquid chromatography-matrix-assisted laser desorption/ionisation time-of-flight tandem mass spectrometry.	Acrolein	103-111	surfactant protein A1	Homo sapiens	51-55
28814727-5	2017	To further confirm this finding, recombinant human SP-A (hSP-A) was incubated with CS extract (CSE) or acrolein and then analysed by western blotting and nanoscale liquid chromatography-matrix-assisted laser desorption/ionisation time-of-flight tandem mass spectrometry.	Acrolein	103-111	surfactant protein A1	Homo sapiens	57-62
28814727-6	2017	These analyses revealed that CSE and acrolein induced hSP-A oligomerisation and that acrolein induced the modification of six residues in hSP-A: His39, His116, Cys155, Lys180, Lys221, and Cys224.	Acrolein	37-45	surfactant protein A1	Homo sapiens	54-59
28814727-8	2017	CSE- or acrolein-induced modification of hSP-A significantly decreased hSP-A"s ability to inhibit bacterial growth and to enhance macrophage phagocytosis.	Acrolein	8-16	surfactant protein A1	Homo sapiens	41-46
28814727-8	2017	CSE- or acrolein-induced modification of hSP-A significantly decreased hSP-A"s ability to inhibit bacterial growth and to enhance macrophage phagocytosis.	Acrolein	8-16	surfactant protein A1	Homo sapiens	71-76
28814727-9	2017	These findings suggest that CS-induced structural and functional defects in SP-A contribute to the dysfunctional innate immune responses observed in the lung during cigarette smoking.	Cesium	28-30	surfactant protein A1	Homo sapiens	76-80
28719181-3	2017	SP-A binds to dipalmitoylphosphatidylcholine (DPPC), the major surfactant lipid component, but not phosphatidylinositol (PI), whereas SP-D shows the opposite preference.	1,2-Dipalmitoylphosphatidylcholine	14-44	surfactant protein A1	Homo sapiens	0-4
28719181-3	2017	SP-A binds to dipalmitoylphosphatidylcholine (DPPC), the major surfactant lipid component, but not phosphatidylinositol (PI), whereas SP-D shows the opposite preference.	1,2-Dipalmitoylphosphatidylcholine	46-50	surfactant protein A1	Homo sapiens	0-4
28719181-9	2017	Structures of mutant complexes with inositol or methyl-mannose revealed an attenuation of the ligand-induced conformational change relative to wild-type SP-A.	Inositol	36-44	surfactant protein A1	Homo sapiens	153-157
28719181-9	2017	Structures of mutant complexes with inositol or methyl-mannose revealed an attenuation of the ligand-induced conformational change relative to wild-type SP-A.	methylmannoside	48-62	surfactant protein A1	Homo sapiens	153-157
27667820-1	2016	The growth of 3, 4, 9, 10-perylene tetracarboxylic dianhydride (PTCDA) on the Ga-polar GaN(0 0 0 1) surface has been studied by x-ray photoelectron spectroscopy (XPS), spot profile analysis low-energy electron diffraction (SPA-LEED), near edge x-ray absorption fine structure (NEXAFS), and scanning tunneling microscopy (STM).	3,4,9,10-perylenetetracarboxylic dianhydride	64-69	surfactant protein A1	Homo sapiens	223-226
28591049-13	2017	In acute exacerbation of IPF, serum SP-A/D were higher than those in stable stage.	Deuterium	41-42	surfactant protein A1	Homo sapiens	36-40
27859014-7	2017	In the PNG cohort, higher PspA-specific IL-5 and IL-6 CBMC responses were associated independently and significantly with increased risk of earlier pneumococcal colonization, while a significant protective effect was found for higher PspA-IL-10 CBMC responses.	cbmc	54-58	surfactant protein A1	Homo sapiens	26-30
27859014-7	2017	In the PNG cohort, higher PspA-specific IL-5 and IL-6 CBMC responses were associated independently and significantly with increased risk of earlier pneumococcal colonization, while a significant protective effect was found for higher PspA-IL-10 CBMC responses.	cbmc	245-249	surfactant protein A1	Homo sapiens	26-30
28063793-9	2017	IL-6 plus AG490 or piceatannol) IL-6-induced increases in SPA and StAR mRNA.	3,3',4,5'-tetrahydroxystilbene	19-30	surfactant protein A1	Homo sapiens	58-61
28791026-6	2017	We analyzed blood and serum samples from 32 patients, suffering from MSDs, who had been treated in the radon spa in Bad Steben (Germany).	steben	120-126	surfactant protein A1	Homo sapiens	109-112
27258774-4	2017	From 2012 to 2013, we experienced seven patients desensitized using SPA IA, initially presenting negative cytotoxic complement dependent (CDC) T-cell crossmatches but positive B and T cell flowcytometric crossmatch, who despite significant DSA reduction developed weakly positive CDC T-cell crossmatch shortly prior to transplantation.	dsa	240-243	surfactant protein A1	Homo sapiens	68-71
28485325-10	2017	In addition, levels of phosphorylated IkappaB-alpha and nuclear NF-kappaB were augmented with LPS exposure for 2 h. LPS-induced SP-A and TLR4 mRNA as well as NF-kappaB expression were significantly inhibited by pretreatment with CLI-095.	ethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-ene-1-carboxylate	229-236	surfactant protein A1	Homo sapiens	128-132
27859014-6	2017	Higher CBMC PspA-IL-5 and PspA-IL-13 responses correlated with a higher proportion of cord CD4 T cells, and higher dPly-IL-6 responses with a higher frequency of cord antigen-presenting cells.	cbmc	7-11	surfactant protein A1	Homo sapiens	12-16
27793398-3	2017	SP-A binds to carbohydrates on the surface of pathogens in a calcium-dependent manner to enable neutralisation, agglutination and clearance of pathogens including RSV.	Carbohydrates	14-27	surfactant protein A1	Homo sapiens	0-4
27793398-3	2017	SP-A binds to carbohydrates on the surface of pathogens in a calcium-dependent manner to enable neutralisation, agglutination and clearance of pathogens including RSV.	Calcium	61-68	surfactant protein A1	Homo sapiens	0-4
28101052-9	2016	Results: CSF-SP concentrations (mean +- standard deviation in ng/ml) were as follows: SP-A 0.71 +- 0.58, SP-B 0.18 +- 0.43, SP-C 0.89 +- 0.77 and SP-D 7.4 +- 5.4.	sp	13-15	surfactant protein A1	Homo sapiens	86-90
27934478-1	2016	Surfactant protein A (SP-A), a lung anti-infective protein, is a lectin with affinity for sugars found on fungal and micrococcal surfaces such as mannose.	Sugars	90-96	surfactant protein A1	Homo sapiens	0-20
27934478-1	2016	Surfactant protein A (SP-A), a lung anti-infective protein, is a lectin with affinity for sugars found on fungal and micrococcal surfaces such as mannose.	Sugars	90-96	surfactant protein A1	Homo sapiens	22-26
27934478-1	2016	Surfactant protein A (SP-A), a lung anti-infective protein, is a lectin with affinity for sugars found on fungal and micrococcal surfaces such as mannose.	Mannose	146-153	surfactant protein A1	Homo sapiens	0-20
27934478-1	2016	Surfactant protein A (SP-A), a lung anti-infective protein, is a lectin with affinity for sugars found on fungal and micrococcal surfaces such as mannose.	Mannose	146-153	surfactant protein A1	Homo sapiens	22-26
27934478-2	2016	We synthesized a mannosylated poly(lactic acid)-poly(ethylene glycol) (PLA-PEG) copolymer and used it to produce nanoparticles with a polyester (PLGA/PLA) core and a PEG shell decorated with mannose residues, designed to be strongly associated with SP-A for an increased uptake by alveolar macrophages.	pla-peg) copolymer	71-89	surfactant protein A1	Homo sapiens	249-253
27934478-4	2016	The presence of mannose on the surface was demonstrated by zeta potential changes according to pH and by a strong aggregation in the presence of concanavalin A. Mannosylated nanoparticles bound to SP-A as demonstrated by dynamic light scattering and transmission electron microscopy.	Mannose	16-23	surfactant protein A1	Homo sapiens	197-201
27667820-6	2016	SPA-LEED moreover clearly shows the presence of homogeneously distributed rotational domains of two-dimensionally isotropic PTCDA.	3,4,9,10-perylenetetracarboxylic dianhydride	124-129	surfactant protein A1	Homo sapiens	0-3
27271568-8	2016	In addition, we found that SP-A bound to human IFN-gamma (KD = 11 +- 0.5 nM) in a Ca(2+)-dependent manner and prevented IFN-gamma interaction with IFN-gammaR1 on human aMphis.	methyl 2-(((2-aminoethyl)amino)methyl)-6-carboxylpyridinehistidinate	168-174	surfactant protein A1	Homo sapiens	27-31
27215389-6	2016	Knockdown of the miR-29 family in cultured HFL type II cells blocked cAMP-induced SP-A expression and accumulation of surfactant-containing lamellar bodies, suggesting their physiological relevance.	Cyclic AMP	69-73	surfactant protein A1	Homo sapiens	82-86
27271568-2	2016	However, the exact role of SP-A and the mechanism by which SP-A affects IFN-gamma-induced activation of alveolar macrophages (aMphis) remains unknown.	methyl 2-(((2-aminoethyl)amino)methyl)-6-carboxylpyridinehistidinate	126-132	surfactant protein A1	Homo sapiens	59-63
27271568-3	2016	To address these questions, we studied the effect of human SP-A on rat and human aMphis stimulated with IFN-gamma, LPS, and combinations thereof and measured the induction of proinflammatory mediators as well as SP-A"s ability to bind to IFN-gamma or IFN-gammaR1.	methyl 2-(((2-aminoethyl)amino)methyl)-6-carboxylpyridinehistidinate	81-87	surfactant protein A1	Homo sapiens	59-63
27656877-9	2016	SP-A is elevated in diseases accompanied by ventricular enlargement (AQS, acute HC w/o AQS) in a significant manner (0.67, 1.21 vs 0.38 ng/ml in control, p&lt;0.001).	Hydrocortisone	80-82	surfactant protein A1	Homo sapiens	0-4
27656877-13	2016	There are significant changes of SP-A and SP-C levels in diseases affecting brain water circulation and elevation of intracranial pressure.	Water	82-87	surfactant protein A1	Homo sapiens	33-37
27795995-6	2016	RESULTS: Surfactant protein A in exhaled particles and the SP-A/albumin ratio were lower (P = 0.002 and P = 0.0001 respectively) in the BOS group compared to the BOS-free group.	N-[4-(Aminosulfonyl)phenyl]-2-Mercaptobenzamide	136-139	surfactant protein A1	Homo sapiens	9-29
27795995-6	2016	RESULTS: Surfactant protein A in exhaled particles and the SP-A/albumin ratio were lower (P = 0.002 and P = 0.0001 respectively) in the BOS group compared to the BOS-free group.	N-[4-(Aminosulfonyl)phenyl]-2-Mercaptobenzamide	136-139	surfactant protein A1	Homo sapiens	59-63
27795995-8	2016	CONCLUSIONS: We conclude that low levels of SP-A in exhaled particles are associated with increased risk of BOS in LTRs.	N-[4-(Aminosulfonyl)phenyl]-2-Mercaptobenzamide	108-111	surfactant protein A1	Homo sapiens	44-48
27508436-3	2016	However, previous studies have shown that SP-A also aids in the formation and biophysical properties of pulmonary surfactant films at the air-water interface.	Water	142-147	surfactant protein A1	Homo sapiens	42-46
27215389-2	2016	Expression of the gene (SFTPA) encoding the major surfactant protein, SP-A, in midgestation human fetal lung (HFL) is dramatically induced by cyclic AMP (cAMP).	Cyclic AMP	142-152	surfactant protein A1	Homo sapiens	70-74
27215389-2	2016	Expression of the gene (SFTPA) encoding the major surfactant protein, SP-A, in midgestation human fetal lung (HFL) is dramatically induced by cyclic AMP (cAMP).	Cyclic AMP	154-158	surfactant protein A1	Homo sapiens	70-74
27215389-3	2016	cAMP induction of SP-A expression is repressed by transforming growth factor beta (TGF-beta) and by hypoxia.	Cyclic AMP	0-4	surfactant protein A1	Homo sapiens	18-22
27559371-16	2016	In conclusion, SP-alpha-Ch dyads are unique in the sense that they can be used to photogenerate both biradicals and singlet oxygen, thus being able to initiate Ch oxidation from their triplet excited states following either of the two competing mechanistic pathways.	Singlet Oxygen	116-130	surfactant protein A1	Homo sapiens	15-23
27324153-2	2016	Bifunctional avidity of SP-A for pathogen-associated molecular patterns (PAMPs) such as lipid A and for dipalmitoylphosphatidylcholine (DPPC), the major component of surfactant membranes lining the air-liquid interface of the lung, ensures that the protein is poised for first-line interactions with inhaled pathogens.	Lipid A	88-95	surfactant protein A1	Homo sapiens	24-28
27324153-2	2016	Bifunctional avidity of SP-A for pathogen-associated molecular patterns (PAMPs) such as lipid A and for dipalmitoylphosphatidylcholine (DPPC), the major component of surfactant membranes lining the air-liquid interface of the lung, ensures that the protein is poised for first-line interactions with inhaled pathogens.	1,2-Dipalmitoylphosphatidylcholine	104-134	surfactant protein A1	Homo sapiens	24-28
27324153-2	2016	Bifunctional avidity of SP-A for pathogen-associated molecular patterns (PAMPs) such as lipid A and for dipalmitoylphosphatidylcholine (DPPC), the major component of surfactant membranes lining the air-liquid interface of the lung, ensures that the protein is poised for first-line interactions with inhaled pathogens.	1,2-Dipalmitoylphosphatidylcholine	136-140	surfactant protein A1	Homo sapiens	24-28
27324153-3	2016	To improve our understanding of the motifs that are required for interactions with microbes and surfactant structures, we explored the role of the tyrosine-rich binding surface on the carbohydrate recognition domain of SP-A in the interaction with DPPC and lipid A using crystallography, site-directed mutagenesis, and molecular dynamics simulations.	Tyrosine	147-155	surfactant protein A1	Homo sapiens	219-223
27324153-3	2016	To improve our understanding of the motifs that are required for interactions with microbes and surfactant structures, we explored the role of the tyrosine-rich binding surface on the carbohydrate recognition domain of SP-A in the interaction with DPPC and lipid A using crystallography, site-directed mutagenesis, and molecular dynamics simulations.	Carbohydrates	184-196	surfactant protein A1	Homo sapiens	219-223
27324153-3	2016	To improve our understanding of the motifs that are required for interactions with microbes and surfactant structures, we explored the role of the tyrosine-rich binding surface on the carbohydrate recognition domain of SP-A in the interaction with DPPC and lipid A using crystallography, site-directed mutagenesis, and molecular dynamics simulations.	1,2-Dipalmitoylphosphatidylcholine	248-252	surfactant protein A1	Homo sapiens	219-223
27324153-3	2016	To improve our understanding of the motifs that are required for interactions with microbes and surfactant structures, we explored the role of the tyrosine-rich binding surface on the carbohydrate recognition domain of SP-A in the interaction with DPPC and lipid A using crystallography, site-directed mutagenesis, and molecular dynamics simulations.	Lipid A	257-264	surfactant protein A1	Homo sapiens	219-223
27324153-5	2016	This basic cluster is also critical for binding of lipid A, a bacterial PAMP and target for SP-A.	Lipid A	51-58	surfactant protein A1	Homo sapiens	92-96
27324153-7	2016	These results suggest that the differential binding properties of SP-A favor transfer of the protein from surfactant DPPC to pathogen membranes containing appropriate lipid PAMPs to effect key host defense functions.	1,2-Dipalmitoylphosphatidylcholine	117-121	surfactant protein A1	Homo sapiens	66-70
27324153-7	2016	These results suggest that the differential binding properties of SP-A favor transfer of the protein from surfactant DPPC to pathogen membranes containing appropriate lipid PAMPs to effect key host defense functions.	lipid pamps	167-178	surfactant protein A1	Homo sapiens	66-70
27337142-8	2016	In post-hoc analysis, SP-A levels differed only between controls and CPFE (p&lt;0.05) and CPFE and emphysema (p&lt;0.05).	cpfe	69-73	surfactant protein A1	Homo sapiens	22-26
27337142-14	2016	CONCLUSION: In conclusion, serum SP-A and SP-D levels were higher where fibrosis exists or coexists and related to disease severity, suggesting that serum SPs relate to alveolar damage in fibrotic lungs and may reflect either local overproduction or overleakage.	Sodium phenolsulfonate	155-158	surfactant protein A1	Homo sapiens	33-37
26220138-8	2016	In patients with CRSsNP and more severe form of the disease, higher levels of SP-A and SP-D in NALF and stronger immunoreactivity of these proteins in nasal mucosa were detected.	crssnp	17-23	surfactant protein A1	Homo sapiens	78-82
26220138-9	2016	Identification of pathogenic bacteria was associated with higher levels of SP-A and SP-D in NALF and nasal mucosa in patients with CRSsNP and control group.	crssnp	131-137	surfactant protein A1	Homo sapiens	75-79
26767511-3	2016	The evolved PVAc corona was significantly enriched compared to that observed on SiO2 nanoparticles (698 vs. 429 proteins identified); however both coronas contained a substantial contribution from innate immunity proteins, including surfactant protein A, napsin A and complement (C1q and C3) proteins.	polyvinyl acetate	12-16	surfactant protein A1	Homo sapiens	233-253
27250970-3	2016	SP-A and SP-D, which are also known as pulmonary collectins, have an important function in the host"s lung immune response; they act as opsonins for different pathogens via a C-terminal carbohydrate recognition domain and enhance the attachment to phagocytic cells or show their own microbicidal activity by increasing the cellular membrane permeability.	Carbohydrates	186-198	surfactant protein A1	Homo sapiens	0-4
27250970-5	2016	SP-A and SP-D bind glucan and mannose residues from fungal cell wall, but there is still a lack of information on their binding to other fungal carbohydrate residues.	Glucans	19-25	surfactant protein A1	Homo sapiens	0-4
27250970-5	2016	SP-A and SP-D bind glucan and mannose residues from fungal cell wall, but there is still a lack of information on their binding to other fungal carbohydrate residues.	Mannose	30-37	surfactant protein A1	Homo sapiens	0-4
27250970-5	2016	SP-A and SP-D bind glucan and mannose residues from fungal cell wall, but there is still a lack of information on their binding to other fungal carbohydrate residues.	Carbohydrates	144-156	surfactant protein A1	Homo sapiens	0-4
26313358-4	2015	DKK-1 and SOST serum levels were assessed at baseline and were compared between the subgroup of patients fulfilling ASAS criteria for SpA (n = 486; 68.6%) and 80 healthy controls.	Aspirin	116-120	surfactant protein A1	Homo sapiens	134-137
26611525-9	2016	Aspect of patients, 0.45% NaCl group and 0.9% NaCl+ambroxol group were significantly different in the levels of SP-A, IL-6, IL-8 and TNF-alpha (P&lt;0.01).	Sodium Chloride	26-30	surfactant protein A1	Homo sapiens	112-116
26611525-9	2016	Aspect of patients, 0.45% NaCl group and 0.9% NaCl+ambroxol group were significantly different in the levels of SP-A, IL-6, IL-8 and TNF-alpha (P&lt;0.01).	Sodium Chloride	46-50	surfactant protein A1	Homo sapiens	112-116
26611525-9	2016	Aspect of patients, 0.45% NaCl group and 0.9% NaCl+ambroxol group were significantly different in the levels of SP-A, IL-6, IL-8 and TNF-alpha (P&lt;0.01).	Ambroxol	51-59	surfactant protein A1	Homo sapiens	112-116
26472220-0	2016	Nicotine reduces the levels of surfactant proteins A and D via Wnt/beta-catenin and PKC signaling in human airway epithelial cells.	Nicotine	0-8	surfactant protein A1	Homo sapiens	31-58
26472220-2	2016	We recently showed that in vitro nicotine exposure induces Wnt3a/beta-catenin activation, which is a pathway that has also been implicated in altering levels of SP-A and SP-D.	Nicotine	33-41	surfactant protein A1	Homo sapiens	161-165
26472220-4	2016	The main aim of this study was to investigate whether human bronchial epithelial cells reduce levels of SP-A and SP-D in vitro following nicotine stimulation via the Wnt3a/beta-catenin and PKC signaling pathway.	Nicotine	137-145	surfactant protein A1	Homo sapiens	104-108
26472220-5	2016	We showed that nicotine activated the Wnt3a/beta-catenin and PKC signaling pathway, and this activation was accompanied by a decrease in SP-A and SP-D expression.	Nicotine	15-23	surfactant protein A1	Homo sapiens	137-141
27607236-11	2016	The results of alizarin red staining and ALP detection showed that SpA treatment suppressed the osteogenic differentiation of hBMSCs.	alizarin	15-27	surfactant protein A1	Homo sapiens	67-70
26792177-6	2016	The mutation (p.Trp211Arg), which segregates with a disease phenotype characterized by either isolated IIP/IPF, or IPF associated with lung adenocarcinoma, is located in the carbohydrate recognition domain (CRD) of SP-A1 and involves a residue invariant throughout evolution, not only in SP-A1, but also in its close paralog SP-A2 and other CRD-containing proteins.	Carbohydrates	174-186	surfactant protein A1	Homo sapiens	215-220
26792177-6	2016	The mutation (p.Trp211Arg), which segregates with a disease phenotype characterized by either isolated IIP/IPF, or IPF associated with lung adenocarcinoma, is located in the carbohydrate recognition domain (CRD) of SP-A1 and involves a residue invariant throughout evolution, not only in SP-A1, but also in its close paralog SP-A2 and other CRD-containing proteins.	Carbohydrates	174-186	surfactant protein A1	Homo sapiens	288-293
26707652-3	2016	SP-A was detected in the exhaled breath condensate (EBC) obtained from patients with COPD and from non-COPD subjects.	NSC638702	52-55	surfactant protein A1	Homo sapiens	0-4
26707652-8	2016	The results demonstrated that SP-A was detectable in the EBC of all subjects.	NSC638702	57-60	surfactant protein A1	Homo sapiens	30-34
26707652-11	2016	Decreased expression levels of SP-A in EBC were associated with a higher degree of airway limitation.	NSC638702	39-42	surfactant protein A1	Homo sapiens	31-35
26707652-12	2016	These results suggested that the measurement of SP-A levels in the EBC may serve as a method for monitoring airway obstruction in patients with COPD.	NSC638702	67-70	surfactant protein A1	Homo sapiens	48-52
26203191-1	2015	Type II cell differentiation and expression of the major surfactant protein, SP-A, in mid-gestation human fetal lung (HFL) are induced by cAMP and inhibited by TGF-beta.	Cyclic AMP	138-142	surfactant protein A1	Homo sapiens	77-81
26203191-2	2015	cAMP induction of SP-A promoter activity is mediated by increased phosphorylation and DNA binding of thyroid transcription factor-1 (TTF-1/Nkx2.1), a master regulator of lung development.	Cyclic AMP	0-4	surfactant protein A1	Homo sapiens	18-22
25619705-14	2015	CONCLUSIONS: Circulating SP-A and SP-D levels are decreased in some individuals with higher HI in OSA, possibly reflecting severity of hypoxia in OSA.	hi	92-94	surfactant protein A1	Homo sapiens	25-29
24674306-7	2014	The development of ADAs increased plasma clearance of SPA.	dSMP	19-23	surfactant protein A1	Homo sapiens	54-57
25724120-7	2015	IC formation between SpA and IgG (SpA-IgG ICs) was confirmed by using native polyacrylamide gel electrophoresis.	polyacrylamide	77-91	surfactant protein A1	Homo sapiens	21-24
25724120-7	2015	IC formation between SpA and IgG (SpA-IgG ICs) was confirmed by using native polyacrylamide gel electrophoresis.	polyacrylamide	77-91	surfactant protein A1	Homo sapiens	34-37
25162121-0	2015	Comparison of the effects of betamethasone and dexamethasone on surfactant protein A mRNA expression in human lung cells.	Betamethasone	29-42	surfactant protein A1	Homo sapiens	64-84
25162121-0	2015	Comparison of the effects of betamethasone and dexamethasone on surfactant protein A mRNA expression in human lung cells.	Dexamethasone	47-60	surfactant protein A1	Homo sapiens	64-84
25162121-2	2015	We compared the dose-dependent effects of various concentrations of two synthetic corticosteroids, betamethasone and dexamethasone, on steady state levels of surfactant protein A (SP-A) mRNA in human lung cells.	Betamethasone	99-112	surfactant protein A1	Homo sapiens	158-178
25162121-2	2015	We compared the dose-dependent effects of various concentrations of two synthetic corticosteroids, betamethasone and dexamethasone, on steady state levels of surfactant protein A (SP-A) mRNA in human lung cells.	Betamethasone	99-112	surfactant protein A1	Homo sapiens	180-184
25162121-2	2015	We compared the dose-dependent effects of various concentrations of two synthetic corticosteroids, betamethasone and dexamethasone, on steady state levels of surfactant protein A (SP-A) mRNA in human lung cells.	Dexamethasone	117-130	surfactant protein A1	Homo sapiens	158-178
25162121-2	2015	We compared the dose-dependent effects of various concentrations of two synthetic corticosteroids, betamethasone and dexamethasone, on steady state levels of surfactant protein A (SP-A) mRNA in human lung cells.	Dexamethasone	117-130	surfactant protein A1	Homo sapiens	180-184
25162121-6	2015	RESULTS: A dose-dependent modification in SP-A mRNA levels was demonstrated with both dexamethasone and betamethasone.	Dexamethasone	86-99	surfactant protein A1	Homo sapiens	42-46
25162121-6	2015	RESULTS: A dose-dependent modification in SP-A mRNA levels was demonstrated with both dexamethasone and betamethasone.	Betamethasone	104-117	surfactant protein A1	Homo sapiens	42-46
25162121-7	2015	Cells treated with cAMP expressed higher levels of SP-A mRNA than untreated cells.	Cyclic AMP	19-23	surfactant protein A1	Homo sapiens	51-55
25162121-8	2015	A biphasic curve in the SP-A mRNA response to corticosteroids was elicited only in the presence of cAMP: at lower concentrations (10-10 through 10-12 M), SP-A mRNA levels were upregulated, whereas at higher concentrations (10-7 and 10-8 M), SP-A mRNA levels were reduced.	Cyclic AMP	99-103	surfactant protein A1	Homo sapiens	24-28
25162121-8	2015	A biphasic curve in the SP-A mRNA response to corticosteroids was elicited only in the presence of cAMP: at lower concentrations (10-10 through 10-12 M), SP-A mRNA levels were upregulated, whereas at higher concentrations (10-7 and 10-8 M), SP-A mRNA levels were reduced.	Cyclic AMP	99-103	surfactant protein A1	Homo sapiens	154-158
25162121-8	2015	A biphasic curve in the SP-A mRNA response to corticosteroids was elicited only in the presence of cAMP: at lower concentrations (10-10 through 10-12 M), SP-A mRNA levels were upregulated, whereas at higher concentrations (10-7 and 10-8 M), SP-A mRNA levels were reduced.	Cyclic AMP	99-103	surfactant protein A1	Homo sapiens	154-158
25162121-10	2015	CONCLUSIONS: Our results support a biphasic effect on SP-A mRNA levels after exposure to corticosteroids in combination with cAMP.	Cyclic AMP	125-129	surfactant protein A1	Homo sapiens	54-58
25162121-11	2015	At higher corticosteroid concentrations, betamethasone is less inhibitory than dexamethasone on SP-A mRNA.	Betamethasone	41-54	surfactant protein A1	Homo sapiens	96-100
25162121-11	2015	At higher corticosteroid concentrations, betamethasone is less inhibitory than dexamethasone on SP-A mRNA.	Dexamethasone	79-92	surfactant protein A1	Homo sapiens	96-100
32262909-0	2015	Thromboresistant and rapid-endothelialization effects of dopamine and staphylococcal protein A mediated anti-CD34 coating on 316L stainless steel for cardiovascular devices.	Stainless Steel	130-145	surfactant protein A1	Homo sapiens	70-94
25522687-0	2015	Cholesterol-mediated surfactant dysfunction is mitigated by surfactant protein A.	Cholesterol	0-11	surfactant protein A1	Homo sapiens	60-80
25522687-3	2015	It was hypothesized that elevated cholesterol levels within surfactant inhibit human surfactant biophysical function and that these effects can be reversed by surfactant protein A (SP-A).	Cholesterol	34-45	surfactant protein A1	Homo sapiens	159-179
25522687-3	2015	It was hypothesized that elevated cholesterol levels within surfactant inhibit human surfactant biophysical function and that these effects can be reversed by surfactant protein A (SP-A).	Cholesterol	34-45	surfactant protein A1	Homo sapiens	181-185
25522687-8	2015	It is concluded that cholesterol-induced surfactant inhibition can actively contribute to physiological impairment of the lungs in mechanically ventilated patients and that SP-A levels may be important to maintain surfactant function in the presence of high cholesterol within surfactant.	Cholesterol	258-269	surfactant protein A1	Homo sapiens	173-177
26309693-0	2015	Effect of edaravone on serum SP-A and arterial blood gas in patients with lobectomy.	Edaravone	10-19	surfactant protein A1	Homo sapiens	29-33
26309693-1	2015	OBJECTIVE: To discuss the effect of edaravone on serum pulmonary surfactant protein A (SP-A) and arterial blood gas (ABG) in patients with thoracoscopic lobectomy.	Edaravone	36-45	surfactant protein A1	Homo sapiens	55-85
26309693-1	2015	OBJECTIVE: To discuss the effect of edaravone on serum pulmonary surfactant protein A (SP-A) and arterial blood gas (ABG) in patients with thoracoscopic lobectomy.	Edaravone	36-45	surfactant protein A1	Homo sapiens	87-91
25533100-5	2015	Pre-incubation of low concentrations of U-PS with SP-A resulted in a reduction of SP-A anti-influenza activity in A549 cells, whereas at higher concentrations there was an increase in SP-A antiviral activity.	u-ps	40-44	surfactant protein A1	Homo sapiens	50-54
25533100-5	2015	Pre-incubation of low concentrations of U-PS with SP-A resulted in a reduction of SP-A anti-influenza activity in A549 cells, whereas at higher concentrations there was an increase in SP-A antiviral activity.	u-ps	40-44	surfactant protein A1	Homo sapiens	82-86
25533100-5	2015	Pre-incubation of low concentrations of U-PS with SP-A resulted in a reduction of SP-A anti-influenza activity in A549 cells, whereas at higher concentrations there was an increase in SP-A antiviral activity.	u-ps	40-44	surfactant protein A1	Homo sapiens	82-86
25533100-7	2015	On the other hand, low concentrations of A-PS particles resulted in a reduction of SP-A activity in TT1 cells and a reduction in SP-D activity in A549 cells.	Adenosine Phosphosulfate	41-45	surfactant protein A1	Homo sapiens	83-87
25078973-1	2014	Spiruchostatin A (SP-A) and spiruchostatin B (SP-B) are the potent histone deacetylase inhibitors (HDACi), that has the potential for chemotherapy of leukemia but the exact mechanism of these compounds remains unclear.	spiruchostatin A	0-16	surfactant protein A1	Homo sapiens	18-22
27129122-1	2014	PRTX-100 is a highly-purified preparation of staphylococcal protein A (SpA), with immunologic activity in vitro and in animal models of immune-mediated inflammation.	prtx-100	0-8	surfactant protein A1	Homo sapiens	45-69
27129122-1	2014	PRTX-100 is a highly-purified preparation of staphylococcal protein A (SpA), with immunologic activity in vitro and in animal models of immune-mediated inflammation.	prtx-100	0-8	surfactant protein A1	Homo sapiens	71-74
24122298-8	2014	FTIR analysis revealed changes in the vibrational bands nuas PO-(2), indicating an interaction of SP-A with the 1-phosphate, but not with the 4"-phosphate.	sphingosine 1-phosphate	112-123	surfactant protein A1	Homo sapiens	98-102
25078973-6	2014	SP-A and SP-B induced apoptosis was accompanied by significant increase in the formation of intracellular reactive oxygen species (ROS).	Reactive Oxygen Species	106-129	surfactant protein A1	Homo sapiens	0-4
25078973-6	2014	SP-A and SP-B induced apoptosis was accompanied by significant increase in the formation of intracellular reactive oxygen species (ROS).	Reactive Oxygen Species	131-134	surfactant protein A1	Homo sapiens	0-4
25078973-7	2014	Pre-treatment with N-acetyl-l-cysteine (NAC), significantly inhibited the SP-A and SP-B mediated apoptosis, suggesting a vital role of ROS involved in the lethality of both agents.	Acetylcysteine	19-38	surfactant protein A1	Homo sapiens	74-78
25078973-7	2014	Pre-treatment with N-acetyl-l-cysteine (NAC), significantly inhibited the SP-A and SP-B mediated apoptosis, suggesting a vital role of ROS involved in the lethality of both agents.	Acetylcysteine	40-43	surfactant protein A1	Homo sapiens	74-78
25078973-7	2014	Pre-treatment with N-acetyl-l-cysteine (NAC), significantly inhibited the SP-A and SP-B mediated apoptosis, suggesting a vital role of ROS involved in the lethality of both agents.	Reactive Oxygen Species	135-138	surfactant protein A1	Homo sapiens	74-78
25078973-8	2014	Moreover, SP-A and SP-B treatment resulted in the loss of mitochondrial membrane potential (MMP), and Fas, caspase-8 and caspase-3 activation.	ammonium ferrous sulfate	102-105	surfactant protein A1	Homo sapiens	10-14
25078973-10	2014	In this study, we suggest that a marked induction of intracellular ROS mediated mitochondrial pathway and the Fas plays a role in the SP-A and SP-B induced apoptosis.	Reactive Oxygen Species	67-70	surfactant protein A1	Homo sapiens	134-138
25025725-4	2014	We further developed a SDS-PAGE-based, multiple reaction monitoring (GeLC-MRM) assay for enrichment and targeted quantitation of total SP-A, the SP-A2 isoform, and the Gln223 and Lys223 variants of SP-A, from as little as one milliliter of bronchoalveolar lavage fluid.	Sodium Dodecyl Sulfate	23-26	surfactant protein A1	Homo sapiens	135-139
24909694-2	2014	Here, we present a new method for multilayered, site-directed immobilization of antibody on polystyrene surface through the linkage of a genetically engineered ligand and the assembly of staphylococcal protein A (SPA) with immunoglobulin G (IgG).	Polystyrenes	92-103	surfactant protein A1	Homo sapiens	187-211
24909694-2	2014	Here, we present a new method for multilayered, site-directed immobilization of antibody on polystyrene surface through the linkage of a genetically engineered ligand and the assembly of staphylococcal protein A (SPA) with immunoglobulin G (IgG).	Polystyrenes	92-103	surfactant protein A1	Homo sapiens	213-216
24936027-10	2014	In contrast, exposure of the fetal ovine lung in vivo to ethanol, a risk factor for preterm birth, reduces pulmonary alveolar development and surfactant protein A expression.	Ethanol	57-64	surfactant protein A1	Homo sapiens	142-162
25262689-13	2014	The LDH, CEA and SP-A levels correlated positively with P(A-a) O2 and negatively with TL(CO)%, PaO2 and SaO2 (P &lt; 0.05).	Oxygen	63-65	surfactant protein A1	Homo sapiens	17-21
25262689-13	2014	The LDH, CEA and SP-A levels correlated positively with P(A-a) O2 and negatively with TL(CO)%, PaO2 and SaO2 (P &lt; 0.05).	pao2	95-99	surfactant protein A1	Homo sapiens	17-21
25262689-13	2014	The LDH, CEA and SP-A levels correlated positively with P(A-a) O2 and negatively with TL(CO)%, PaO2 and SaO2 (P &lt; 0.05).	sao2	104-108	surfactant protein A1	Homo sapiens	17-21
24660775-5	2014	Analysis by gel electrophoresis and mass spectrometry revealed transfer of this fluorophore from IgG to specific lysines of its binding partner SpA but not to bovine serum albumin (BSA) as a nonbinding control.	Lysine	113-120	surfactant protein A1	Homo sapiens	144-147
24660775-6	2014	Examination of an X-ray structure of IgG bound to SpA revealed that the fluorophore was selectively transferred between amino groups of lysines that reside within ~10 A at the protein-protein interface.	Lysine	136-143	surfactant protein A1	Homo sapiens	50-53
24388860-3	2014	The system consists on a chemically oxidized PSi platform derivatized with 3-aminopropyltriethoxysilane (APTS) that is coupled to Staphylococcus protein A (SpA).	amino-propyl-triethoxysilane	75-103	surfactant protein A1	Homo sapiens	156-159
24116373-3	2013	An Au-GO composite with the Au spheres size of 15-20 nm was synthesized and modified with staphylococcal protein A (SPA).	Gold	3-5	surfactant protein A1	Homo sapiens	116-119
23620014-6	2013	Dexamethasone promoted the transcription of the SFTPB, SFTPC and SFTPD genes in the A549 and H441 cells and reduced the transcription of the SFTPA1 and SFTPA2 genes in the H441 cells (SFTPA mRNA expression was not detected in A549 cells).	Dexamethasone	0-13	surfactant protein A1	Homo sapiens	141-147
23925886-4	2013	With these modifications separately or in combination, rabbit antisera to the recombinant alpha-helical or proline-rich domains of PspA mediated &gt;50% killing of the target strain.	Proline	107-114	surfactant protein A1	Homo sapiens	131-135
23925886-6	2013	Passive protection of mice against pneumococci and killing in the modified OPKA were lost when normal human sera were adsorbed with recombinant PspA (rPspA) on Sepharose, thus supporting the potential utility of the modified OPKA to detect protective antibodies to PspA.	Sepharose	160-169	surfactant protein A1	Homo sapiens	144-148
23925886-6	2013	Passive protection of mice against pneumococci and killing in the modified OPKA were lost when normal human sera were adsorbed with recombinant PspA (rPspA) on Sepharose, thus supporting the potential utility of the modified OPKA to detect protective antibodies to PspA.	Sepharose	160-169	surfactant protein A1	Homo sapiens	151-155
23707200-4	2013	Breakdown of SP-A was markedly decreased in CF sputum by E-64 and Mu-Leu-Hph-VSPh, a Cat S inhibitor.	mu-leu-hph-vsph	66-81	surfactant protein A1	Homo sapiens	13-17
23707200-5	2013	Cat S cleaved efficiently and specifically SP-A within critical residues of the solvent-exposed loop of its carbohydrate recognition (C-type lectin) domain that allows binding to pathogens.	Carbohydrates	108-120	surfactant protein A1	Homo sapiens	43-47
23707200-6	2013	Cat S decreased aggregation properties of SP-A (self-aggregation, aggregation of phospholipid vesicles and rough LPS).	Phospholipids	81-93	surfactant protein A1	Homo sapiens	42-46
23747872-1	2013	Surfactant Protein A (SP-A) and D (SP-D) are calcium-dependent collagen-containing lectins, also called collectins, which play a significant role in surfactant homeostasis and pulmonary immunity.	Calcium	45-52	surfactant protein A1	Homo sapiens	0-20
23747872-1	2013	Surfactant Protein A (SP-A) and D (SP-D) are calcium-dependent collagen-containing lectins, also called collectins, which play a significant role in surfactant homeostasis and pulmonary immunity.	Calcium	45-52	surfactant protein A1	Homo sapiens	22-33
23072893-5	2012	In this study, sera of children with history of pneumococcal colonization were analyzed for presence of IgG antibodies to the conserved proline-rich region (PRR) of PspA.	Proline	136-143	surfactant protein A1	Homo sapiens	165-169
23628053-8	2013	In response to phytohemagglutinin (PHA, 1 microg/ml), PBMNC from SpA patients secreted more IL-17 than that from healthy control [(573.95 +- 171.68) pg/ml vs (115.53 +- 40.41) pg/ml (P &lt; 0.01)].	pbmnc	54-59	surfactant protein A1	Homo sapiens	65-68
23328605-8	2013	There was a significant correlation between the serum SP-A concentration and thoracic radiographic changes in dogs with BTLI.	btli	120-124	surfactant protein A1	Homo sapiens	54-58
23544079-4	2013	Other proteins of the innate immune system, namely human surfactant protein A and porcine surfactant protein D, have been reported to express sialylated glycans which facilitate inhibition of particular IAV strains, yet the specific viral determinants for recognition of these inhibitors have not been defined.	Polysaccharides	153-160	surfactant protein A1	Homo sapiens	57-77
22966120-2	2012	SP-A prevented the invasion of AEC by alginate-producing P. aeruginosa strains because of a direct effect on the AEC.	Alginates	38-46	surfactant protein A1	Homo sapiens	0-4
22966120-4	2012	Treatment of AEC with SP-A, monoclonal antibodies to CKAP4/P63, or CKAP4/P63-specific siRNA decreased the binding of purified alginate exopolysaccharide to AEC.	alginate exopolysaccharide	126-152	surfactant protein A1	Homo sapiens	22-26
22966120-4	2012	Treatment of AEC with SP-A, monoclonal antibodies to CKAP4/P63, or CKAP4/P63-specific siRNA decreased the binding of purified alginate exopolysaccharide to AEC.	Urea, 1-acetyl-3-(2-ethylcrotonyl)-, (Z)-	13-16	surfactant protein A1	Homo sapiens	22-26
22966120-5	2012	Alginate binding to AEC reduced SP-A release by these cells.	Alginates	0-8	surfactant protein A1	Homo sapiens	32-36
22966120-6	2012	Because the alginate exopolysaccharide is surface-exposed, levels of SP-A may be crucial to modulate the interaction of P. aeruginosa with AEC.	Alginates	12-20	surfactant protein A1	Homo sapiens	69-73
22966120-6	2012	Because the alginate exopolysaccharide is surface-exposed, levels of SP-A may be crucial to modulate the interaction of P. aeruginosa with AEC.	exopolysaccharide	21-38	surfactant protein A1	Homo sapiens	69-73
23499372-9	2013	Taking into account that SP-A did not directly activate NK cells, these results suggest that SP-A inhibited lung cancer progression by recruiting and activating NK cells via controlling the polarization of TAMs.	tams	206-210	surfactant protein A1	Homo sapiens	93-97
32260835-1	2013	In this study, a reductively cleavable photoreactive linker, disulfide-phenylazide (SPA), was synthesized and used to functionalize inorganic mesoporous silica nanoparticles (MSNs) by simple amidation reaction.	disulfide-phenylazide	61-82	surfactant protein A1	Homo sapiens	84-87
32260835-1	2013	In this study, a reductively cleavable photoreactive linker, disulfide-phenylazide (SPA), was synthesized and used to functionalize inorganic mesoporous silica nanoparticles (MSNs) by simple amidation reaction.	mesoporous silica	142-159	surfactant protein A1	Homo sapiens	84-87
23031213-0	2012	Lipoteichoic acid induces surfactant protein-A biosynthesis in human alveolar type II epithelial cells through activating the MEK1/2-ERK1/2-NF-kappaB pathway.	lipoteichoic acid	0-17	surfactant protein A1	Homo sapiens	26-46
23031213-9	2012	Pretreatment with BAY 11-7082, an inhibitor of NF-kappaB activation, significantly inhibited LTA-induced SP-A mRNA expression.	3-(4-methylphenylsulfonyl)-2-propenenitrile	18-29	surfactant protein A1	Homo sapiens	105-109
23031213-12	2012	CONCLUSIONS: Therefore, this study showed that LTA can increase SP-A synthesis in human alveolar type II epithelial cells through sequentially activating the MEK1-ERK1/2-NF-kappaB-dependent pathway.	lipoteichoic acid	47-50	surfactant protein A1	Homo sapiens	64-68
22803352-5	2012	The expressed recombinant SP-A was identified by Western blot and purified from culture medium by Ni-NTA-Agarose beads.	ni-nta	98-104	surfactant protein A1	Homo sapiens	26-30
22879717-8	2012	In addition, spa spring water attenuated the differentiation process of subsets of CD4(+) T cells, i.e., Th1, Th2 and Th17 cells.	Water	24-29	surfactant protein A1	Homo sapiens	13-16
22879717-10	2012	CONCLUSION: Spa spring water treatment suppressed the inflammatory cytokines production and also modulated the differentiation of CD4(+) T cells into Th1, Th2, and Th17 cells, but not the T(regs) cells.	Water	23-28	surfactant protein A1	Homo sapiens	12-15
22701116-1	2012	Surfactant proteins SP-A and SP-D are hydrophilic, collagen-containing calcium-dependent lectins, which appear to have a range of innate immune functions at pulmonary as well as extrapulmonary sites.	Calcium	71-78	surfactant protein A1	Homo sapiens	20-24
22803352-5	2012	The expressed recombinant SP-A was identified by Western blot and purified from culture medium by Ni-NTA-Agarose beads.	Sepharose	105-112	surfactant protein A1	Homo sapiens	26-30
22718593-4	2012	METHODS: Here we evaluate the expression and presence of SPs (SP-A, SP-B, SP-C, and SP-D) in human gingiva and saliva.	Sodium phenolsulfonate	57-60	surfactant protein A1	Homo sapiens	62-66
21833746-7	2012	SP-A and SP-D levels were elevated significantly in the workers with moderately high indium exposure.	Indium	85-91	surfactant protein A1	Homo sapiens	0-4
22418431-8	2012	Furthermore, we found that the functional region of SP-A lies within Tyr(161)-Lys(201).	Tyrosine	69-72	surfactant protein A1	Homo sapiens	52-56
22418431-8	2012	Furthermore, we found that the functional region of SP-A lies within Tyr(161)-Lys(201).	Lysine	78-81	surfactant protein A1	Homo sapiens	52-56
22100538-7	2012	SP-A detection rates were 100%, 21%, and 89% for PEx, EBC and serum, respectively.	NSC638702	54-57	surfactant protein A1	Homo sapiens	0-4
21989137-0	2012	Dissociation of transforming growth factors beta1 and beta2 from surfactant protein A (SP-A) by deglycosylation or deoxycholate treatment.	Deoxycholic Acid	115-127	surfactant protein A1	Homo sapiens	87-91
21989137-5	2012	Deglycosylation of SP-A released TGF-beta1,2 from SP-A indicating a role for the carbohydrate moieties of SP-A in binding of TGF-beta1,2.	Carbohydrates	81-93	surfactant protein A1	Homo sapiens	19-23
21989137-6	2012	TGF-beta-free SP-A was obtained by incubating SP-A with 5 mM deoxycholate at pH 9.2 followed by size-exclusion chromatography, a protocol which can be used to study the biological activities of SP-A and TGF-beta1,2 separately.	Deoxycholic Acid	61-73	surfactant protein A1	Homo sapiens	14-18
21989137-6	2012	TGF-beta-free SP-A was obtained by incubating SP-A with 5 mM deoxycholate at pH 9.2 followed by size-exclusion chromatography, a protocol which can be used to study the biological activities of SP-A and TGF-beta1,2 separately.	Deoxycholic Acid	61-73	surfactant protein A1	Homo sapiens	46-50
21989137-6	2012	TGF-beta-free SP-A was obtained by incubating SP-A with 5 mM deoxycholate at pH 9.2 followed by size-exclusion chromatography, a protocol which can be used to study the biological activities of SP-A and TGF-beta1,2 separately.	Deoxycholic Acid	61-73	surfactant protein A1	Homo sapiens	46-50
22246864-5	2012	The effect of SpA on fibroproliferation in serum-containing medium +- transforming growth factor (TGF)-beta(1) was quantified by methylene blue binding.	Methylene Blue	129-143	surfactant protein A1	Homo sapiens	14-17
22487281-3	2012	This study aimed to reveal the consequences  of systemic methylprednisolone treatment on levels of SP-A and SP-D, which play a role in innate immunity, in patients with CRSwNP.	Methylprednisolone	57-75	surfactant protein A1	Homo sapiens	99-103
22487281-12	2012	Statistically significant up-regulation was detected  in SP-A and SP-D levels after oral methylprednisolone (p = 0.0002 and p = 0.0004, respectively).	Methylprednisolone	89-107	surfactant protein A1	Homo sapiens	57-61
22487281-13	2012	CONCLUSION: In this study, significant up-regulation of SP-A and SP-D was revealed in patients with CRSwNP after systemic steroid treatment.	Steroids	122-129	surfactant protein A1	Homo sapiens	56-60
22718593-7	2012	RESULTS: Our results indicate that SP-A, SP-B, SP-C, and SP-D are peptides produced by healthy gingiva that reveal a changed expression pattern in cases of gingival disease.	Peptides	66-74	surfactant protein A1	Homo sapiens	35-39
22815690-7	2012	AEC-II stimulated with Roflumilast-N-oxide showed a minor increase in SP-A1, SP-C and SP-D mRNA mainly in low expressing preparations.	roflumilast N-oxide	23-42	surfactant protein A1	Homo sapiens	70-75
22739240-7	2012	The H(2)O(2)-induced gene repression or activation of SP-A, SP-B, SP-D and ABCA3 was blocked by pretreatment with the antioxidants N-acetyl-L-cysteine (NAC) and catalase.	Acetylcysteine	131-150	surfactant protein A1	Homo sapiens	54-58
22739240-9	2012	The analyses of signal transduction pathways that may play a role in the regulation of gene expression by H(2)O(2 )using several specific inhibitors showed that U0126, an inhibitor of ERK1/2 upstream kinase MEK1/2, blocked both H(2)O(2)-induced inhibition of SP-A and SP-B gene expression, whereas SB203580, an inhibitor of p38 MAPK, partially blocked H(2)O(2)-mediated inhibition of SP-A gene expression but not SP-B expression.	U 0126	161-166	surfactant protein A1	Homo sapiens	259-263
22739240-9	2012	The analyses of signal transduction pathways that may play a role in the regulation of gene expression by H(2)O(2 )using several specific inhibitors showed that U0126, an inhibitor of ERK1/2 upstream kinase MEK1/2, blocked both H(2)O(2)-induced inhibition of SP-A and SP-B gene expression, whereas SB203580, an inhibitor of p38 MAPK, partially blocked H(2)O(2)-mediated inhibition of SP-A gene expression but not SP-B expression.	U 0126	161-166	surfactant protein A1	Homo sapiens	384-388
22362238-5	2012	Drinking SPA treatment was effected with sulphurous mineral water from Terme of Telese SpA (Benevento - Italy) and the pharmacological treatment provided the use of hypoglycemic drugs normally used in diabetic disease.	Water	60-65	surfactant protein A1	Homo sapiens	9-12
22362238-9	2012	CONCLUSIONS: The data from this preliminary investigation suggest that the drinking SPA therapy with sulphurous mineral water, especially in combination with antidiabetic drug treatment, may be useful in type 2 diabetes mellitus for the improvement redox state of the organism.	Water	120-125	surfactant protein A1	Homo sapiens	84-87
22815690-9	2012	Under these conditions SP-A1, SP-A2, SP-B and SP-D are increased by roflumilast-N-oxide in low expressing preparations.	roflumilast N-oxide	68-87	surfactant protein A1	Homo sapiens	23-28
21733365-16	2011	The TBA concentration in cord blood was positively correlated with SP-A concentration as well (r(3) = 0.494, P &lt; 0.05).	tba	4-7	surfactant protein A1	Homo sapiens	67-71
21474333-9	2011	Pretreatment with PD98059, an inhibitor of ERK1/2, significantly decreased LPS-induced TLR2 and SP-A mRNA expression.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	18-25	surfactant protein A1	Homo sapiens	96-100
21553841-4	2011	However, one of the findings of this study is that when SP-A is bound to detergent and lipid micelles that mimic lung surfactant phospholipids, it exists predominantly as smaller oligomers, in sharp contrast to the much larger forms observed when alone in water.	Phospholipids	129-142	surfactant protein A1	Homo sapiens	56-60
21553841-4	2011	However, one of the findings of this study is that when SP-A is bound to detergent and lipid micelles that mimic lung surfactant phospholipids, it exists predominantly as smaller oligomers, in sharp contrast to the much larger forms observed when alone in water.	Water	256-261	surfactant protein A1	Homo sapiens	56-60
21402781-2	2011	Cyclic AMP (cAMP) induction of SP-A expression in human fetal lung type II cells is O(2) dependent and is mediated by increased binding of TTF-1/Nkx2.1 and NF-kappaB to a critical response element (TBE).	Cyclic AMP	12-16	surfactant protein A1	Homo sapiens	31-35
21402781-2	2011	Cyclic AMP (cAMP) induction of SP-A expression in human fetal lung type II cells is O(2) dependent and is mediated by increased binding of TTF-1/Nkx2.1 and NF-kappaB to a critical response element (TBE).	tbe	198-201	surfactant protein A1	Homo sapiens	31-35
21402781-4	2011	Using chromatin immunoprecipitation analysis of fetal lung between 15.5 and 19.0 days of gestation, we observed that the developmental induction of SP-A was associated with increased recruitment of TTF-1, NF-kappaB, PCAF, and CBP, as well as enhanced acetylation and decreased methylation of histone H3K9 at the TBE.	tbe	312-315	surfactant protein A1	Homo sapiens	148-152
21402781-5	2011	Importantly, expression and TBE binding of the H3K9 methyltransferases, Suv39h1 and Suv39h2, was inversely correlated with the developmental upregulation of SP-A.	tbe	28-31	surfactant protein A1	Homo sapiens	157-161
21402781-6	2011	In human fetal lung epithelial cells, Suv39H1 and Suv39H2 mRNA levels declined with cAMP induction of SP-A.	Cyclic AMP	84-88	surfactant protein A1	Homo sapiens	102-106
21402781-7	2011	Moreover, hypoxia, which inhibits cAMP stimulation of SP-A, markedly increased Suv39h1 and Suv39h2 binding to the TBE.	Cyclic AMP	34-38	surfactant protein A1	Homo sapiens	54-58
21402781-7	2011	Moreover, hypoxia, which inhibits cAMP stimulation of SP-A, markedly increased Suv39h1 and Suv39h2 binding to the TBE.	tbe	114-117	surfactant protein A1	Homo sapiens	54-58
21153920-6	2011	The results showed troglitazone-activated PPARgamma could inhibit the production of TNF-alpha, one of the most important inflammatory factors, and then increased the expression of surfactant-associated protein A (SP-A) and attenuate the apoptosis of alveolar type II epithelial cells.	Troglitazone	19-31	surfactant protein A1	Homo sapiens	180-211
21153920-6	2011	The results showed troglitazone-activated PPARgamma could inhibit the production of TNF-alpha, one of the most important inflammatory factors, and then increased the expression of surfactant-associated protein A (SP-A) and attenuate the apoptosis of alveolar type II epithelial cells.	Troglitazone	19-31	surfactant protein A1	Homo sapiens	213-217
21261566-0	2011	Effect of perfluorohexane on the expression of cellular adhesion molecules and surfactant protein A in human mesothelial cells in vitro.	perflexane	10-25	surfactant protein A1	Homo sapiens	79-99
21261566-5	2011	Concentration of intracellular surfactant protein A tended to be higher in perfluorohexane treated cells compared to controls.	perflexane	75-90	surfactant protein A1	Homo sapiens	31-51
21112663-10	2011	Pretreatment of A549 cells with SP600125, an inhibitor of JNK1, significantly lowered LPS-induced SP-A mRNA production.	pyrazolanthrone	32-40	surfactant protein A1	Homo sapiens	98-102
21402781-2	2011	Cyclic AMP (cAMP) induction of SP-A expression in human fetal lung type II cells is O(2) dependent and is mediated by increased binding of TTF-1/Nkx2.1 and NF-kappaB to a critical response element (TBE).	Cyclic AMP	0-10	surfactant protein A1	Homo sapiens	31-35
21056657-0	2011	Interaction of metal oxide nanoparticles with lung surfactant protein A.	metal oxide	15-26	surfactant protein A1	Homo sapiens	51-71
21425823-7	2011	For SpA, residues F132, Y133, H137, E143, R146, and K154 contribute significantly.	Fast Green FCF	36-40	surfactant protein A1	Homo sapiens	4-7
21172435-0	2011	Surfactant protein A (SP-A)-tacrolimus complexes have a greater anti-inflammatory effect than either SP-A or tacrolimus alone on human macrophage-like U937 cells.	Tacrolimus	28-38	surfactant protein A1	Homo sapiens	0-20
21172435-0	2011	Surfactant protein A (SP-A)-tacrolimus complexes have a greater anti-inflammatory effect than either SP-A or tacrolimus alone on human macrophage-like U937 cells.	Tacrolimus	28-38	surfactant protein A1	Homo sapiens	22-26
21172435-0	2011	Surfactant protein A (SP-A)-tacrolimus complexes have a greater anti-inflammatory effect than either SP-A or tacrolimus alone on human macrophage-like U937 cells.	Tacrolimus	109-119	surfactant protein A1	Homo sapiens	0-20
21056657-2	2011	We here report for the first time significant differences for metal oxide nanoparticles to the binding of surfactant protein A (SP-A), the predominant protein component of ALF.	metal oxide	62-73	surfactant protein A1	Homo sapiens	106-126
21172435-0	2011	Surfactant protein A (SP-A)-tacrolimus complexes have a greater anti-inflammatory effect than either SP-A or tacrolimus alone on human macrophage-like U937 cells.	Tacrolimus	109-119	surfactant protein A1	Homo sapiens	22-26
21172435-2	2011	Nanoparticles of tacrolimus (FK506) might interact with human SP-A, which is the most abundant lipoprotein in the alveolar fluid.	Tacrolimus	17-27	surfactant protein A1	Homo sapiens	62-66
21056657-2	2011	We here report for the first time significant differences for metal oxide nanoparticles to the binding of surfactant protein A (SP-A), the predominant protein component of ALF.	metal oxide	62-73	surfactant protein A1	Homo sapiens	128-132
21172435-2	2011	Nanoparticles of tacrolimus (FK506) might interact with human SP-A, which is the most abundant lipoprotein in the alveolar fluid.	Tacrolimus	29-34	surfactant protein A1	Homo sapiens	62-66
20401612-3	2011	In this study, we evaluated prospectively whether surfactant protein-A (SP-A) and -D (SP-D) may be new conventional predictors of the efficacy of gefitinib treatment.	Gefitinib	146-155	surfactant protein A1	Homo sapiens	50-70
21172435-3	2011	This study was undertaken to determine whether the formation of FK506/SP-A complexes interferes with FK506 immunosuppressive actions on stimulated human macrophage-like U937 cells.	Tacrolimus	64-69	surfactant protein A1	Homo sapiens	70-74
21172435-3	2011	This study was undertaken to determine whether the formation of FK506/SP-A complexes interferes with FK506 immunosuppressive actions on stimulated human macrophage-like U937 cells.	Tacrolimus	101-106	surfactant protein A1	Homo sapiens	70-74
21172435-4	2011	We found that SP-A was avidly bound to FK506 (K(d) = 35 +- 4nM), as determined by solid phase-binding assays and dynamic light scattering.	Tacrolimus	39-44	surfactant protein A1	Homo sapiens	14-18
21172435-8	2011	FK506 bound to SP-A was delivered to macrophages by endocytosis, since several endocytosis inhibitors blocked FK506/SP-A anti-inflammatory effects.	Tacrolimus	0-5	surfactant protein A1	Homo sapiens	15-19
21172435-8	2011	FK506 bound to SP-A was delivered to macrophages by endocytosis, since several endocytosis inhibitors blocked FK506/SP-A anti-inflammatory effects.	Tacrolimus	0-5	surfactant protein A1	Homo sapiens	116-120
21172435-8	2011	FK506 bound to SP-A was delivered to macrophages by endocytosis, since several endocytosis inhibitors blocked FK506/SP-A anti-inflammatory effects.	Tacrolimus	110-115	surfactant protein A1	Homo sapiens	15-19
21270323-0	2011	Surfactant protein-A (SP-A) selectively inhibits prostaglandin F2alpha (PGF2alpha) production in term decidua: implications for the onset of labor.	Dinoprost	49-70	surfactant protein A1	Homo sapiens	0-20
21270323-0	2011	Surfactant protein-A (SP-A) selectively inhibits prostaglandin F2alpha (PGF2alpha) production in term decidua: implications for the onset of labor.	Dinoprost	49-70	surfactant protein A1	Homo sapiens	22-26
21270323-0	2011	Surfactant protein-A (SP-A) selectively inhibits prostaglandin F2alpha (PGF2alpha) production in term decidua: implications for the onset of labor.	Dinoprost	72-81	surfactant protein A1	Homo sapiens	0-20
21270323-0	2011	Surfactant protein-A (SP-A) selectively inhibits prostaglandin F2alpha (PGF2alpha) production in term decidua: implications for the onset of labor.	Dinoprost	72-81	surfactant protein A1	Homo sapiens	22-26
21270323-8	2011	The effect of SP-A on eicosanoid gene expression was measured by quantitative RT-PCR.	Eicosanoids	22-32	surfactant protein A1	Homo sapiens	14-18
21270323-10	2011	High-dose SP-A (100 mug/ml) inhibited PGF(2alpha) by term decidual stromal cells without affecting the production of other inflammatory mediators, and this effect occurred at a posttranscriptional level.	Prostaglandins F	38-41	surfactant protein A1	Homo sapiens	10-14
21270323-13	2011	CONCLUSIONS: SP-A is produced by human endometrium/decidua, where it significantly and selectively inhibits PGF(2alpha) production.	Prostaglandins F	108-111	surfactant protein A1	Homo sapiens	13-17
21270323-15	2011	These novel observations suggest that decidual SP-A likely plays a critical role in regulating prostaglandin production within the uterus, culminating at term in decidual activation and the onset of labor.	Prostaglandins	95-108	surfactant protein A1	Homo sapiens	47-51
21338074-1	2011	To investigate the effect of antibody orientation on its immunological activities, we developed a novel and versatile platform consisting of a well-defined phospholipid polymer surface on which staphylococcal protein A (SpA) was site-selectively immobilized.	phospholipid polymer	156-176	surfactant protein A1	Homo sapiens	220-223
21338074-4	2011	An enzymatic reaction was performed for orientation-selective coupling of SpA molecules to the polymer brush surface.	Polymers	95-102	surfactant protein A1	Homo sapiens	74-77
20401612-3	2011	In this study, we evaluated prospectively whether surfactant protein-A (SP-A) and -D (SP-D) may be new conventional predictors of the efficacy of gefitinib treatment.	Gefitinib	146-155	surfactant protein A1	Homo sapiens	72-84
20423923-8	2010	By contrast, SP-A shows features consistent with its preference for lipid ligands, including lipid A and the major surfactant lipid, dipalmitoylphosphatidylcholine.	Lipid A	93-100	surfactant protein A1	Homo sapiens	13-17
21047777-3	2011	This study describes crystal structures of calcium-dependent complexes of the C-terminal neck and carbohydrate recognition domain of SP-A with d-mannose, D-alpha-methylmannose, and glycerol, which represent subdomains of glycans on pathogen surfaces.	Calcium	43-50	surfactant protein A1	Homo sapiens	133-137
21047777-3	2011	This study describes crystal structures of calcium-dependent complexes of the C-terminal neck and carbohydrate recognition domain of SP-A with d-mannose, D-alpha-methylmannose, and glycerol, which represent subdomains of glycans on pathogen surfaces.	Carbohydrates	98-110	surfactant protein A1	Homo sapiens	133-137
21047777-3	2011	This study describes crystal structures of calcium-dependent complexes of the C-terminal neck and carbohydrate recognition domain of SP-A with d-mannose, D-alpha-methylmannose, and glycerol, which represent subdomains of glycans on pathogen surfaces.	Mannose	143-152	surfactant protein A1	Homo sapiens	133-137
21047777-3	2011	This study describes crystal structures of calcium-dependent complexes of the C-terminal neck and carbohydrate recognition domain of SP-A with d-mannose, D-alpha-methylmannose, and glycerol, which represent subdomains of glycans on pathogen surfaces.	d-alpha-methylmannose	154-175	surfactant protein A1	Homo sapiens	133-137
21047777-3	2011	This study describes crystal structures of calcium-dependent complexes of the C-terminal neck and carbohydrate recognition domain of SP-A with d-mannose, D-alpha-methylmannose, and glycerol, which represent subdomains of glycans on pathogen surfaces.	Glycerol	181-189	surfactant protein A1	Homo sapiens	133-137
21047777-3	2011	This study describes crystal structures of calcium-dependent complexes of the C-terminal neck and carbohydrate recognition domain of SP-A with d-mannose, D-alpha-methylmannose, and glycerol, which represent subdomains of glycans on pathogen surfaces.	Polysaccharides	221-228	surfactant protein A1	Homo sapiens	133-137
21047777-6	2011	The Glu-202 side chain of unliganded SP-A extends out into the solvent and away from the calcium ion; however, in the complexes, the Glu-202 side chain translocates 12.8 A to bind the calcium.	Glutamic Acid	4-7	surfactant protein A1	Homo sapiens	37-41
21047777-6	2011	The Glu-202 side chain of unliganded SP-A extends out into the solvent and away from the calcium ion; however, in the complexes, the Glu-202 side chain translocates 12.8 A to bind the calcium.	Calcium	89-96	surfactant protein A1	Homo sapiens	37-41
21047777-6	2011	The Glu-202 side chain of unliganded SP-A extends out into the solvent and away from the calcium ion; however, in the complexes, the Glu-202 side chain translocates 12.8 A to bind the calcium.	Glutamic Acid	133-136	surfactant protein A1	Homo sapiens	37-41
21047777-6	2011	The Glu-202 side chain of unliganded SP-A extends out into the solvent and away from the calcium ion; however, in the complexes, the Glu-202 side chain translocates 12.8 A to bind the calcium.	Calcium	184-191	surfactant protein A1	Homo sapiens	37-41
21047777-10	2011	The ability to undergo conformational changes may help SP-A adapt to different ligand classes, including microbial glycolipids and surfactant lipids.	Glycolipids	115-126	surfactant protein A1	Homo sapiens	55-59
20473679-7	2010	Oleic acid-induced lung injury resulted in a marked influx of neutrophils into BAL, and this influx was reduced by 70% by pretreatment with the antibody to SP-A receptor.	Oleic Acid	0-10	surfactant protein A1	Homo sapiens	156-160
21092225-5	2010	METHODS: Anti-SP-A antibodies fixed to latex beads bound SP-A at its N-terminal end and allowed the interaction with other SP-A molecules in a given sample by their C-terminal carbohydrate recognition domain (CRD) to agglutinate the beads to aggregates, which were quantified by light microscopy.	Carbohydrates	176-188	surfactant protein A1	Homo sapiens	14-18
21092225-6	2010	RESULTS: SP-A aggregation was dependent on its concentration, the presence of calcium, and was dose-dependently inhibited by mannose.	Calcium	78-85	surfactant protein A1	Homo sapiens	9-13
21092225-6	2010	RESULTS: SP-A aggregation was dependent on its concentration, the presence of calcium, and was dose-dependently inhibited by mannose.	Mannose	125-132	surfactant protein A1	Homo sapiens	9-13
20870746-5	2010	cAMP exposure resulted in enrichment of P63 on the cell surface as shown by stimulation of SP-A binding, enhanced association of labeled P63 antibody with type II cells, and promotion of SP-A-mediated liposome uptake, all of which were inhibited by competing P63 antibody.	Cyclic AMP	0-4	surfactant protein A1	Homo sapiens	91-95
20870746-5	2010	cAMP exposure resulted in enrichment of P63 on the cell surface as shown by stimulation of SP-A binding, enhanced association of labeled P63 antibody with type II cells, and promotion of SP-A-mediated liposome uptake, all of which were inhibited by competing P63 antibody.	Cyclic AMP	0-4	surfactant protein A1	Homo sapiens	187-191
20870746-8	2010	Treatment with LY-294002, an inhibitor of the PI3-kinase pathway, prevented the SP-A-induced PM enrichment of P63.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	15-24	surfactant protein A1	Homo sapiens	80-84
20683585-3	2010	A simple electrochemical procedure was formulated to prepare sulphonyl chloride terminated gold surfaces that form a strong sulphonamide bond with the receptor protein staphylococcal protein A (SpA).	sulfonyl chloride	61-79	surfactant protein A1	Homo sapiens	168-192
20683585-3	2010	A simple electrochemical procedure was formulated to prepare sulphonyl chloride terminated gold surfaces that form a strong sulphonamide bond with the receptor protein staphylococcal protein A (SpA).	sulfonyl chloride	61-79	surfactant protein A1	Homo sapiens	194-197
20683585-3	2010	A simple electrochemical procedure was formulated to prepare sulphonyl chloride terminated gold surfaces that form a strong sulphonamide bond with the receptor protein staphylococcal protein A (SpA).	Sulfanilamide	124-136	surfactant protein A1	Homo sapiens	168-192
20683585-3	2010	A simple electrochemical procedure was formulated to prepare sulphonyl chloride terminated gold surfaces that form a strong sulphonamide bond with the receptor protein staphylococcal protein A (SpA).	Sulfanilamide	124-136	surfactant protein A1	Homo sapiens	194-197
20423923-8	2010	By contrast, SP-A shows features consistent with its preference for lipid ligands, including lipid A and the major surfactant lipid, dipalmitoylphosphatidylcholine.	1,2-Dipalmitoylphosphatidylcholine	133-163	surfactant protein A1	Homo sapiens	13-17
20153410-13	2010	In addition, the mRNA levels of surfactant proteins (SPs), namely, SP-A, SP-B, SP-C, and SP-D (alveolar epithelial cell functional markers) were significantly decreased.	Sodium phenolsulfonate	53-56	surfactant protein A1	Homo sapiens	67-71
20448439-10	2010	r-UTI patients with 19Ala/Ala or 223Gln/Gln genotype were associated with high serum and low urine SP-A levels (p &lt; 0.01).	Alanine	22-25	surfactant protein A1	Homo sapiens	99-103
20448439-10	2010	r-UTI patients with 19Ala/Ala or 223Gln/Gln genotype were associated with high serum and low urine SP-A levels (p &lt; 0.01).	Glutamine	36-39	surfactant protein A1	Homo sapiens	99-103
19860445-4	2010	A final amphiphile resulted from the conjugation of DAB-dendr-(NH(2))(16) with 1,2-distearoyl-sn-glycero-3-phosphoethanolamine-succinimidylpropionate (DSPE-PEG(3400)-SPA), i.e.: DPD5 (with 4 DSPE-PEG arms).	dab-dendr-(nh(2))	52-69	surfactant protein A1	Homo sapiens	166-169
20336594-1	2010	Dutogliptin (PHX-1149T), being developed by Phenomix Corp, Forest Laboratories Inc and Chiesi Farmaceutici SpA, is a small-molecule dipeptidyl peptidase-4 (DPP-4) inhibitor for the potential oral treatment of type 2 diabetes mellitus (T2DM).	dutogliptin	0-11	surfactant protein A1	Homo sapiens	107-110
19860445-4	2010	A final amphiphile resulted from the conjugation of DAB-dendr-(NH(2))(16) with 1,2-distearoyl-sn-glycero-3-phosphoethanolamine-succinimidylpropionate (DSPE-PEG(3400)-SPA), i.e.: DPD5 (with 4 DSPE-PEG arms).	1,2-distearoyl-sn-glycero-3-phosphoethanolamine-succinimidylpropionate	79-149	surfactant protein A1	Homo sapiens	166-169
19741063-5	2010	Additionally, the SP-A expression pattern was evaluated by immunohistochemistry in formalin-fixed, paraffin-embedded lung tissue sections from the same subjects.	Formaldehyde	83-91	surfactant protein A1	Homo sapiens	18-22
21203987-2	2010	Here we present evidence that phosphatidylserine (PS) is a relevant binding molecule for human SP-A.	Phosphatidylserines	30-48	surfactant protein A1	Homo sapiens	95-99
21203987-2	2010	Here we present evidence that phosphatidylserine (PS) is a relevant binding molecule for human SP-A.	Phosphatidylserines	50-52	surfactant protein A1	Homo sapiens	95-99
21203987-3	2010	The binding is Ca(2+)-dependent and is not inhibited by mannose, suggesting that the sugar-binding site of the carbohydrate recognition domain (CRD) of SP-A is not involved.	Sugars	85-90	surfactant protein A1	Homo sapiens	152-156
21203987-3	2010	The binding is Ca(2+)-dependent and is not inhibited by mannose, suggesting that the sugar-binding site of the carbohydrate recognition domain (CRD) of SP-A is not involved.	Carbohydrates	111-123	surfactant protein A1	Homo sapiens	152-156
21203987-6	2010	However, we cannot conclude that this inhibition is exclusively due to the binding of SP-A to PS on the cell surface, as annexin V is not wholly specific for PS and SP-A also interacts with other phospholipids that might become exposed on the apoptotic cell surface.	Phosphatidylserines	94-96	surfactant protein A1	Homo sapiens	86-90
20054141-3	2010	There are four surfactant proteins named SP-A, SP-B, SP-C, and SP-D; their distinct interactions with surfactant phospholipids are necessary for the ultra-structural organization, stability, metabolism, and lowering of surface tension.	Phospholipids	113-126	surfactant protein A1	Homo sapiens	41-45
19741063-5	2010	Additionally, the SP-A expression pattern was evaluated by immunohistochemistry in formalin-fixed, paraffin-embedded lung tissue sections from the same subjects.	Paraffin	99-107	surfactant protein A1	Homo sapiens	18-22
19517319-1	2009	Elocalcitol, which had been under development by BioXell SpA, is a synthetic derivative of vitamin D3 that regulates cell proliferation and apoptosis via its binding to the vitamin D receptor.	BXL628	0-11	surfactant protein A1	Homo sapiens	57-60
19712733-7	2009	Pretreatment of A549 cells with SP600125, an inhibitor of c-Jun N-terminal kinase, decreased c-Jun translocation, and significantly ameliorated LPS-induced SP-A mRNA production.	pyrazolanthrone	32-40	surfactant protein A1	Homo sapiens	156-160
19394213-4	2009	Affinities of PEG, BSA, human immunoglobulin G (hIgG), and Staphylococcus protein A (SPA) for alpha-SiO(2)(quartz), Au thin film, PEG, and BSA are systematically studied by the homebuilt flow-injection system.	Polyethylene Glycols	130-133	surfactant protein A1	Homo sapiens	85-88
19423113-3	2009	Efficiencies were similar in sodium dodecylsulphate polyacrylamide gel electrophoresis and size-exclusion chromatography; however, 2-D DIGE revealed higher efficiency with SpA than with CEX capture.	Echothiophate Iodide	131-134	surfactant protein A1	Homo sapiens	172-175
19423113-3	2009	Efficiencies were similar in sodium dodecylsulphate polyacrylamide gel electrophoresis and size-exclusion chromatography; however, 2-D DIGE revealed higher efficiency with SpA than with CEX capture.	dige	135-139	surfactant protein A1	Homo sapiens	172-175
19566962-2	2009	We have recently demonstrated that SP-A enhances the killing of bacillus Calmette-Guerin (BCG) by rat macrophages through a nitric oxide-dependent pathway.	Nitric Oxide	124-136	surfactant protein A1	Homo sapiens	35-39
19566962-5	2009	BCG-SP-A complexes were routinely prepared by incubation of a ratio of 20 microg of SP-A to 5 x 105 BCG for 30 min at 37 degrees C. Cells were incubated with PBS, SP-A, BCG, or SP-A-BCG complexes for the times indicated.	Lead	158-161	surfactant protein A1	Homo sapiens	4-8
19566962-8	2009	RESULTS: Involvement of tyrosine kinases was demonstrated by herbimycin A-mediated inhibition of the SP-A-enhanced nitric oxide production and BCG killing.	herbimycin	61-73	surfactant protein A1	Homo sapiens	101-105
19566962-8	2009	RESULTS: Involvement of tyrosine kinases was demonstrated by herbimycin A-mediated inhibition of the SP-A-enhanced nitric oxide production and BCG killing.	Nitric Oxide	115-127	surfactant protein A1	Homo sapiens	101-105
19566962-10	2009	An inhibitor of upstream kinases required for ERK activation inhibited BCG- and SP-A-BCG-enhanced production of nitric oxide by approximately 35%.	Nitric Oxide	112-124	surfactant protein A1	Homo sapiens	80-84
19566962-12	2009	Finally, lactacystin, an inhibitor of IkappaB degradation, reduced BCG- and SP-A-BCG-induced nitric oxide production by 60% and 80% respectively.	lactacystin	9-20	surfactant protein A1	Homo sapiens	76-80
19566962-12	2009	Finally, lactacystin, an inhibitor of IkappaB degradation, reduced BCG- and SP-A-BCG-induced nitric oxide production by 60% and 80% respectively.	Nitric Oxide	93-105	surfactant protein A1	Homo sapiens	76-80
19517319-1	2009	Elocalcitol, which had been under development by BioXell SpA, is a synthetic derivative of vitamin D3 that regulates cell proliferation and apoptosis via its binding to the vitamin D receptor.	Cholecalciferol	91-101	surfactant protein A1	Homo sapiens	57-60
19000577-8	2008	Research on wild-type and mutant recombinant molecules in vivo and in vitro showed that SP-A and SP-D bind carbohydrates, lipids, and nucleic acids with a broad-spectrum specificity and initiate phagocytosis of inhaled pathogens as well as apoptotic cells.	Carbohydrates	107-120	surfactant protein A1	Homo sapiens	88-92
19264843-0	2009	cAMP enhances estrogen-related receptor alpha (ERRalpha) transcriptional activity at the SP-A promoter by increasing its interaction with protein kinase A and steroid receptor coactivator 2 (SRC-2).	Cyclic AMP	0-4	surfactant protein A1	Homo sapiens	89-93
19264843-4	2009	cAMP/PKA stimulation of ERRalpha activation of the SP-A promoter was blocked by the PKA inhibitor, H89, whereas the MAPK P38 inhibitor, SB203580, and the MAPK kinase inhibitor, PD98059, had negligible to modest effects.	Cyclic AMP	0-4	surfactant protein A1	Homo sapiens	51-55
19264843-4	2009	cAMP/PKA stimulation of ERRalpha activation of the SP-A promoter was blocked by the PKA inhibitor, H89, whereas the MAPK P38 inhibitor, SB203580, and the MAPK kinase inhibitor, PD98059, had negligible to modest effects.	N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide	99-102	surfactant protein A1	Homo sapiens	51-55
19264843-10	2009	Collectively, these findings indicate that cAMP/PKA signaling enhances ERRalpha phosphorylation and nuclear localization, recruitment to the SP-A promoter, and interaction with PKAcat and SRC-2, resulting in the up-regulation of SP-A gene transcription.	Cyclic AMP	43-47	surfactant protein A1	Homo sapiens	141-145
19264843-10	2009	Collectively, these findings indicate that cAMP/PKA signaling enhances ERRalpha phosphorylation and nuclear localization, recruitment to the SP-A promoter, and interaction with PKAcat and SRC-2, resulting in the up-regulation of SP-A gene transcription.	Cyclic AMP	43-47	surfactant protein A1	Homo sapiens	229-233
19112099-8	2009	Surfactant protein (SP)-A and SP-B mRNA levels were approximately one third of control levels following ethanol exposure (P &lt; 0.05).	Ethanol	104-111	surfactant protein A1	Homo sapiens	0-25
19848584-4	2008	To attenuate these effects we used monomethoxy polyethylene glycol-succinimidyl propionate (mPEG-SPA) to modify first-generation vectors that express an anti-HBV RNAi effector.	monomethoxy polyethylene glycol-succinimidyl propionate	35-90	surfactant protein A1	Homo sapiens	97-100
19848584-4	2008	To attenuate these effects we used monomethoxy polyethylene glycol-succinimidyl propionate (mPEG-SPA) to modify first-generation vectors that express an anti-HBV RNAi effector.	monomethoxypolyethylene glycol	92-96	surfactant protein A1	Homo sapiens	97-100
18566427-3	2008	Our data demonstrate that SP-A binds to HIV in a calcium-dependent manner that is inhibitable by mannose and EDTA.	Calcium	49-56	surfactant protein A1	Homo sapiens	26-30
18599636-3	2008	In the presence of calcium, large interconnected aggregates of fluorescently labeled TR-SP-A were observed on the surface of Re-LPS films by epifluorescence microscopy.	Calcium	19-26	surfactant protein A1	Homo sapiens	88-92
18599636-7	2008	Taken together, our results seem to indicate that the calcium-dependent permeabilization of Re-LPS membranes by SP-A is related to the extraction of LPS molecules from the membrane due to the formation of calcium-mediated protein aggregates that contain LPS.	Calcium	54-61	surfactant protein A1	Homo sapiens	112-116
18599636-7	2008	Taken together, our results seem to indicate that the calcium-dependent permeabilization of Re-LPS membranes by SP-A is related to the extraction of LPS molecules from the membrane due to the formation of calcium-mediated protein aggregates that contain LPS.	Calcium	205-212	surfactant protein A1	Homo sapiens	112-116
18463356-9	2008	Stimulation of myometrial cells with SFTPA1 markedly enhanced the intensity of the filamentous-actin pool stained with fluorescein isothiocyanate-phalloidin.	fluorescein isothiocyanate-phalloidin	119-156	surfactant protein A1	Homo sapiens	37-43
18754883-4	2008	Gefitinib treatment suppressed surfactant protein (SP)-A expression in H441 human lung adenocarcinoma cells expressing SP-A, -B, -C and -D by inhibiting epidermal growth factor signal.	Gefitinib	0-9	surfactant protein A1	Homo sapiens	31-56
18754883-4	2008	Gefitinib treatment suppressed surfactant protein (SP)-A expression in H441 human lung adenocarcinoma cells expressing SP-A, -B, -C and -D by inhibiting epidermal growth factor signal.	Gefitinib	0-9	surfactant protein A1	Homo sapiens	119-138
18754883-7	2008	Daily administration of gefitinib gradually reduced SP-A level in the bronchoalveolar lavage fluid.	Gefitinib	24-33	surfactant protein A1	Homo sapiens	52-56
18754883-10	2008	These results demonstrated that pretreatment with gefitinib exacerbated LPS-induced lung inflammation by reducing SP-A expression in the lung.	Gefitinib	50-59	surfactant protein A1	Homo sapiens	114-118
18566427-5	2008	Digestion of gp120 with endoglycosidase H abrogates the binding of SP-A, indicating that the high mannose structures on gp120 are the target of the collectin.	Mannose	98-105	surfactant protein A1	Homo sapiens	67-71
18566427-3	2008	Our data demonstrate that SP-A binds to HIV in a calcium-dependent manner that is inhibitable by mannose and EDTA.	Mannose	97-104	surfactant protein A1	Homo sapiens	26-30
18566427-3	2008	Our data demonstrate that SP-A binds to HIV in a calcium-dependent manner that is inhibitable by mannose and EDTA.	Edetic Acid	109-113	surfactant protein A1	Homo sapiens	26-30
18522535-11	2008	Methylation-bisulfite sequencing detected methylated CpG sites within three Sp motifs (Sp a, Sp b and Sp c) and GC-rich flanking sequences, and demethylation by 5-aza-2"-deoxycytidine up-regulated Axl and Sp3 expression in low-Axl-expressing Colo206f/WiDr cells, but not in high-Axl-expressing Rko cells.	hydrogen sulfite	12-21	surfactant protein A1	Homo sapiens	87-91
18285549-4	2008	RESULTS: Circulating SP-A concentration was significantly higher among patients with glucose intolerance and type 2 diabetes than in subjects with normal glucose tolerance, even after adjustment for BMI, age, and smoking status (ex/never).	Glucose	85-92	surfactant protein A1	Homo sapiens	21-25
18407667-7	2008	SP-A also recognized in vitro polymerized filaments in a calcium-dependent manner at a physiological ionic strength but not the C1q receptor gC1qR.	Calcium	57-64	surfactant protein A1	Homo sapiens	0-4
18407667-8	2008	Furthermore, Texas Red-labeled SP-A colocalized with desmin filaments in myometrial cells.	Texas red	13-22	surfactant protein A1	Homo sapiens	31-35
18407667-9	2008	Interestingly, vimentin, the IF characteristic of leukocytes, is one of the major proteins recognized by SP-A in protein extracts of U937 cells after PMA-induced differentiation of this monocytic cell line.	Tetradecanoylphorbol Acetate	150-153	surfactant protein A1	Homo sapiens	105-109
18285549-5	2008	The most significant differences were found in overweight and obese subjects with altered glucose tolerance (n = 59) who showed significantly increased serum SP-A concentrations (by a mean of 24%) compared with obese subjects with normal glucose tolerance (n = 58) (log SP-A 1.54 +/- 0.13 vs. 1.44 +/- 0.13; P &lt; 0.0001).	Glucose	90-97	surfactant protein A1	Homo sapiens	158-162
18285549-7	2008	In subjects with altered glucose tolerance, insulin sensitivity (P = 0.01) and fasting triglycerides (P = 0.02) contributed to 37% of SP-A variance.	Triglycerides	87-100	surfactant protein A1	Homo sapiens	134-138
18079322-1	2008	Surfactant protein-A (SP-A) gene expression in human fetal lung type II cells is stimulated by cAMP and IL-1 and is inhibited by glucocorticoids.	Cyclic AMP	95-99	surfactant protein A1	Homo sapiens	0-20
18458694-8	2008	In the trail of human vaginal doughing water, in contrast to the control group, the levels of SP-A of VVC group were higher, which was considered to be significant (P&lt;0.05).	Water	39-44	surfactant protein A1	Homo sapiens	94-98
17520282-4	2008	We found that both SP-A1 and SP-A2 equally displayed alpha(2,3)-linked sialic acids, and had similar activity against a strain (PR-8) that preferentially binds to alpha(2,3)-linked sialic acids.	Sialic Acids	71-83	surfactant protein A1	Homo sapiens	19-24
17520282-4	2008	We found that both SP-A1 and SP-A2 equally displayed alpha(2,3)-linked sialic acids, and had similar activity against a strain (PR-8) that preferentially binds to alpha(2,3)-linked sialic acids.	Sialic Acids	181-193	surfactant protein A1	Homo sapiens	19-24
18079322-1	2008	Surfactant protein-A (SP-A) gene expression in human fetal lung type II cells is stimulated by cAMP and IL-1 and is inhibited by glucocorticoids.	Cyclic AMP	95-99	surfactant protein A1	Homo sapiens	22-26
18079322-2	2008	cAMP/IL-1 stimulation of SP-A expression is mediated by increased binding of thyroid transcription factor-1 and nuclear factor (NF)-kappaB to the TTF-1-binding element (TBE) in the SP-A promoter.	Cyclic AMP	0-4	surfactant protein A1	Homo sapiens	25-29
18079322-2	2008	cAMP/IL-1 stimulation of SP-A expression is mediated by increased binding of thyroid transcription factor-1 and nuclear factor (NF)-kappaB to the TTF-1-binding element (TBE) in the SP-A promoter.	Cyclic AMP	0-4	surfactant protein A1	Homo sapiens	181-185
17905854-2	2007	The goal of the current study is to test the hypothesis that SP-A regulates IgG-mediated phagocytosis by neutrophils, which are major effector cells of the innate immune response that remove invading pathogens by phagocytosis and by extracellular killing mediated by reactive oxygen and nitrogen.	reactive oxygen and nitrogen	267-295	surfactant protein A1	Homo sapiens	61-65
17579843-5	2007	The result of the BALF proteome analysis show the presence of several isoforms of SP-A, in which an N-non-glycosylierte form and several proline hydroxylations were identified.	Nitrogen	100-101	surfactant protein A1	Homo sapiens	82-86
17693477-0	2007	Surfactant protein A forms extensive lattice-like structures on 1,2-dipalmitoylphosphatidylcholine/rough-lipopolysaccharide-mixed monolayers.	1,2-Dipalmitoylphosphatidylcholine	64-98	surfactant protein A1	Homo sapiens	0-20
17693477-1	2007	Due to the inhalation of airborne particles containing bacterial lipopolysaccharide (LPS), these molecules might incorporate into the 1,2-dipalmitoylphosphatidylcholine (DPPC)-rich monolayer and interact with surfactant protein A (SP-A), the major surfactant protein component involved in host defense.	,2-dipalmitoylphosphatidylcholine	135-168	surfactant protein A1	Homo sapiens	231-235
17693477-1	2007	Due to the inhalation of airborne particles containing bacterial lipopolysaccharide (LPS), these molecules might incorporate into the 1,2-dipalmitoylphosphatidylcholine (DPPC)-rich monolayer and interact with surfactant protein A (SP-A), the major surfactant protein component involved in host defense.	1,2-Dipalmitoylphosphatidylcholine	170-174	surfactant protein A1	Homo sapiens	209-229
17693477-1	2007	Due to the inhalation of airborne particles containing bacterial lipopolysaccharide (LPS), these molecules might incorporate into the 1,2-dipalmitoylphosphatidylcholine (DPPC)-rich monolayer and interact with surfactant protein A (SP-A), the major surfactant protein component involved in host defense.	1,2-Dipalmitoylphosphatidylcholine	170-174	surfactant protein A1	Homo sapiens	231-235
17693477-2	2007	In this study, epifluorescence microscopy combined with a surface balance was used to examine the interaction of SP-A with mixed monolayers of DPPC/rough LPS (Re-LPS).	1,2-Dipalmitoylphosphatidylcholine	143-147	surfactant protein A1	Homo sapiens	113-117
17693477-6	2007	SP-A interacted strongly with Re-LPS and promoted the formation of DPPC-rich solid domains.	1,2-Dipalmitoylphosphatidylcholine	67-71	surfactant protein A1	Homo sapiens	0-4
17693477-7	2007	Fluorescently labeled Texas red-SP-A accumulated at the fluid-solid boundary regions and formed networks of interconnected filaments in the fluid phase of DPPC/Re-LPS monolayers in a Ca(2+)-independent manner.	1,2-Dipalmitoylphosphatidylcholine	155-159	surfactant protein A1	Homo sapiens	32-36
17693477-8	2007	These lattice-like structures were also observed when TR-SP-A interacted with lipid A monolayers.	Lipid A	78-85	surfactant protein A1	Homo sapiens	57-61
17693477-9	2007	These novel results deepen our understanding of the specific interaction of SP-A with the lipid A moiety of bacterial LPS.	Lipid A	90-97	surfactant protein A1	Homo sapiens	76-80
18022079-6	2007	RESULTS: Among 11 differentially expressed proteins, we identified 2 locally produced factors: peroxiredoxin II (PRXII), exclusively expressed in BOS; and surfactant protein A (SP-A), expressed consistently less in BOS patients than in stable LTRs.	N-[4-(Aminosulfonyl)phenyl]-2-Mercaptobenzamide	215-218	surfactant protein A1	Homo sapiens	155-175
18022079-6	2007	RESULTS: Among 11 differentially expressed proteins, we identified 2 locally produced factors: peroxiredoxin II (PRXII), exclusively expressed in BOS; and surfactant protein A (SP-A), expressed consistently less in BOS patients than in stable LTRs.	N-[4-(Aminosulfonyl)phenyl]-2-Mercaptobenzamide	215-218	surfactant protein A1	Homo sapiens	177-181
18022079-8	2007	Finally, the time course of SP-A was studied in 5 LTRs who subsequently developed BOS.	N-[4-(Aminosulfonyl)phenyl]-2-Mercaptobenzamide	82-85	surfactant protein A1	Homo sapiens	28-32
18022079-10	2007	CONCLUSIONS: Our results suggest that testing SP-A levels in BALf could predict LTR patients who are at higher risk of BOS development.	N-[4-(Aminosulfonyl)phenyl]-2-Mercaptobenzamide	119-122	surfactant protein A1	Homo sapiens	46-50
17579843-5	2007	The result of the BALF proteome analysis show the presence of several isoforms of SP-A, in which an N-non-glycosylierte form and several proline hydroxylations were identified.	Proline	137-144	surfactant protein A1	Homo sapiens	82-86
17659477-1	2007	Merck Serono SA (formerly Serono), under license from Newron Pharmaceuticals SpA (following its acquisition of the rights from Pharmacia and Upjohn AB [now Pfizer Inc]), is developing the oral alpha-aminoamide derivative of milacemide, safinamide, a monoamine oxidase-B and glutamate release inhibitor, for the potential treatment of Parkinson"s disease, epilepsy and restless legs syndrome.	serono	6-12	surfactant protein A1	Homo sapiens	77-80
17678872-0	2007	Differential effects of human SP-A1 and SP-A2 variants on phospholipid monolayers containing surfactant protein B.	Phospholipids	58-70	surfactant protein A1	Homo sapiens	30-35
17678872-4	2007	We have found that the human in vitro expressed variants, SP-A1 (6A(2)) and SP-A2 (1A(0)), and the coexpressed SP-A1/SP-A2 (6A(2)/1A(0)) protein have a differential influence on the organization of phospholipid monolayers containing surfactant protein B (SP-B).	Phospholipids	198-210	surfactant protein A1	Homo sapiens	111-116
17678872-9	2007	The results indicate that human SP-A1 and SP-A2 variants exhibit differential effects on characteristics of phospholipid monolayers containing SP-B.	Phospholipids	108-120	surfactant protein A1	Homo sapiens	32-37
17580966-0	2007	Effect of cysteine 85 on biochemical properties and biological function of human surfactant protein A variants.	Cysteine	10-18	surfactant protein A1	Homo sapiens	81-101
17580966-2	2007	One of these, cysteine 85 that could form intermolecular disulfide bonds, is present in SP-A1 (Cys85) and absent in SP-A2 (Arg85).	Cysteine	14-22	surfactant protein A1	Homo sapiens	88-93
17580966-2	2007	One of these, cysteine 85 that could form intermolecular disulfide bonds, is present in SP-A1 (Cys85) and absent in SP-A2 (Arg85).	Disulfides	57-66	surfactant protein A1	Homo sapiens	88-93
17542781-9	2007	On the one hand, SP-A1/SP-A2, like SP-A2, had a higher degree of oligomerization than SP-A1, and consequently had lower K(d) for binding to bacterial Re-LPS (rough lipopolysaccharide), higher self-association in the presence of calcium and greater capability to aggregate Re-LPS and phospholipids than SP-A1.	Calcium	228-235	surfactant protein A1	Homo sapiens	17-22
17542781-9	2007	On the one hand, SP-A1/SP-A2, like SP-A2, had a higher degree of oligomerization than SP-A1, and consequently had lower K(d) for binding to bacterial Re-LPS (rough lipopolysaccharide), higher self-association in the presence of calcium and greater capability to aggregate Re-LPS and phospholipids than SP-A1.	Phospholipids	283-296	surfactant protein A1	Homo sapiens	17-22
17434940-1	2007	Deuterium nuclear magnetic resonance was used to monitor lipid acyl-chain orientational order in suspensions of dipalmitoylphosphatidylcholine (DPPC) and dipalmitoylphosphatidylglycerol (DPPG) containing Ca(2+) and the lung surfactant proteins SP-A and SP-B separately and together.	Deuterium	0-9	surfactant protein A1	Homo sapiens	244-248
17434940-4	2007	SP-A had little effect on DPPC-d(62) chain order but did narrow the temperature range over which DPPG-d(62) ordered at the liquid-crystal-to-gel transition.	dppg-d	97-103	surfactant protein A1	Homo sapiens	0-4
17434940-6	2007	Near the transition, though, there was evidence that SP-A promoted preferential depletion of DPPG from liquid crystalline domains in the temperature range over which gel and liquid crystal domains coexist.	1,2-dipalmitoylphosphatidylglycerol	93-97	surfactant protein A1	Homo sapiens	53-57
17659477-1	2007	Merck Serono SA (formerly Serono), under license from Newron Pharmaceuticals SpA (following its acquisition of the rights from Pharmacia and Upjohn AB [now Pfizer Inc]), is developing the oral alpha-aminoamide derivative of milacemide, safinamide, a monoamine oxidase-B and glutamate release inhibitor, for the potential treatment of Parkinson"s disease, epilepsy and restless legs syndrome.	serono	26-32	surfactant protein A1	Homo sapiens	77-80
17220308-5	2007	Here we used SP-A1 (6A(2), 6A(4)) and SP-A2 (1A(0), 1A(1)) allele variants expressed by CHO (Chinese hamster ovary) mammalian cells to study their effect on association and/or internalization of P. aeruginosa by rAMs and/or human AMs (hAMs) and to study if phagocytosis can be modulated differentially and/or more effectively by CHO cell-expressed SP-A variants than by insect-cell expressed SP-A variants.	cho	88-91	surfactant protein A1	Homo sapiens	13-18
17318528-9	2007	The binding of the mimotopes to the Fab part of the IgG1 antibody and binding of SpA to the Fc part of the IgG1 antibody were mainly driven by hydrophobic effects and associated with a relatively large change in water-accessible surface area.	Water	212-217	surfactant protein A1	Homo sapiens	81-84
17599561-7	2007	CONCLUSION: SPA1, A2, and D are upregulated in various forms of CRS, but are significantly elevated in cystic fibrosis CRS.	3-cresol	64-67	surfactant protein A1	Homo sapiens	12-16
17364965-0	2007	Inhibition of ozone-induced SP-A oxidation by plant polyphenols.	Ozone	14-19	surfactant protein A1	Homo sapiens	28-32
17364965-0	2007	Inhibition of ozone-induced SP-A oxidation by plant polyphenols.	Polyphenols	52-63	surfactant protein A1	Homo sapiens	28-32
17364965-2	2007	It has been shown that ozone-induced oxidation of SP-A protein changes its functional and biochemical properties.	Ozone	23-28	surfactant protein A1	Homo sapiens	50-54
17364965-3	2007	In the present study, eight plant polyphenols (three flavonoids, three hydroxycinnamic acids, and two hydroxybenzoic acids) known as strong antioxidants, were tested for their ability to inhibit ozone-induced SP-A oxidation as a mechanism for chemoprevention against lung damage.	Polyphenols	34-45	surfactant protein A1	Homo sapiens	209-213
17364965-3	2007	In the present study, eight plant polyphenols (three flavonoids, three hydroxycinnamic acids, and two hydroxybenzoic acids) known as strong antioxidants, were tested for their ability to inhibit ozone-induced SP-A oxidation as a mechanism for chemoprevention against lung damage.	Hydroxybenzoates	102-122	surfactant protein A1	Homo sapiens	209-213
17364965-4	2007	SP-A isolated from alveolar proteinosis patients was exposed to ozone (1 ppm) for 4 h. The flavonoids protected SP-A from oxidation in a dose dependent manner.	Flavonoids	91-101	surfactant protein A1	Homo sapiens	0-4
17364965-4	2007	SP-A isolated from alveolar proteinosis patients was exposed to ozone (1 ppm) for 4 h. The flavonoids protected SP-A from oxidation in a dose dependent manner.	Flavonoids	91-101	surfactant protein A1	Homo sapiens	112-116
17364965-6	2007	Hydroxybenzoic acids inhibited SP-A oxidation in a dose-dependent manner although they were less potent than flavonoids.	Hydroxybenzoates	0-20	surfactant protein A1	Homo sapiens	31-35
17364965-9	2007	The results indicate that inhibition of SP-A oxidation by plant polyphenols may be a mechanism accounting for the protective activity of natural antioxidants against the effects of ozone exposure on lungs.	Polyphenols	64-75	surfactant protein A1	Homo sapiens	40-44
17378767-4	2007	Using a fluorescein-labeled PEG-SPA linker (SPA, succinimidyl ester of PEG propionic acid) with a 5-kDa linear PEG moiety, multiple preparations of fluoro-PEG-rAds were produced under various reaction conditions, purified, and analyzed by size-exclusion high-performance liquid chromatography (HPLC) with fluorescence quantification of the virus peak.	Fluorescein	8-19	surfactant protein A1	Homo sapiens	32-35
17378767-4	2007	Using a fluorescein-labeled PEG-SPA linker (SPA, succinimidyl ester of PEG propionic acid) with a 5-kDa linear PEG moiety, multiple preparations of fluoro-PEG-rAds were produced under various reaction conditions, purified, and analyzed by size-exclusion high-performance liquid chromatography (HPLC) with fluorescence quantification of the virus peak.	Fluorescein	8-19	surfactant protein A1	Homo sapiens	44-47
17378767-4	2007	Using a fluorescein-labeled PEG-SPA linker (SPA, succinimidyl ester of PEG propionic acid) with a 5-kDa linear PEG moiety, multiple preparations of fluoro-PEG-rAds were produced under various reaction conditions, purified, and analyzed by size-exclusion high-performance liquid chromatography (HPLC) with fluorescence quantification of the virus peak.	Polyethylene Glycols	28-31	surfactant protein A1	Homo sapiens	32-35
17378767-4	2007	Using a fluorescein-labeled PEG-SPA linker (SPA, succinimidyl ester of PEG propionic acid) with a 5-kDa linear PEG moiety, multiple preparations of fluoro-PEG-rAds were produced under various reaction conditions, purified, and analyzed by size-exclusion high-performance liquid chromatography (HPLC) with fluorescence quantification of the virus peak.	Polyethylene Glycols	28-31	surfactant protein A1	Homo sapiens	44-47
17056727-0	2007	Effect of surfactant protein A on the physical properties and surface activity of KL4-surfactant.	sinapultide	82-85	surfactant protein A1	Homo sapiens	10-30
17426003-3	2007	RESULTS: After platelet CD42a modification by 5 kD and 20 kD mPEG-SPA, the fluorescence intensity of CD42a decreased sharply by 85.54% and 88.65%, respectively, and multiple lysine regions were identified on the surface of CD42a molecule.	Lysine	174-180	surfactant protein A1	Homo sapiens	66-69
17056727-5	2007	We found that SP-A had a concentration-dependent effect on the surface activity of KL(4)-DPPC/POPG/PA membranes but not on that of an animal-derived LES.	kl(4)-dppc/	83-94	surfactant protein A1	Homo sapiens	14-18
17056727-5	2007	We found that SP-A had a concentration-dependent effect on the surface activity of KL(4)-DPPC/POPG/PA membranes but not on that of an animal-derived LES.	1-palmitoyl-2-oleoylglycero-3-phosphoglycerol	94-98	surfactant protein A1	Homo sapiens	14-18
17056727-5	2007	We found that SP-A had a concentration-dependent effect on the surface activity of KL(4)-DPPC/POPG/PA membranes but not on that of an animal-derived LES.	Protactinium	99-101	surfactant protein A1	Homo sapiens	14-18
17056727-6	2007	The surface activity of KL(4)-surfactant significantly improved after enrichment with 2.5-5 wt % SP-A.	sinapultide	24-29	surfactant protein A1	Homo sapiens	97-101
17056727-8	2007	This was due to the fluidizing effect of supraphysiological SP-A concentrations on KL(4)-DPPC/POPG/PA membranes as determined by fluorescence anisotropy measurements, calorimetric studies, and confocal fluorescence microscopy of GUVs.	kl(4)-dppc	83-93	surfactant protein A1	Homo sapiens	60-64
17056727-8	2007	This was due to the fluidizing effect of supraphysiological SP-A concentrations on KL(4)-DPPC/POPG/PA membranes as determined by fluorescence anisotropy measurements, calorimetric studies, and confocal fluorescence microscopy of GUVs.	1-palmitoyl-2-oleoylglycero-3-phosphoglycerol	94-98	surfactant protein A1	Homo sapiens	60-64
17056727-8	2007	This was due to the fluidizing effect of supraphysiological SP-A concentrations on KL(4)-DPPC/POPG/PA membranes as determined by fluorescence anisotropy measurements, calorimetric studies, and confocal fluorescence microscopy of GUVs.	Protactinium	99-101	surfactant protein A1	Homo sapiens	60-64
17056727-9	2007	High SP-A concentrations caused disappearance of the solid/fluid phase coexistence of KL(4)-surfactant, suggesting that phase coexistence might be important for the surface adsorption process.	sinapultide	86-91	surfactant protein A1	Homo sapiens	5-9
17514488-8	2007	SP-D had greater NA inhibitory activity than mannose-binding lectin, which in turn had greater activity than SP-A.	Mannose	45-52	surfactant protein A1	Homo sapiens	109-113
17283573-2	2007	Toll-like receptors (TLRs) are known to bind pathogen-associated molecular patterns in addition to sinonasally secreted surfactant proteins (SP) such as SP-A and SP-D.	sp	141-143	surfactant protein A1	Homo sapiens	153-157
16905641-5	2007	Proteasome inhibitors lactacystin and MG132 reduced the levels of SP-A, SP-B, and SP-C mRNAs in a concentration-dependent manner in H441 and MLE-12 cells.	lactacystin	22-33	surfactant protein A1	Homo sapiens	66-70
16905641-5	2007	Proteasome inhibitors lactacystin and MG132 reduced the levels of SP-A, SP-B, and SP-C mRNAs in a concentration-dependent manner in H441 and MLE-12 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	38-43	surfactant protein A1	Homo sapiens	66-70
17204705-1	2007	UNLABELLED: (18)F-Labeled substance P antagonist-receptor quantifier ([(18)F]SPA-RQ) [2-fluoromethoxy-5-(5-trifluoromethyl-tetrazol-1-yl)-benzyl]-[(2S,3S)-2-phenyl-piperidin-3-yl)amine] is a selective radioligand for in vivo quantification of tachykinin NK(1) receptors with PET.	2-fluoromethoxy-5-(5-trifluoromethyl-tetrazol-1-yl)-benzyl]-[(2s,3s)-2-phenyl-piperidin-3-yl)amine	86-184	surfactant protein A1	Homo sapiens	77-80
17544823-3	2007	SP-A and SP-D are pattern-recognition molecules with the lectin domains binding preferentially to sugars on a broad spectrum of pathogen surfaces and thereby facilitating immune functions including viral neutralization, clearance of bacteria, fungi and apoptotic and necrotic cells, modulation of allergic reactions, and resolution of inflammation.	Sugars	98-104	surfactant protein A1	Homo sapiens	0-4
17544824-2	2007	Studies on allergen-sensitized murine models, and asthmatic patients, show that SP-A and SP-D can: specifically bind to aero-allergens; inhibit mast cell degranulation and histamine release; and modulate the activation of alveolar macrophages and dendritic cells during the acute hypersensitive phase of allergic response.	Histamine	172-181	surfactant protein A1	Homo sapiens	80-84
17128993-0	2006	Surfactant protein A without the interruption of Gly-X-Y repeats loses a kink of oligomeric structure and exhibits impaired phospholipid liposome aggregation ability.	Phospholipids	124-136	surfactant protein A1	Homo sapiens	0-20
17313021-7	2007	In summary, we report here an elderly case of drug-induced pneumonitis successfully weaned from mechanical ventilation by early treatment with corticosteroid and sivelestat sodium, monitored by changes of markers for interstitial pneumonitis (KL-6, SP-A, SP-D).	Sivelestat sodium	162-179	surfactant protein A1	Homo sapiens	249-253
17128993-3	2006	A collagen-like domain of human SP-A consists of 23 Gly-X-Y repeats with an interruption near the midpoint of this domain.	Glycine	52-55	surfactant protein A1	Homo sapiens	32-36
17128993-8	2006	Both SP-ADEL and SP-AINS mutants as well as wild-type SP-A bound to liposomes containing dipalmitoylphosphatidylcholine and galactosylceramide at equivalent levels, but the abilities of the mutants to induce phospholipid liposome aggregation were significantly less developed than that of the wild type.	1,2-Dipalmitoylphosphatidylcholine	89-119	surfactant protein A1	Homo sapiens	5-9
17128993-8	2006	Both SP-ADEL and SP-AINS mutants as well as wild-type SP-A bound to liposomes containing dipalmitoylphosphatidylcholine and galactosylceramide at equivalent levels, but the abilities of the mutants to induce phospholipid liposome aggregation were significantly less developed than that of the wild type.	Galactosylceramides	124-142	surfactant protein A1	Homo sapiens	5-9
17128993-8	2006	Both SP-ADEL and SP-AINS mutants as well as wild-type SP-A bound to liposomes containing dipalmitoylphosphatidylcholine and galactosylceramide at equivalent levels, but the abilities of the mutants to induce phospholipid liposome aggregation were significantly less developed than that of the wild type.	Phospholipids	208-220	surfactant protein A1	Homo sapiens	5-9
17128993-9	2006	The mutants SP-ADEL and SP-AINS augmented liposome uptake by alveolar type II cells and inhibited secretion of phospholipids from type II cells at a level comparable to that of wild-type SP-A.	Phospholipids	111-124	surfactant protein A1	Homo sapiens	12-16
17128993-10	2006	These results indicate that the interruption of Gly-X-Y repeats in the SP-A molecule is critical for the formation of a flower bouquet-like octadecamer and contributes to SP-A"s capacity to aggregate phospholipid liposomes.	Glycine	48-51	surfactant protein A1	Homo sapiens	71-75
17128993-10	2006	These results indicate that the interruption of Gly-X-Y repeats in the SP-A molecule is critical for the formation of a flower bouquet-like octadecamer and contributes to SP-A"s capacity to aggregate phospholipid liposomes.	Glycine	48-51	surfactant protein A1	Homo sapiens	171-175
17128993-10	2006	These results indicate that the interruption of Gly-X-Y repeats in the SP-A molecule is critical for the formation of a flower bouquet-like octadecamer and contributes to SP-A"s capacity to aggregate phospholipid liposomes.	Phospholipids	200-212	surfactant protein A1	Homo sapiens	71-75
17128993-10	2006	These results indicate that the interruption of Gly-X-Y repeats in the SP-A molecule is critical for the formation of a flower bouquet-like octadecamer and contributes to SP-A"s capacity to aggregate phospholipid liposomes.	Phospholipids	200-212	surfactant protein A1	Homo sapiens	171-175
17003084-0	2006	Induction of surfactant protein A expression by cortisol facilitates prostaglandin synthesis in human chorionic trophoblasts.	Hydrocortisone	48-56	surfactant protein A1	Homo sapiens	13-33
17090701-7	2006	Binding is calcium dependent but not inhibited by saccharides known to bind to SP-A"s carbohydrate recognition domain.	Calcium	11-18	surfactant protein A1	Homo sapiens	79-83
17090701-7	2006	Binding is calcium dependent but not inhibited by saccharides known to bind to SP-A"s carbohydrate recognition domain.	Carbohydrates	50-61	surfactant protein A1	Homo sapiens	79-83
17090701-7	2006	Binding is calcium dependent but not inhibited by saccharides known to bind to SP-A"s carbohydrate recognition domain.	Carbohydrates	86-98	surfactant protein A1	Homo sapiens	79-83
17003084-0	2006	Induction of surfactant protein A expression by cortisol facilitates prostaglandin synthesis in human chorionic trophoblasts.	Prostaglandins	69-82	surfactant protein A1	Homo sapiens	13-33
17003084-3	2006	OBJECTIVE: Our objective was to examine SP-A expression and the effect of SP-A on prostaglandin synthesis in human fetal membranes.	Prostaglandins	82-95	surfactant protein A1	Homo sapiens	74-78
17003084-5	2006	The effect of SP-A on prostaglandin synthesis was investigated in cultured human chorionic trophoblasts.	Prostaglandins	22-35	surfactant protein A1	Homo sapiens	14-18
17003084-8	2006	Cortisol (10(-7) and 10(-6) M, 24 h) induced SP-A expression in cultured chorionic trophoblasts, which could be blocked by the glucocorticoid receptor antagonist RU486.	Mifepristone	162-167	surfactant protein A1	Homo sapiens	45-49
17003084-9	2006	Treatment of chorionic trophoblasts with SP-A (10-100 microg/ml, 24 h) caused a dose-dependent increase of prostaglandin E2 release and an induction of cyclooxygenase type 2 but not cytosolic phospholipase A2 and microsomal prostaglandin E synthase expression.	Dinoprostone	107-123	surfactant protein A1	Homo sapiens	41-45
17003084-11	2006	SP-A appeared to induce prostaglandin E2 synthesis in chorionic trophoblasts via induction of cyclooxygenase type 2 expression.	Dinoprostone	24-40	surfactant protein A1	Homo sapiens	0-4
16916954-1	2006	Surfactant protein-A (SP-A) gene expression is developmentally regulated in fetal lung type II cells in concert with surfactant glycerophospholipid synthesis.	Glycerophospholipids	128-147	surfactant protein A1	Homo sapiens	0-20
16916954-9	2006	The ERRalpha-specific inverse agonist XCT790 inhibited cAMP induced hSP-A expression in human fetal lung type II cells in a concentration-dependent manner, suggesting a role of peroxisome proliferator-activated receptor-gamma coactivator 1alpha.	Cyclic AMP	55-59	surfactant protein A1	Homo sapiens	68-73
16916954-1	2006	Surfactant protein-A (SP-A) gene expression is developmentally regulated in fetal lung type II cells in concert with surfactant glycerophospholipid synthesis.	Glycerophospholipids	128-147	surfactant protein A1	Homo sapiens	22-26
16916954-10	2006	These findings suggest that ERRalpha acting through NRE(SP-A) is an important mediator of hSP-A gene expression and its induction by cAMP.	Cyclic AMP	133-137	surfactant protein A1	Homo sapiens	56-60
16916954-10	2006	These findings suggest that ERRalpha acting through NRE(SP-A) is an important mediator of hSP-A gene expression and its induction by cAMP.	Cyclic AMP	133-137	surfactant protein A1	Homo sapiens	90-95
16916954-7	2006	ERRalpha overexpression in lung type II cells enhanced cAMP induction of endogenous hSP-A expression, whereas cotransfection of protein kinase A catalytic subunit enhanced ERRalpha stimulation of hSP-A promoter activity in lung adenocarcinoma cells.	Cyclic AMP	55-59	surfactant protein A1	Homo sapiens	84-89
16916954-9	2006	The ERRalpha-specific inverse agonist XCT790 inhibited cAMP induced hSP-A expression in human fetal lung type II cells in a concentration-dependent manner, suggesting a role of peroxisome proliferator-activated receptor-gamma coactivator 1alpha.	XCT790	38-44	surfactant protein A1	Homo sapiens	68-73
16867155-1	2006	Pulmonary surfactant protein A (SP-A) is an oligomeric collectin that recognizes lipid and carbohydrate moieties present on broad range of micro-organisms, and mediates microbial lysis and clearance.	Carbohydrates	91-103	surfactant protein A1	Homo sapiens	0-30
17040017-8	2006	Demonstrated expression of SP-A and SP-D in diseased and normal sinus tissue may mean that these SPs are excreted into the airway-lining fluid of the sinuses.	Sodium phenolsulfonate	97-100	surfactant protein A1	Homo sapiens	27-31
16754682-4	2006	SP-A bound to sTLR4 and MD-2 in a Ca2+-dependent manner, and an anti-SP-A monoclonal antibody whose epitope lies in the region Thr184-Gly194 blocked the SP-A binding to sTLR4 and MD-2, indicating the involvement of the carbohydrate recognition domain (CRD) in the binding.	Carbohydrates	219-231	surfactant protein A1	Homo sapiens	69-73
16754682-4	2006	SP-A bound to sTLR4 and MD-2 in a Ca2+-dependent manner, and an anti-SP-A monoclonal antibody whose epitope lies in the region Thr184-Gly194 blocked the SP-A binding to sTLR4 and MD-2, indicating the involvement of the carbohydrate recognition domain (CRD) in the binding.	Carbohydrates	219-231	surfactant protein A1	Homo sapiens	69-73
16889547-8	2006	BALF with high levels of bile acids also had significantly lower SP-A, SP-D, dipalmitoylphosphatidylcholine; PG and higher SM levels (Mann-Whitney, p &lt; 0.05).	Bile Acids and Salts	25-35	surfactant protein A1	Homo sapiens	65-69
16867155-1	2006	Pulmonary surfactant protein A (SP-A) is an oligomeric collectin that recognizes lipid and carbohydrate moieties present on broad range of micro-organisms, and mediates microbial lysis and clearance.	Carbohydrates	91-103	surfactant protein A1	Homo sapiens	32-36
16867155-7	2006	We demonstrated calcium-dependent binding between MFAP4 and human SP-A1 and SP-A2.	Calcium	16-23	surfactant protein A1	Homo sapiens	66-71
16867155-8	2006	No binding was seen to recombinant SP-A composed of the neck region and carbohydrate recognition domain of SP-A indicating that the interaction between MFAP4 and SP-A is mediated via the collagen domain of SP-A.	Carbohydrates	72-84	surfactant protein A1	Homo sapiens	107-111
16867155-8	2006	No binding was seen to recombinant SP-A composed of the neck region and carbohydrate recognition domain of SP-A indicating that the interaction between MFAP4 and SP-A is mediated via the collagen domain of SP-A.	Carbohydrates	72-84	surfactant protein A1	Homo sapiens	107-111
16867155-8	2006	No binding was seen to recombinant SP-A composed of the neck region and carbohydrate recognition domain of SP-A indicating that the interaction between MFAP4 and SP-A is mediated via the collagen domain of SP-A.	Carbohydrates	72-84	surfactant protein A1	Homo sapiens	107-111
20641909-0	2004	[2-[(18)F]Fluoromethoxy-5-(5-trifluoromethyl-tetrazol-1-yl)-benzyl]([2S,3S]2-phenyl-piperidin-3-yl)-amine [2-[(18)F]Fluoromethoxy-5-(5-trifluoromethyl-tetrazol-1-yl)-benzyl]([2S,3S]2-phenyl-piperidin-3-yl)-amine ([(18)F]SPA-RQ) is a radioligand developed for positron emission tomography (PET) imaging of NK1 receptors (SP receptors) in the central nervous system (CNS) (1).	[2-[(18)f]fluoromethoxy-5-(5-trifluoromethyl-tetrazol-1-yl)-benzyl]([	0-69	surfactant protein A1	Homo sapiens	220-223
16709567-5	2006	Using a collection of glutathione S-transferase fusions to the intact IgG binding region of SpA and to each of the individual binding domains, we found that the SpA IgG binding domains also mediate binding to human airway cells.	Glutathione	22-33	surfactant protein A1	Homo sapiens	161-164
20641909-0	2004	[2-[(18)F]Fluoromethoxy-5-(5-trifluoromethyl-tetrazol-1-yl)-benzyl]([2S,3S]2-phenyl-piperidin-3-yl)-amine [2-[(18)F]Fluoromethoxy-5-(5-trifluoromethyl-tetrazol-1-yl)-benzyl]([2S,3S]2-phenyl-piperidin-3-yl)-amine ([(18)F]SPA-RQ) is a radioligand developed for positron emission tomography (PET) imaging of NK1 receptors (SP receptors) in the central nervous system (CNS) (1).	,3s]2-phenyl-piperidin-3-yl)-amine	71-105	surfactant protein A1	Homo sapiens	220-223
16714591-9	2006	In contrast, SP-A and SP-D effects on bacterial adherence to SAEC differed between the two strains.	saec	61-65	surfactant protein A1	Homo sapiens	13-17
16983827-13	2006	The weak protection conferred on the IPT could be explained by the inefficacy of the SP a failing in prenatal record andlor by the low compliance of the mothers with this strategy This is the reason why we strongly recommend a large-scale evaluation of this strategy.	isoprothiolane	37-40	surfactant protein A1	Homo sapiens	85-89
16581766-0	2006	Permissive effects of oxygen on cyclic AMP and interleukin-1 stimulation of surfactant protein A gene expression are mediated by epigenetic mechanisms.	Oxygen	22-28	surfactant protein A1	Homo sapiens	76-96
16263772-0	2006	11Beta-hydroxysteroid dehydrogenase type 2 and the regulation of surfactant protein A by dexamethasone metabolites.	Dexamethasone	89-102	surfactant protein A1	Homo sapiens	65-85
16263772-8	2006	We also show that the Dex-mediated regulation of surfactant protein A is attenuated by inhibition of HSD2 activity.	Dexamethasone	22-25	surfactant protein A1	Homo sapiens	49-69
16581766-4	2006	In this study, we found that O(2) also was permissive for IL-1 induction of SP-A expression and for cAMP and IL-1 stimulation of type II cell nuclear protein binding to the TBE.	Oxygen	29-33	surfactant protein A1	Homo sapiens	76-80
16581766-2	2006	Cyclic AMP (cAMP) stimulation of SP-A expression in lung type II cells is O(2) dependent and mediated by increased phosphorylation and binding of thyroid transcription factor 1 (TTF-1) to an upstream response element (TTF-1-binding element [TBE]).	Cyclic AMP	0-10	surfactant protein A1	Homo sapiens	33-37
16581766-5	2006	Using chromatin immunoprecipitation, we observed that when type II cells were cultured in 20% O(2), cAMP and IL-1 stimulated the recruitment of TTF-1, p65, CBP, and steroid receptor coactivator 1 to the TBE region of the SP-A promoter and increased local acetylation of histone H3; these effects were prevented by hypoxia.	Oxygen	94-98	surfactant protein A1	Homo sapiens	221-225
16581766-2	2006	Cyclic AMP (cAMP) stimulation of SP-A expression in lung type II cells is O(2) dependent and mediated by increased phosphorylation and binding of thyroid transcription factor 1 (TTF-1) to an upstream response element (TTF-1-binding element [TBE]).	Cyclic AMP	12-16	surfactant protein A1	Homo sapiens	33-37
16581766-5	2006	Using chromatin immunoprecipitation, we observed that when type II cells were cultured in 20% O(2), cAMP and IL-1 stimulated the recruitment of TTF-1, p65, CBP, and steroid receptor coactivator 1 to the TBE region of the SP-A promoter and increased local acetylation of histone H3; these effects were prevented by hypoxia.	Cyclic AMP	100-104	surfactant protein A1	Homo sapiens	221-225
16581766-3	2006	Interleukin-1 (IL-1) stimulation of SP-A expression is mediated by NF-kappaB (p65/p50) activation and increased binding to the TBE.	tbe	127-130	surfactant protein A1	Homo sapiens	36-40
16330552-9	2006	Interaction of SP-A and Prdx6 at pH 7.4 was shown by Prdx6-mediated inhibition of SP-A binding to agarose beads, a pull-down assay using His-tagged Prdx6 and Ni(2) -chelating beads, co-immunoprecipitation from lung epithelial cells and from a binary mixture of the two proteins, binding after treatment with a trifunctional cross-linker, and size-exclusion chromatography.	Sepharose	98-105	surfactant protein A1	Homo sapiens	15-19
16581766-8	2006	These results, together with findings that the histone deacetylase inhibitor trichostatin A and the methyltransferase inhibitor 5"-deoxy(5"-methylthio)adenosine markedly enhanced SP-A expression in lung type II cells, suggest that increased O(2) availability to type II cells late in gestation causes epigenetic changes that permit access of TTF-1 and NF-kappaB to the SP-A promoter.	trichostatin A	77-91	surfactant protein A1	Homo sapiens	179-183
16581766-8	2006	These results, together with findings that the histone deacetylase inhibitor trichostatin A and the methyltransferase inhibitor 5"-deoxy(5"-methylthio)adenosine markedly enhanced SP-A expression in lung type II cells, suggest that increased O(2) availability to type II cells late in gestation causes epigenetic changes that permit access of TTF-1 and NF-kappaB to the SP-A promoter.	trichostatin A	77-91	surfactant protein A1	Homo sapiens	369-373
16581766-8	2006	These results, together with findings that the histone deacetylase inhibitor trichostatin A and the methyltransferase inhibitor 5"-deoxy(5"-methylthio)adenosine markedly enhanced SP-A expression in lung type II cells, suggest that increased O(2) availability to type II cells late in gestation causes epigenetic changes that permit access of TTF-1 and NF-kappaB to the SP-A promoter.	5'-methylthioadenosine	128-160	surfactant protein A1	Homo sapiens	179-183
16581766-8	2006	These results, together with findings that the histone deacetylase inhibitor trichostatin A and the methyltransferase inhibitor 5"-deoxy(5"-methylthio)adenosine markedly enhanced SP-A expression in lung type II cells, suggest that increased O(2) availability to type II cells late in gestation causes epigenetic changes that permit access of TTF-1 and NF-kappaB to the SP-A promoter.	5'-methylthioadenosine	128-160	surfactant protein A1	Homo sapiens	369-373
16581766-8	2006	These results, together with findings that the histone deacetylase inhibitor trichostatin A and the methyltransferase inhibitor 5"-deoxy(5"-methylthio)adenosine markedly enhanced SP-A expression in lung type II cells, suggest that increased O(2) availability to type II cells late in gestation causes epigenetic changes that permit access of TTF-1 and NF-kappaB to the SP-A promoter.	Oxygen	241-245	surfactant protein A1	Homo sapiens	179-183
16330552-9	2006	Interaction of SP-A and Prdx6 at pH 7.4 was shown by Prdx6-mediated inhibition of SP-A binding to agarose beads, a pull-down assay using His-tagged Prdx6 and Ni(2) -chelating beads, co-immunoprecipitation from lung epithelial cells and from a binary mixture of the two proteins, binding after treatment with a trifunctional cross-linker, and size-exclusion chromatography.	Sepharose	98-105	surfactant protein A1	Homo sapiens	82-86
16330552-9	2006	Interaction of SP-A and Prdx6 at pH 7.4 was shown by Prdx6-mediated inhibition of SP-A binding to agarose beads, a pull-down assay using His-tagged Prdx6 and Ni(2) -chelating beads, co-immunoprecipitation from lung epithelial cells and from a binary mixture of the two proteins, binding after treatment with a trifunctional cross-linker, and size-exclusion chromatography.	ni(2)	158-163	surfactant protein A1	Homo sapiens	15-19
16330552-10	2006	Analysis by static light scattering and surface plasmon resonance showed calcium-independent SP-A binding to Prdx6 at pH 4.0 and partial Ca(2+) dependence of binding at pH 7.4.	Calcium	73-80	surfactant protein A1	Homo sapiens	93-97
16548909-6	2006	A previous study of three cases of lethal lung toxicity resulting from gefitinib administration revealed a significant and almost equal increase in KL-6, SP-A and SP-D.	Gefitinib	71-80	surfactant protein A1	Homo sapiens	154-158
16548909-7	2006	These results suggest that SP-A and SP-D may be indicators of gefitinib-induced ILD and that KL-6 is a predictor of outcome.	Gefitinib	62-71	surfactant protein A1	Homo sapiens	27-31
15932345-4	2005	Fluorescence intensity and anisotropy measurements of FITC-labelled Re-LPS in the presence and absence of SP-A indicated that SP-A bound to Re-LPS in solution in a Ca2+-independent manner, with a dissociation constant of 2.8x10(-8) M. In the presence of calcium, a high-mobility complex of SP-A and [3H]Rb-LPS (Rb mutant of LPS from Escherichia coli strain LCD 25) micelles was formed, as detected by sucrose density gradients.	Calcium	254-261	surfactant protein A1	Homo sapiens	126-130
16169899-1	2006	In the noninflamed lung, surfactant protein A (SP-A) acts as an anti-inflammatory molecule through its effects on macrophage (MPhi) function, modulating cytokine and reactive oxygen and nitrogen intermediate production.	Nitrogen	186-194	surfactant protein A1	Homo sapiens	25-45
16169899-1	2006	In the noninflamed lung, surfactant protein A (SP-A) acts as an anti-inflammatory molecule through its effects on macrophage (MPhi) function, modulating cytokine and reactive oxygen and nitrogen intermediate production.	Nitrogen	186-194	surfactant protein A1	Homo sapiens	47-51
16169899-4	2006	SP-A binding was inhibited by EGTA, indicating calcium dependence.	Egtazic Acid	30-34	surfactant protein A1	Homo sapiens	0-4
16169899-4	2006	SP-A binding was inhibited by EGTA, indicating calcium dependence.	Calcium	47-54	surfactant protein A1	Homo sapiens	0-4
16478858-5	2006	Diffusing capacities of the lung for carbon monoxide (15.3 +/- 3.5 mL/min/mm Hg vs 18.8 +/- 3.7 mL/min/mm Hg, p = 0.0493) were lower, and KL-6 (607 +/- 297 U/mL vs 318 +/- 143 U/mL, p = 0.0090), SP-A (59 +/- 24 ng/mL vs 34 +/- 12 ng/mL, p = 0.0207), and SP-D (112 +/- 54 ng/mL vs 42 +/- 24 ng/mL, p = 0.0028) were higher in the true abnormalities group than in the control group (+/- SD).	Carbon Monoxide	37-52	surfactant protein A1	Homo sapiens	195-199
17278394-9	2006	SP-A and SP-D are most abundant in the lungs, and also bind to microorganisms and inhaled particulates, mainly by lectin-sugar interactions.	Sugars	121-126	surfactant protein A1	Homo sapiens	0-4
16423264-7	2006	Analysis of the interaction of SP-A with the bacteria revealed that the major ligand was a phospholipid.	Phospholipids	91-103	surfactant protein A1	Homo sapiens	31-35
16423264-9	2006	The mass spectrometry demonstrated that the SP-A reactive lipid consisted of several disaturated molecular species of phosphatidylglycerol (PtdGro).	Phosphatidylglycerols	118-138	surfactant protein A1	Homo sapiens	44-48
16423264-9	2006	The mass spectrometry demonstrated that the SP-A reactive lipid consisted of several disaturated molecular species of phosphatidylglycerol (PtdGro).	Phosphatidylglycerols	140-146	surfactant protein A1	Homo sapiens	44-48
16351724-3	2005	METHODS AND RESULTS: At an alpha1-antitrypsin:SP-A molar ratio of 1:1, the interaction resulted in a calcium-dependent decrease of 84.6% in the association rate constant of alpha1-antitrypsin for neutrophil elastase.	Calcium	101-108	surfactant protein A1	Homo sapiens	46-50
16351724-5	2005	The carbohydrate recognition domain of SP-A appeared to be a major determinant of the interaction, by recognizing alpha1-antitrypsin carbohydrate chains.	Carbohydrates	4-16	surfactant protein A1	Homo sapiens	39-43
16351724-5	2005	The carbohydrate recognition domain of SP-A appeared to be a major determinant of the interaction, by recognizing alpha1-antitrypsin carbohydrate chains.	Carbohydrates	133-145	surfactant protein A1	Homo sapiens	39-43
16351724-6	2005	However, binding of SP-A carbohydrate chains to the alpha1-antitrypsin amino acid backbone and interaction between carbohydrates of both proteins are also possible.	Carbohydrates	115-128	surfactant protein A1	Homo sapiens	20-24
15951333-5	2005	In type II cells, 1,25(OH)(2)D(3) alone had no significant effect on SP-A mRNA or protein levels but reduced SP-A mRNA and protein in a dose-dependent manner when the cells were incubated with cAMP.	Cyclic AMP	193-197	surfactant protein A1	Homo sapiens	109-113
15951333-6	2005	SP-A mRNA levels in NCI-H441 cells, a nonciliated bronchiolar epithelial (Clara) cell line, were decreased in a dose-dependent manner in the absence or presence of cAMP.	Cyclic AMP	164-168	surfactant protein A1	Homo sapiens	0-4
16489761-6	2006	At a human SP-A concentration of 100 microg/mL, the permeability of the J5 LPS/POPE membranes increased 4.4-fold (p &lt; 0.02) compared to the control with no added SP-A.	1-palmitoyl-2-oleoyl-sn-glycero-3-phosphoethanolamine	79-83	surfactant protein A1	Homo sapiens	11-15
16489761-8	2006	Incorporation of cholesterol into J5 LPS/POPE liposomes at a POPE:cholesterol molar ratio of 1:0.15 blocked human SP-A or melittin-induced permeability (p &lt; 0.05) compared to cholesterol-free liposomes.	Cholesterol	17-28	surfactant protein A1	Homo sapiens	114-118
16489761-10	2006	We conclude that SP-A permeabilizes phospholipid membranes in an LPS-dependent and rough LPS-specific manner, that the effect is neither SP-A- nor species-specific, and that oxidative damage to SP-A abolishes its membrane destabilizing properties.	Phospholipids	36-48	surfactant protein A1	Homo sapiens	17-21
16489761-11	2006	Incorporation of cholesterol into the membrane enhances resistance to permeabilization by SP-A, most likely by increasing the packing density and membrane rigidity.	Cholesterol	17-28	surfactant protein A1	Homo sapiens	90-94
16030018-4	2005	Competition studies indicated that such binding is mediated by the recognition of lipoteichoic acid (LTA) and lipopolysaccharide (LPS), respectively, through nonoverlapping sites on the Sp alpha molecule.	lipoteichoic acid	82-99	surfactant protein A1	Homo sapiens	186-194
16030018-4	2005	Competition studies indicated that such binding is mediated by the recognition of lipoteichoic acid (LTA) and lipopolysaccharide (LPS), respectively, through nonoverlapping sites on the Sp alpha molecule.	lipoteichoic acid	101-104	surfactant protein A1	Homo sapiens	186-194
16030018-5	2005	The most conserved part of LPS (2-keto-3-deoxyoctulosonic acid and lipid A) was shown to be involved in the recognition by Sp alpha.	2-keto-3-deoxyoctonate	32-62	surfactant protein A1	Homo sapiens	123-131
16030018-5	2005	The most conserved part of LPS (2-keto-3-deoxyoctulosonic acid and lipid A) was shown to be involved in the recognition by Sp alpha.	Lipid A	67-74	surfactant protein A1	Homo sapiens	123-131
15932345-4	2005	Fluorescence intensity and anisotropy measurements of FITC-labelled Re-LPS in the presence and absence of SP-A indicated that SP-A bound to Re-LPS in solution in a Ca2+-independent manner, with a dissociation constant of 2.8x10(-8) M. In the presence of calcium, a high-mobility complex of SP-A and [3H]Rb-LPS (Rb mutant of LPS from Escherichia coli strain LCD 25) micelles was formed, as detected by sucrose density gradients.	Fluorescein-5-isothiocyanate	54-58	surfactant protein A1	Homo sapiens	126-130
15932345-4	2005	Fluorescence intensity and anisotropy measurements of FITC-labelled Re-LPS in the presence and absence of SP-A indicated that SP-A bound to Re-LPS in solution in a Ca2+-independent manner, with a dissociation constant of 2.8x10(-8) M. In the presence of calcium, a high-mobility complex of SP-A and [3H]Rb-LPS (Rb mutant of LPS from Escherichia coli strain LCD 25) micelles was formed, as detected by sucrose density gradients.	Fluorescein-5-isothiocyanate	54-58	surfactant protein A1	Homo sapiens	126-130
15932345-4	2005	Fluorescence intensity and anisotropy measurements of FITC-labelled Re-LPS in the presence and absence of SP-A indicated that SP-A bound to Re-LPS in solution in a Ca2+-independent manner, with a dissociation constant of 2.8x10(-8) M. In the presence of calcium, a high-mobility complex of SP-A and [3H]Rb-LPS (Rb mutant of LPS from Escherichia coli strain LCD 25) micelles was formed, as detected by sucrose density gradients.	Calcium	254-261	surfactant protein A1	Homo sapiens	126-130
15932345-4	2005	Fluorescence intensity and anisotropy measurements of FITC-labelled Re-LPS in the presence and absence of SP-A indicated that SP-A bound to Re-LPS in solution in a Ca2+-independent manner, with a dissociation constant of 2.8x10(-8) M. In the presence of calcium, a high-mobility complex of SP-A and [3H]Rb-LPS (Rb mutant of LPS from Escherichia coli strain LCD 25) micelles was formed, as detected by sucrose density gradients.	Tritium	300-302	surfactant protein A1	Homo sapiens	126-130
15932345-4	2005	Fluorescence intensity and anisotropy measurements of FITC-labelled Re-LPS in the presence and absence of SP-A indicated that SP-A bound to Re-LPS in solution in a Ca2+-independent manner, with a dissociation constant of 2.8x10(-8) M. In the presence of calcium, a high-mobility complex of SP-A and [3H]Rb-LPS (Rb mutant of LPS from Escherichia coli strain LCD 25) micelles was formed, as detected by sucrose density gradients.	Tritium	300-302	surfactant protein A1	Homo sapiens	126-130
15932345-4	2005	Fluorescence intensity and anisotropy measurements of FITC-labelled Re-LPS in the presence and absence of SP-A indicated that SP-A bound to Re-LPS in solution in a Ca2+-independent manner, with a dissociation constant of 2.8x10(-8) M. In the presence of calcium, a high-mobility complex of SP-A and [3H]Rb-LPS (Rb mutant of LPS from Escherichia coli strain LCD 25) micelles was formed, as detected by sucrose density gradients.	Sucrose	401-408	surfactant protein A1	Homo sapiens	126-130
15932345-4	2005	Fluorescence intensity and anisotropy measurements of FITC-labelled Re-LPS in the presence and absence of SP-A indicated that SP-A bound to Re-LPS in solution in a Ca2+-independent manner, with a dissociation constant of 2.8x10(-8) M. In the presence of calcium, a high-mobility complex of SP-A and [3H]Rb-LPS (Rb mutant of LPS from Escherichia coli strain LCD 25) micelles was formed, as detected by sucrose density gradients.	Sucrose	401-408	surfactant protein A1	Homo sapiens	126-130
15932345-8	2005	SP-A decreased the binding of Re-LPS to CD14, but not to LBP, as detected by cross-linking experiments with 125I-ASD-Re-LPS [125I-labelled sulphosuccinimidyl-2-(p-azidosalicylamido)-1,3-dithiopropionate derivative of Re-LPS] and fluorescence analysis with FITC-Re-LPS.	125i-asd-re-lps	108-123	surfactant protein A1	Homo sapiens	0-4
15932345-8	2005	SP-A decreased the binding of Re-LPS to CD14, but not to LBP, as detected by cross-linking experiments with 125I-ASD-Re-LPS [125I-labelled sulphosuccinimidyl-2-(p-azidosalicylamido)-1,3-dithiopropionate derivative of Re-LPS] and fluorescence analysis with FITC-Re-LPS.	sulphosuccinimidyl-2-(p-azidosalicylamido)-1,3-dithiopropionate	139-202	surfactant protein A1	Homo sapiens	0-4
15932345-8	2005	SP-A decreased the binding of Re-LPS to CD14, but not to LBP, as detected by cross-linking experiments with 125I-ASD-Re-LPS [125I-labelled sulphosuccinimidyl-2-(p-azidosalicylamido)-1,3-dithiopropionate derivative of Re-LPS] and fluorescence analysis with FITC-Re-LPS.	fitc-re	256-263	surfactant protein A1	Homo sapiens	0-4
16081790-0	2005	Pulmonary surfactant protein A activates a phosphatidylinositol 3-kinase/calcium signal transduction pathway in human macrophages: participation in the up-regulation of mannose receptor activity.	Calcium	73-80	surfactant protein A1	Homo sapiens	0-30
16006630-5	2005	Natural hydrophilic polymers, like the SP-A present in native surfactant, or hyaluronan, normally present in the alveolar fluids, can enhance adsorption in the presence of serum to eliminate inactivation.	Polymers	20-28	surfactant protein A1	Homo sapiens	39-43
16162765-2	2005	Pulmonary surfactant protein A (SP-A), the most abundant surfactant protein, has potent antioxidant properties and protects unsaturated phospholipids and growing cells from oxidative injury.	unsaturated phospholipids	124-149	surfactant protein A1	Homo sapiens	0-30
16162765-2	2005	Pulmonary surfactant protein A (SP-A), the most abundant surfactant protein, has potent antioxidant properties and protects unsaturated phospholipids and growing cells from oxidative injury.	unsaturated phospholipids	124-149	surfactant protein A1	Homo sapiens	32-36
16081790-4	2005	SP-A induced a refractory state specific for SP-A consistent with homologous desensitization of a receptor(s) linked to calcium mobilization because a second application of SP-A did not induce a rise in cytosolic Ca2+ whereas the addition of platelet-activating factor did.	Calcium	120-127	surfactant protein A1	Homo sapiens	0-4
16081790-5	2005	Using site-directed mutations in SP-A, we determined that both the attached sugars and the collagen-like domain of SP-A are necessary to optimize Ca2+ mobilization.	Sugars	76-82	surfactant protein A1	Homo sapiens	33-37
16081790-6	2005	SP-A triggered the increase in cytosolic Ca2+ by inducing activation of phospholipase C, which leads to the hydrolysis of membrane phospholipids, yielding inositol 1,4,5-trisphosphate and mobilizing intracellularly stored Ca2+ by inositol triphosphate-sensitive channels.	Phospholipids	131-144	surfactant protein A1	Homo sapiens	0-4
16081790-6	2005	SP-A triggered the increase in cytosolic Ca2+ by inducing activation of phospholipase C, which leads to the hydrolysis of membrane phospholipids, yielding inositol 1,4,5-trisphosphate and mobilizing intracellularly stored Ca2+ by inositol triphosphate-sensitive channels.	Inositol	155-163	surfactant protein A1	Homo sapiens	0-4
16081790-6	2005	SP-A triggered the increase in cytosolic Ca2+ by inducing activation of phospholipase C, which leads to the hydrolysis of membrane phospholipids, yielding inositol 1,4,5-trisphosphate and mobilizing intracellularly stored Ca2+ by inositol triphosphate-sensitive channels.	4,5-trisphosphate	166-183	surfactant protein A1	Homo sapiens	0-4
16061856-6	2005	In the cells isolated from paraffin-embedded tissue blocks, SP-A was deleted from 87% of the carcinoma tissues and 32% of the adjacent normal-appearing bronchial tissues.	Paraffin	27-35	surfactant protein A1	Homo sapiens	60-64
15640287-5	2005	Exposure to a NO donor, S-nitroso-N-acetylpenicillamine (SNAP), decreased surfactant protein (SP)-A, (SP)-B, and (SP)-C mRNA levels in type II pneumocytes in a time- and dose-dependent manner.	S-Nitroso-N-Acetylpenicillamine	24-55	surfactant protein A1	Homo sapiens	74-107
15890661-5	2005	Exposure of human SP-A to copper-initiated surfactant phospholipid peroxidation or to free radicals generated by human neutrophils in vitro increased the level of SP-A-associated carbonyl moieties and blocked the permeabilizing function of the protein.	Copper	26-32	surfactant protein A1	Homo sapiens	18-22
15890661-5	2005	Exposure of human SP-A to copper-initiated surfactant phospholipid peroxidation or to free radicals generated by human neutrophils in vitro increased the level of SP-A-associated carbonyl moieties and blocked the permeabilizing function of the protein.	Copper	26-32	surfactant protein A1	Homo sapiens	163-167
15890661-5	2005	Exposure of human SP-A to copper-initiated surfactant phospholipid peroxidation or to free radicals generated by human neutrophils in vitro increased the level of SP-A-associated carbonyl moieties and blocked the permeabilizing function of the protein.	Phospholipids	54-66	surfactant protein A1	Homo sapiens	18-22
15890661-5	2005	Exposure of human SP-A to copper-initiated surfactant phospholipid peroxidation or to free radicals generated by human neutrophils in vitro increased the level of SP-A-associated carbonyl moieties and blocked the permeabilizing function of the protein.	Phospholipids	54-66	surfactant protein A1	Homo sapiens	163-167
15890661-5	2005	Exposure of human SP-A to copper-initiated surfactant phospholipid peroxidation or to free radicals generated by human neutrophils in vitro increased the level of SP-A-associated carbonyl moieties and blocked the permeabilizing function of the protein.	Free Radicals	86-99	surfactant protein A1	Homo sapiens	18-22
15890661-5	2005	Exposure of human SP-A to copper-initiated surfactant phospholipid peroxidation or to free radicals generated by human neutrophils in vitro increased the level of SP-A-associated carbonyl moieties and blocked the permeabilizing function of the protein.	Free Radicals	86-99	surfactant protein A1	Homo sapiens	163-167
15608147-9	2005	The commercial NA inhibitor oseltamivir had a similar effect and also enhanced the neutralizing activity of SP-A and bronchoalveolar lavage fluid.	Oseltamivir	28-39	surfactant protein A1	Homo sapiens	108-112
15608147-3	2005	By contrast, gp340 and SP-A act like mucins in that they provide sialic acid ligands that bind to the viral HA.	N-Acetylneuraminic Acid	65-76	surfactant protein A1	Homo sapiens	23-27
15498759-10	2005	The bacteriostatic effects of SP-A were reversed by dipalmitoylphosphatidylglycerol.	1,2-dipalmitoylphosphatidylglycerol	52-83	surfactant protein A1	Homo sapiens	30-34
15615713-2	2005	This Cys(6) mutant lacked the NH(2)-terminal Ala(-3)-Val(-2)-Cys(-1) (DeltaAVC) extension present in some SP-A1 isoforms.	Cysteine	5-8	surfactant protein A1	Homo sapiens	106-111
15615713-2	2005	This Cys(6) mutant lacked the NH(2)-terminal Ala(-3)-Val(-2)-Cys(-1) (DeltaAVC) extension present in some SP-A1 isoforms.	deltaavc	70-78	surfactant protein A1	Homo sapiens	106-111
15615713-7	2005	Although SP-A1(DeltaAVC,C6S) was capable of binding to calcium, rough lipopolysaccharide, and phospholipid vesicles, this mutant was unable to induce rough lipopolysaccharide and phospholipid vesicle aggregation, to enhance the interfacial adsorption of SP-B/SP-C-surfactant membranes, and to undergo self-association in the presence of Ca(2+).	deltaavc	15-23	surfactant protein A1	Homo sapiens	9-14
15615713-7	2005	Although SP-A1(DeltaAVC,C6S) was capable of binding to calcium, rough lipopolysaccharide, and phospholipid vesicles, this mutant was unable to induce rough lipopolysaccharide and phospholipid vesicle aggregation, to enhance the interfacial adsorption of SP-B/SP-C-surfactant membranes, and to undergo self-association in the presence of Ca(2+).	Calcium	55-62	surfactant protein A1	Homo sapiens	9-14
15615713-7	2005	Although SP-A1(DeltaAVC,C6S) was capable of binding to calcium, rough lipopolysaccharide, and phospholipid vesicles, this mutant was unable to induce rough lipopolysaccharide and phospholipid vesicle aggregation, to enhance the interfacial adsorption of SP-B/SP-C-surfactant membranes, and to undergo self-association in the presence of Ca(2+).	Phospholipids	94-106	surfactant protein A1	Homo sapiens	9-14
15698989-2	2005	METHODS: AFM was used to acquire the images of SPA-G binding to the surface of mica under physiological condition for determining the 3D conformation of the molecule.	mica	79-83	surfactant protein A1	Homo sapiens	47-50
15802130-0	2005	Equilibrium studies of a fluorescent tacrolimus binding to surfactant protein A.	Tacrolimus	37-47	surfactant protein A1	Homo sapiens	59-79
15802130-2	2005	The objective of this study was to characterize the binding of FK506 to surfactant protein A (SP-A), an abundant lipoprotein found in the alveolar fluid that functions as part of the innate immune system in the lung.	Tacrolimus	63-68	surfactant protein A1	Homo sapiens	72-92
15802130-2	2005	The objective of this study was to characterize the binding of FK506 to surfactant protein A (SP-A), an abundant lipoprotein found in the alveolar fluid that functions as part of the innate immune system in the lung.	Tacrolimus	63-68	surfactant protein A1	Homo sapiens	94-98
15802130-4	2005	Using the fluorescence and anisotropy properties of DNS-FK, we demonstrated that tacrolimus avidly binds to SP-A with an apparent equilibrium association constant (K(app)) of 10(7)M(-1) and a Gibbs binding free energy of -40 kJ mol(-1)K(-1).	dns-fk	52-58	surfactant protein A1	Homo sapiens	108-112
15802130-4	2005	Using the fluorescence and anisotropy properties of DNS-FK, we demonstrated that tacrolimus avidly binds to SP-A with an apparent equilibrium association constant (K(app)) of 10(7)M(-1) and a Gibbs binding free energy of -40 kJ mol(-1)K(-1).	Tacrolimus	81-91	surfactant protein A1	Homo sapiens	108-112
15845487-5	2005	Initially, we found that viable M. pneumoniae cells bound to immobilized hSP-A in a dose- and calcium (Ca(2+))-dependent manner.	Calcium	94-101	surfactant protein A1	Homo sapiens	73-78
15845487-8	2005	The presence of Ca(2+) enhanced binding of the 65-kDa protein to hSP-A, which was reduced by the divalent cation-chelating agent, EDTA.	Edetic Acid	130-134	surfactant protein A1	Homo sapiens	65-70
15828763-4	2005	As a model system, a competitive phase-separation immunoassay based on the ELP-SpA format was established for paclitaxel (taxol) with IC(50) (20.18 nM) and the lower detection limit (2.94 nM) very similar to those reported for the ELISA format.	Paclitaxel	110-120	surfactant protein A1	Homo sapiens	79-82
15828763-4	2005	As a model system, a competitive phase-separation immunoassay based on the ELP-SpA format was established for paclitaxel (taxol) with IC(50) (20.18 nM) and the lower detection limit (2.94 nM) very similar to those reported for the ELISA format.	Paclitaxel	122-127	surfactant protein A1	Homo sapiens	79-82
15466251-3	2005	We have shown previously that O(3) exposure of surfactant protein (SP)-A decreases its ability to modulate proinflammatory cytokine production by cells of monocyte/macrophage lineage (THP-1 cells).	Ozone	30-34	surfactant protein A1	Homo sapiens	47-72
15466251-6	2005	These findings indicate that O(3) exposure may mediate its effect on macrophage function both directly and indirectly (via SP-A oxidation) and by involving different mechanisms.	Ozone	29-33	surfactant protein A1	Homo sapiens	123-127
15949147-2	2005	The two hydrophilic surfactant components SP-A and SP-D are proteins with collagen-like and lectin domains (collectins) able to interact with carbohydrate-containing ligands present on microbial membranes, and with defined regions of LPS.	Carbohydrates	142-154	surfactant protein A1	Homo sapiens	42-46
15544801-5	2004	However, we demonstrated recently that the molecular recognition of ManLAM terminal mannose units by human pulmonary surfactant protein A (hSP-A) carbohydrate recognition domains depends on the presence of the lipid moiety of the ManLAMs as proposed by Sidobre et al.	Mannose	84-91	surfactant protein A1	Homo sapiens	107-137
15544801-5	2004	However, we demonstrated recently that the molecular recognition of ManLAM terminal mannose units by human pulmonary surfactant protein A (hSP-A) carbohydrate recognition domains depends on the presence of the lipid moiety of the ManLAMs as proposed by Sidobre et al.	Carbohydrates	146-158	surfactant protein A1	Homo sapiens	107-137
15544801-5	2004	However, we demonstrated recently that the molecular recognition of ManLAM terminal mannose units by human pulmonary surfactant protein A (hSP-A) carbohydrate recognition domains depends on the presence of the lipid moiety of the ManLAMs as proposed by Sidobre et al.	manlams	230-237	surfactant protein A1	Homo sapiens	107-137
15500109-7	2004	Plasma concentrations of SP-A and SP-D decreased after sivelestat administration, but concentration of KL-6 was still elevated.	sivelestat	55-65	surfactant protein A1	Homo sapiens	25-29
15500109-8	2004	In this case, sivelestat was effective for ARDS in the patient not responding to steroid pulse therapy, and clinical finding and plasma concentrations of SP-A and SP-D were correlated well.	sivelestat	14-24	surfactant protein A1	Homo sapiens	154-158
15187452-0	2004	Neutralizing antibody evasion ability of adenovirus vector induced by the bioconjugation of methoxypolyethylene glycol succinimidyl propionate (MPEG-SPA).	methoxypolyethylene glycol succinimidyl propionate	92-142	surfactant protein A1	Homo sapiens	149-152
15274124-4	2004	Several protein bands corresponding to SP-A and SP-D were identified by MALDI-FT-ICR MS after electrophoretic separation by one- and two-dimensional gel electrophoresis, and provided the identification of structural modifications (hydroxy-proline) and degradation products.	Hydroxyproline	231-246	surfactant protein A1	Homo sapiens	39-43
14751851-2	2004	SP-A mRNA and protein are downregulated by phorbol esters (TPA) via inhibition of gene transcription.	Phorbol Esters	43-57	surfactant protein A1	Homo sapiens	0-4
15153505-0	2004	Pulmonary surfactant protein a inhibits macrophage reactive oxygen intermediate production in response to stimuli by reducing NADPH oxidase activity.	reactive oxygen	51-66	surfactant protein A1	Homo sapiens	0-30
15026426-4	2004	We found that SP-A inhibited copper-initiated LPO to an extent similar to BSA (P &lt; 0.05).	Copper	29-35	surfactant protein A1	Homo sapiens	14-18
15026426-6	2004	LPO initiated by an azo-compound also resulted in enhanced protein oxidation and markedly inhibited SP-A-mediated liposome aggregation.	anthrone	20-23	surfactant protein A1	Homo sapiens	100-104
15026426-8	2004	Oxidative inactivation of SP-A did not occur upon direct incubation of the protein with malondialdehyde alone.	Malondialdehyde	88-103	surfactant protein A1	Homo sapiens	26-30
15153505-6	2004	SP-A significantly reduced Mphi superoxide production in response to the phorbol ester PMA and to serum-opsonized zymosan (OpZy), independent of any effect by SP-A on zymosan phagocytosis.	Superoxides	32-42	surfactant protein A1	Homo sapiens	0-4
15026426-9	2004	We conclude that exposure of SP-A to LPO results in oxidative modification and functional inactivation of SP-A by phospholipid radicals.	Phospholipids	114-126	surfactant protein A1	Homo sapiens	29-33
15026426-9	2004	We conclude that exposure of SP-A to LPO results in oxidative modification and functional inactivation of SP-A by phospholipid radicals.	Phospholipids	114-126	surfactant protein A1	Homo sapiens	106-110
15153505-6	2004	SP-A significantly reduced Mphi superoxide production in response to the phorbol ester PMA and to serum-opsonized zymosan (OpZy), independent of any effect by SP-A on zymosan phagocytosis.	Phorbol Esters	73-86	surfactant protein A1	Homo sapiens	0-4
15153505-6	2004	SP-A significantly reduced Mphi superoxide production in response to the phorbol ester PMA and to serum-opsonized zymosan (OpZy), independent of any effect by SP-A on zymosan phagocytosis.	Zymosan	114-121	surfactant protein A1	Homo sapiens	0-4
15153505-9	2004	SP-A significantly decreased Mphi oxygen consumption in response to PMA and OpZy.	Oxygen	34-40	surfactant protein A1	Homo sapiens	0-4
15065867-8	2004	(iv) Oxidation is observed after ozone exposure, involving several SP-A residues that include cysteine, methionine, and tryptophan.	Cysteine	94-102	surfactant protein A1	Homo sapiens	67-71
15065867-8	2004	(iv) Oxidation is observed after ozone exposure, involving several SP-A residues that include cysteine, methionine, and tryptophan.	Methionine	104-114	surfactant protein A1	Homo sapiens	67-71
15065867-8	2004	(iv) Oxidation is observed after ozone exposure, involving several SP-A residues that include cysteine, methionine, and tryptophan.	Tryptophan	120-130	surfactant protein A1	Homo sapiens	67-71
15047952-4	2004	RESULTS: Very low levels of the neutrophil granule serine proteases cathepsin G, elastase, and proteinase-3 rapidly degraded pure SP-A when tested in buffered saline.	buffered saline	150-165	surfactant protein A1	Homo sapiens	130-134
14633512-1	2004	Induction of surfactant protein-A (SP-A) gene expression in fetal lung type II cells by cAMP and IL-1 is mediated by increased binding of thyroid transcription factor-1 (TTF-1) and NF-B proteins p50 and p65 to the TTF-1-binding element (TBE) at -183 bp.	Cyclic AMP	88-92	surfactant protein A1	Homo sapiens	13-33
14633512-1	2004	Induction of surfactant protein-A (SP-A) gene expression in fetal lung type II cells by cAMP and IL-1 is mediated by increased binding of thyroid transcription factor-1 (TTF-1) and NF-B proteins p50 and p65 to the TTF-1-binding element (TBE) at -183 bp.	Cyclic AMP	88-92	surfactant protein A1	Homo sapiens	35-39
14633512-1	2004	Induction of surfactant protein-A (SP-A) gene expression in fetal lung type II cells by cAMP and IL-1 is mediated by increased binding of thyroid transcription factor-1 (TTF-1) and NF-B proteins p50 and p65 to the TTF-1-binding element (TBE) at -183 bp.	tbe	237-240	surfactant protein A1	Homo sapiens	13-33
14633512-1	2004	Induction of surfactant protein-A (SP-A) gene expression in fetal lung type II cells by cAMP and IL-1 is mediated by increased binding of thyroid transcription factor-1 (TTF-1) and NF-B proteins p50 and p65 to the TTF-1-binding element (TBE) at -183 bp.	tbe	237-240	surfactant protein A1	Homo sapiens	35-39
14633512-5	2004	Cotransfection of primary cultures of type II cells with a GR expression vector abrogated cAMP induction of SP-A promoter activity while, at the same time, causing a 60-fold induction of cotransfected mouse mammary tumor virus (MMTV) promoter.	Cyclic AMP	90-94	surfactant protein A1	Homo sapiens	108-112
14633512-6	2004	In lung cells transfected with a fusion gene containing three TBEs fused to the basal SP-A promoter, Dex prevented the stimulatory effect of IL-1 on TTF-1 induction of SP-A promoter activity, suggesting that the GR inhibits SP-A promoter activity through the TBE.	Dexamethasone	101-104	surfactant protein A1	Homo sapiens	86-90
14633512-6	2004	In lung cells transfected with a fusion gene containing three TBEs fused to the basal SP-A promoter, Dex prevented the stimulatory effect of IL-1 on TTF-1 induction of SP-A promoter activity, suggesting that the GR inhibits SP-A promoter activity through the TBE.	Dexamethasone	101-104	surfactant protein A1	Homo sapiens	168-172
14633512-6	2004	In lung cells transfected with a fusion gene containing three TBEs fused to the basal SP-A promoter, Dex prevented the stimulatory effect of IL-1 on TTF-1 induction of SP-A promoter activity, suggesting that the GR inhibits SP-A promoter activity through the TBE.	Dexamethasone	101-104	surfactant protein A1	Homo sapiens	168-172
15009805-7	2004	The monoclonal antibodies revealed the existence of two Spalpha isoforms of 38 and 40 kDa, resulting from different sialic acid content.	N-Acetylneuraminic Acid	116-127	surfactant protein A1	Homo sapiens	56-63
15047952-9	2004	The degradation of SP-A by protease(s) in BAL fluid of patients with CF was abrogated by diisopropylfluorophosphate and monocyte/neutrophil elastase inhibitor.	Isoflurophate	89-115	surfactant protein A1	Homo sapiens	19-23
14617519-0	2004	Human SP-A genetic variants and bleomycin-induced cytokine production by THP-1 cells: effect of ozone-induced SP-A oxidation.	Ozone	96-101	surfactant protein A1	Homo sapiens	110-114
14617519-5	2004	We found 1) cytokine levels induced by SP-A2 (1A, 1A(0)) were significantly higher than those by SP-A1 (6A(2), 6A(4)) in the presence of bleomycin.	Bleomycin	137-146	surfactant protein A1	Homo sapiens	97-102
14617519-7	2004	3) The synergistic effect of bleomycin/SP-A, either before or after oxidation, can be inhibited to the level of bleomycin alone by surfactant lipids.	Bleomycin	112-121	surfactant protein A1	Homo sapiens	39-43
14617519-9	2004	The results indicate that differences among SP-A variants may partly explain the individual variability of pulmonary complications observed during bleomycin chemotherapy and/or in an environment that may promote protein oxidation.	Bleomycin	147-156	surfactant protein A1	Homo sapiens	44-48
15293882-2	2004	SP-A regulates the innate host defense by enhancing phagocytosis of pathogens and modulating the production of nitric oxide and cytokines by immune cells.	Nitric Oxide	111-123	surfactant protein A1	Homo sapiens	0-4
14640570-3	2003	The maximal induction of SP-A1 gene of H441 occurred at treating 150 nM of baicalin for 48 h. In the present study, cDNA subtraction analysis is performed to examine the differential expression in H441 cell upon baicalin treatment with a view to investigating the regulatory mechanism.	baicalin	75-83	surfactant protein A1	Homo sapiens	25-30
14612363-3	2003	SP-A and SP-D are calcium dependent carbohydrate binding proteins of the innate immune system important in the first line defence of the lung against microorganisms and in the control of lung inflammation.	Calcium	18-25	surfactant protein A1	Homo sapiens	0-4
15033771-2	2003	We hypothesized that collectins, such as pulmonary surfactant protein (SP-) A and D and mannose-binding lectin (MBL), could bind nucleic acid, which is a pentameric sugar-based anionic polymer.	Sugars	165-170	surfactant protein A1	Homo sapiens	51-77
15033771-2	2003	We hypothesized that collectins, such as pulmonary surfactant protein (SP-) A and D and mannose-binding lectin (MBL), could bind nucleic acid, which is a pentameric sugar-based anionic polymer.	Polymers	185-192	surfactant protein A1	Homo sapiens	51-77
12882765-2	2003	Surfactant protein A (SP-A) blocks secretagogue-stimulated phospholipid (PL) release, even in the presence of surfactant-like lipid.	Phospholipids	59-71	surfactant protein A1	Homo sapiens	0-20
12882765-2	2003	Surfactant protein A (SP-A) blocks secretagogue-stimulated phospholipid (PL) release, even in the presence of surfactant-like lipid.	Phospholipids	59-71	surfactant protein A1	Homo sapiens	22-26
12882765-2	2003	Surfactant protein A (SP-A) blocks secretagogue-stimulated phospholipid (PL) release, even in the presence of surfactant-like lipid.	Phospholipids	73-75	surfactant protein A1	Homo sapiens	0-20
12882765-2	2003	Surfactant protein A (SP-A) blocks secretagogue-stimulated phospholipid (PL) release, even in the presence of surfactant-like lipid.	Phospholipids	73-75	surfactant protein A1	Homo sapiens	22-26
12882765-5	2003	Although the ATP-stimulated secretion of PL was blocked by SP-A, the cell association of iodinated MAb 3C9 was not altered, indicating no effect on LB movement.	Adenosine Triphosphate	13-16	surfactant protein A1	Homo sapiens	59-63
12882765-5	2003	Although the ATP-stimulated secretion of PL was blocked by SP-A, the cell association of iodinated MAb 3C9 was not altered, indicating no effect on LB movement.	Phospholipids	41-43	surfactant protein A1	Homo sapiens	59-63
14612363-3	2003	SP-A and SP-D are calcium dependent carbohydrate binding proteins of the innate immune system important in the first line defence of the lung against microorganisms and in the control of lung inflammation.	Carbohydrates	36-48	surfactant protein A1	Homo sapiens	0-4
12913002-0	2003	Crystal structure of trimeric carbohydrate recognition and neck domains of surfactant protein A.	Carbohydrates	30-42	surfactant protein A1	Homo sapiens	75-95
12913002-1	2003	Surfactant protein A (SP-A), one of four proteins associated with pulmonary surfactant, binds with high affinity to alveolar phospholipid membranes, positioning the protein at the first line of defense against inhaled pathogens.	Phospholipids	125-137	surfactant protein A1	Homo sapiens	0-20
12913002-1	2003	Surfactant protein A (SP-A), one of four proteins associated with pulmonary surfactant, binds with high affinity to alveolar phospholipid membranes, positioning the protein at the first line of defense against inhaled pathogens.	Phospholipids	125-137	surfactant protein A1	Homo sapiens	22-26
12913002-2	2003	SP-A exhibits both calcium-dependent carbohydrate binding, a characteristic of the collectin family, and specific interactions with lipid membrane components.	Calcium	19-26	surfactant protein A1	Homo sapiens	0-4
12913002-2	2003	SP-A exhibits both calcium-dependent carbohydrate binding, a characteristic of the collectin family, and specific interactions with lipid membrane components.	Carbohydrates	37-49	surfactant protein A1	Homo sapiens	0-4
12913002-3	2003	The crystal structure of the trimeric carbohydrate recognition domain and neck domain of SP-A was solved to 2.1-A resolution with multiwavelength anomalous dispersion phasing from samarium.	Carbohydrates	38-50	surfactant protein A1	Homo sapiens	89-93
12913002-5	2003	The interdomain carbohydrate recognition domain-neck angle is significantly less in SP-A than in the homologous collectins, surfactant protein D, and mannose-binding protein.	Carbohydrates	16-28	surfactant protein A1	Homo sapiens	84-88
12913002-5	2003	The interdomain carbohydrate recognition domain-neck angle is significantly less in SP-A than in the homologous collectins, surfactant protein D, and mannose-binding protein.	Mannose	150-157	surfactant protein A1	Homo sapiens	84-88
12913002-7	2003	The appearance of this surface suggests a putative binding region for membrane-derived SP-A ligands such as phosphatidylcholine and lipid A, the endotoxic lipid component of bacterial lipopolysaccharide that mediates the potentially lethal effects of Gram-negative bacterial infection.	Phosphatidylcholines	108-127	surfactant protein A1	Homo sapiens	87-91
12913002-7	2003	The appearance of this surface suggests a putative binding region for membrane-derived SP-A ligands such as phosphatidylcholine and lipid A, the endotoxic lipid component of bacterial lipopolysaccharide that mediates the potentially lethal effects of Gram-negative bacterial infection.	Lipid A	132-139	surfactant protein A1	Homo sapiens	87-91
14507703-0	2003	Interaction of pulmonary surfactant protein SP-A with DPPC/egg-PG bilayers.	1,2-Dipalmitoylphosphatidylcholine	54-58	surfactant protein A1	Homo sapiens	44-48
12842807-5	2003	Vitamin D3-differentiated THP-1 cells and peripheral blood mononuclear cells were stimulated in vitro with several concentrations of SP-A for different incubation times.	Cholecalciferol	0-10	surfactant protein A1	Homo sapiens	133-137
14507703-2	2003	SP-A forms octadecamers that interact with phospholipid bilayer surfaces in the presence of calcium.	Calcium	92-99	surfactant protein A1	Homo sapiens	0-4
14507703-2	2003	SP-A forms octadecamers that interact with phospholipid bilayer surfaces in the presence of calcium.	Phospholipids	43-55	surfactant protein A1	Homo sapiens	0-4
14515273-4	2003	RSV infectivity determined by viral titers and the uptake of FITC-labeled RSV were also increased by SP-A, but decreased by LF.	Fluorescein-5-isothiocyanate	61-65	surfactant protein A1	Homo sapiens	101-105
14507703-3	2003	Deuterium NMR was used to characterize the perturbation by SP-A, in the presence of 5 mM Ca(2+), of dipalmitoyl phosphatidylcholine (DPPC) properties in DPPC/egg-PG (7:3) bilayers.	Deuterium	0-9	surfactant protein A1	Homo sapiens	59-63
14507703-3	2003	Deuterium NMR was used to characterize the perturbation by SP-A, in the presence of 5 mM Ca(2+), of dipalmitoyl phosphatidylcholine (DPPC) properties in DPPC/egg-PG (7:3) bilayers.	1,2-Dipalmitoylphosphatidylcholine	100-131	surfactant protein A1	Homo sapiens	59-63
14507703-3	2003	Deuterium NMR was used to characterize the perturbation by SP-A, in the presence of 5 mM Ca(2+), of dipalmitoyl phosphatidylcholine (DPPC) properties in DPPC/egg-PG (7:3) bilayers.	1,2-Dipalmitoylphosphatidylcholine	133-137	surfactant protein A1	Homo sapiens	59-63
14507703-3	2003	Deuterium NMR was used to characterize the perturbation by SP-A, in the presence of 5 mM Ca(2+), of dipalmitoyl phosphatidylcholine (DPPC) properties in DPPC/egg-PG (7:3) bilayers.	1,2-Dipalmitoylphosphatidylcholine	153-157	surfactant protein A1	Homo sapiens	59-63
14507703-4	2003	Effects of SP-A were uniformly distributed over the observed DPPC population.	1,2-Dipalmitoylphosphatidylcholine	61-65	surfactant protein A1	Homo sapiens	11-15
14507703-5	2003	SP-A reduced DPPC chain orientational order significantly in the gel phase but only slightly in the liquid-crystalline phase.	1,2-Dipalmitoylphosphatidylcholine	13-17	surfactant protein A1	Homo sapiens	0-4
14507703-6	2003	Quadrupole echo decay times for DPPC chain deuterons were sensitive to SP-A in the liquid-crystalline mixture but not in the gel phase.	1,2-Dipalmitoylphosphatidylcholine	32-36	surfactant protein A1	Homo sapiens	71-75
14507703-6	2003	Quadrupole echo decay times for DPPC chain deuterons were sensitive to SP-A in the liquid-crystalline mixture but not in the gel phase.	Deuterium	43-52	surfactant protein A1	Homo sapiens	71-75
14507703-7	2003	SP-A reduced quadrupole splittings of DPPC choline beta-deuterons but had little effect on choline alpha-deuteron splittings.	dppc choline	38-50	surfactant protein A1	Homo sapiens	0-4
14507703-7	2003	SP-A reduced quadrupole splittings of DPPC choline beta-deuterons but had little effect on choline alpha-deuteron splittings.	beta-deuterons	51-65	surfactant protein A1	Homo sapiens	0-4
14507703-7	2003	SP-A reduced quadrupole splittings of DPPC choline beta-deuterons but had little effect on choline alpha-deuteron splittings.	Choline	43-50	surfactant protein A1	Homo sapiens	0-4
14507703-7	2003	SP-A reduced quadrupole splittings of DPPC choline beta-deuterons but had little effect on choline alpha-deuteron splittings.	Deuterium	56-64	surfactant protein A1	Homo sapiens	0-4
14507703-8	2003	The observed effects of SP-A on DPPC/egg-PG bilayer properties differ from those of the hydrophobic surfactant proteins SP-B and SP-C.	1,2-Dipalmitoylphosphatidylcholine	32-36	surfactant protein A1	Homo sapiens	24-28
12887296-1	2003	Mannose- or mannan-binding lectin (MBL) is a member of the collectin protein family, which includes lung surfactant proteins SP-A and SP-D.	Mannose	0-7	surfactant protein A1	Homo sapiens	125-129
14500493-5	2003	Only the two related choline binding proteins, PspA and CbpA, were immunogenic in colonized subjects as determined by a statistically significant rise in the serum IgG titer.	Choline	21-28	surfactant protein A1	Homo sapiens	47-51
12911295-0	2003	Effect of hydroxylation and N187-linked glycosylation on molecular and functional properties of recombinant human surfactant protein A.	bafetinib	28-32	surfactant protein A1	Homo sapiens	114-134
12911295-1	2003	The objective of this study was to determine the effects of proline hydroxylation in the collagen-like domain and Asn(187)-linked glycosylation in the globular domain on the molecular and functional properties of human surfactant protein A1 (SP-A1).	Proline	60-67	surfactant protein A1	Homo sapiens	219-240
12911295-1	2003	The objective of this study was to determine the effects of proline hydroxylation in the collagen-like domain and Asn(187)-linked glycosylation in the globular domain on the molecular and functional properties of human surfactant protein A1 (SP-A1).	Asparagine	114-117	surfactant protein A1	Homo sapiens	219-240
12874235-7	2003	The greater hemagglutination inhibitory activity of pSP-A is due to porcine-specific structural features of the conserved asparagine-linked oligosaccharide in the carbohydrate recognition domain of SP-A.	Asparagine	122-132	surfactant protein A1	Homo sapiens	52-57
12874235-7	2003	The greater hemagglutination inhibitory activity of pSP-A is due to porcine-specific structural features of the conserved asparagine-linked oligosaccharide in the carbohydrate recognition domain of SP-A.	Asparagine	122-132	surfactant protein A1	Homo sapiens	53-57
12874235-7	2003	The greater hemagglutination inhibitory activity of pSP-A is due to porcine-specific structural features of the conserved asparagine-linked oligosaccharide in the carbohydrate recognition domain of SP-A.	Oligosaccharides	140-155	surfactant protein A1	Homo sapiens	52-57
12874235-7	2003	The greater hemagglutination inhibitory activity of pSP-A is due to porcine-specific structural features of the conserved asparagine-linked oligosaccharide in the carbohydrate recognition domain of SP-A.	Oligosaccharides	140-155	surfactant protein A1	Homo sapiens	53-57
12874235-7	2003	The greater hemagglutination inhibitory activity of pSP-A is due to porcine-specific structural features of the conserved asparagine-linked oligosaccharide in the carbohydrate recognition domain of SP-A.	Carbohydrates	163-175	surfactant protein A1	Homo sapiens	52-57
12874235-7	2003	The greater hemagglutination inhibitory activity of pSP-A is due to porcine-specific structural features of the conserved asparagine-linked oligosaccharide in the carbohydrate recognition domain of SP-A.	Carbohydrates	163-175	surfactant protein A1	Homo sapiens	53-57
12676764-0	2003	Human SP-A 3"-UTR variants mediate differential gene expression in basal levels and in response to dexamethasone.	Dexamethasone	99-112	surfactant protein A1	Homo sapiens	6-10
12964784-7	2003	CONCLUSION: Antibodies purified by SPA method are better than those by CAASP method, and Met monoclonal antibodies purified by SPA method can be used to prepare gold-labelled testing paper for analyzing Met residue in vegetable and drink water.	Water	238-243	surfactant protein A1	Homo sapiens	127-130
12505869-0	2003	Recombinant human SP-A1 and SP-A2 proteins have different carbohydrate-binding characteristics.	Carbohydrates	58-70	surfactant protein A1	Homo sapiens	18-23
12505869-2	2003	SP-A binds to the carbohydrates of lung pathogens via its calcium-dependant carbohydrate-binding domain.	Carbohydrates	18-31	surfactant protein A1	Homo sapiens	0-4
12505869-2	2003	SP-A binds to the carbohydrates of lung pathogens via its calcium-dependant carbohydrate-binding domain.	Calcium	58-65	surfactant protein A1	Homo sapiens	0-4
12505869-2	2003	SP-A binds to the carbohydrates of lung pathogens via its calcium-dependant carbohydrate-binding domain.	Carbohydrates	18-30	surfactant protein A1	Homo sapiens	0-4
12676764-4	2003	We found: 1) both basal mRNA and protein levels of the reporter gene of SP-A 3"-UTR constructs are significantly (P &lt; 0.01) reduced compared with controls (vector pGL3 and surfactant protein B pGL3) and that differences exist among alleles; and 2) after dexamethasone (Dex) treatment (100 nM for 16 h), mRNA was reduced (31-51%).	Dexamethasone	257-270	surfactant protein A1	Homo sapiens	72-76
12505869-5	2003	We hypothesized that SP-A1 and SP-A2 might have different carbohydrate-binding properties.	Carbohydrates	58-70	surfactant protein A1	Homo sapiens	21-26
12676764-4	2003	We found: 1) both basal mRNA and protein levels of the reporter gene of SP-A 3"-UTR constructs are significantly (P &lt; 0.01) reduced compared with controls (vector pGL3 and surfactant protein B pGL3) and that differences exist among alleles; and 2) after dexamethasone (Dex) treatment (100 nM for 16 h), mRNA was reduced (31-51%).	Dexamethasone	272-275	surfactant protein A1	Homo sapiens	72-76
12505869-6	2003	In this study, we characterized the carbohydrate-binding specificities of native human alveolar SP-A and recombinant human SP-A1 and SP-A2 in the presence of either 1 or 5 mM Ca(2+).	Carbohydrates	36-48	surfactant protein A1	Homo sapiens	96-100
12676764-7	2003	The data indicate that the 3"-UTR of SP-As play a differential role in SP-A basal expression and in response to Dex.	Dexamethasone	112-115	surfactant protein A1	Homo sapiens	37-41
12505869-6	2003	In this study, we characterized the carbohydrate-binding specificities of native human alveolar SP-A and recombinant human SP-A1 and SP-A2 in the presence of either 1 or 5 mM Ca(2+).	Carbohydrates	36-48	surfactant protein A1	Homo sapiens	123-128
12654643-2	2003	Incubation of SP-A with P. aeruginosa organisms from several clinical isolates resulted in concentration- and temperature-dependent degradation of SP-A that was inhibited by a metalloproteinase inhibitor, phosphoramidon.	phosphoramidon	205-219	surfactant protein A1	Homo sapiens	14-18
12505869-7	2003	We found that all of the SP-A proteins bind carbohydrates but with different affinities.	Carbohydrates	44-57	surfactant protein A1	Homo sapiens	25-29
12505869-8	2003	All of the SP-A proteins bind to fucose with the greatest affinity.	Fucose	33-39	surfactant protein A1	Homo sapiens	11-15
12722173-6	2003	At T4, spa therapy improved significantly several dimensions of PDQ-39 and SF-36, part IV of the UPDRS, and GHQ-28.	ghq	108-111	surfactant protein A1	Homo sapiens	7-10
12654643-2	2003	Incubation of SP-A with P. aeruginosa organisms from several clinical isolates resulted in concentration- and temperature-dependent degradation of SP-A that was inhibited by a metalloproteinase inhibitor, phosphoramidon.	phosphoramidon	205-219	surfactant protein A1	Homo sapiens	147-151
12672413-7	2003	The assay is based on GlcNAc6ST-2-mediated [35S]sulfate transfer from [35S]PAPS to the biotinylated glycoside and subsequent detection using streptavidin-coated SPA beads.	Glycosides	100-109	surfactant protein A1	Homo sapiens	161-164
12709894-8	2003	The maximal expression of the SP-A gene, 1.7-fold greater than control, is induced at 150 nM of baicalin treated for 48 h.	baicalin	96-104	surfactant protein A1	Homo sapiens	30-34
12660950-2	2003	PspA could be detected in some (but not all) lots of 23-valent polysaccharide vaccine.	23-valent polysaccharide	53-77	surfactant protein A1	Homo sapiens	0-4
14575179-1	2003	BACKGROUND &amp; OBJECTIVES: The decrease in surfactant protein-A (SP-A level) has recently been implicated in the pathophysiology of acute respiratory distress syndrome (ARDS).	Adenosine Monophosphate	12-15	surfactant protein A1	Homo sapiens	45-65
14575179-1	2003	BACKGROUND &amp; OBJECTIVES: The decrease in surfactant protein-A (SP-A level) has recently been implicated in the pathophysiology of acute respiratory distress syndrome (ARDS).	Adenosine Monophosphate	12-15	surfactant protein A1	Homo sapiens	67-71
14575179-10	2003	INTERPRETATION &amp; CONCLUSION: The present study showed a progressive increase in the SP-A levels in patients with ARDS on mechanical ventilation.	Adenosine Monophosphate	16-19	surfactant protein A1	Homo sapiens	88-92
12437362-11	2002	(3) The ability of SP-A to undergo self-aggregation and induce phospholipid and bacterial lipopolysaccharide aggregation is greater for SP-A2 than for coexpressed SP-A1/SP-A2, which in turn is greater than that observed for SP-A1.	Phospholipids	63-75	surfactant protein A1	Homo sapiens	19-23
12765221-6	2003	If we used both SMT and SP-A, we could diagnose with 100% accuracy that a case with measurements of SMT &gt; or = 2 and SP-A &gt; or = 420 ng/ml would not complicate with RDS (24/24).	S-Methylisothiourea hemisulfate	16-19	surfactant protein A1	Homo sapiens	120-124
12524383-2	2003	The human collectins, mannan-binding lectin (MBL) and surfactant protein A and D (SP-A and SP-D), are oligomeric proteins composed of carbohydrate-recognition domains (CRDs) attached to collagenous regions and are thus structurally similar to the ficolins, L-ficolin, M-ficolin, and H-ficolin.	Carbohydrates	134-146	surfactant protein A1	Homo sapiens	54-80
12524383-2	2003	The human collectins, mannan-binding lectin (MBL) and surfactant protein A and D (SP-A and SP-D), are oligomeric proteins composed of carbohydrate-recognition domains (CRDs) attached to collagenous regions and are thus structurally similar to the ficolins, L-ficolin, M-ficolin, and H-ficolin.	Carbohydrates	134-146	surfactant protein A1	Homo sapiens	82-86
12488138-0	2002	Inhibition of human surfactant protein A function by oxidation intermediates of nitrite.	Nitrites	80-87	surfactant protein A1	Homo sapiens	20-40
12488138-3	2002	We report here that a mixture of hypochlorous acid (HOCl) and nitrite (NO 2 - ) induces nitration, oxidation, and chlorination of tyrosine residues in human SP-A and inhibits SP-A"s ability to aggregate lipids and bind mannose.	Hypochlorous Acid	33-50	surfactant protein A1	Homo sapiens	157-161
12488138-3	2002	We report here that a mixture of hypochlorous acid (HOCl) and nitrite (NO 2 - ) induces nitration, oxidation, and chlorination of tyrosine residues in human SP-A and inhibits SP-A"s ability to aggregate lipids and bind mannose.	Hypochlorous Acid	33-50	surfactant protein A1	Homo sapiens	175-179
12488138-3	2002	We report here that a mixture of hypochlorous acid (HOCl) and nitrite (NO 2 - ) induces nitration, oxidation, and chlorination of tyrosine residues in human SP-A and inhibits SP-A"s ability to aggregate lipids and bind mannose.	Hypochlorous Acid	52-56	surfactant protein A1	Homo sapiens	157-161
12488138-3	2002	We report here that a mixture of hypochlorous acid (HOCl) and nitrite (NO 2 - ) induces nitration, oxidation, and chlorination of tyrosine residues in human SP-A and inhibits SP-A"s ability to aggregate lipids and bind mannose.	Hypochlorous Acid	52-56	surfactant protein A1	Homo sapiens	175-179
12488138-3	2002	We report here that a mixture of hypochlorous acid (HOCl) and nitrite (NO 2 - ) induces nitration, oxidation, and chlorination of tyrosine residues in human SP-A and inhibits SP-A"s ability to aggregate lipids and bind mannose.	Nitrites	62-69	surfactant protein A1	Homo sapiens	157-161
12488138-3	2002	We report here that a mixture of hypochlorous acid (HOCl) and nitrite (NO 2 - ) induces nitration, oxidation, and chlorination of tyrosine residues in human SP-A and inhibits SP-A"s ability to aggregate lipids and bind mannose.	Nitrites	62-69	surfactant protein A1	Homo sapiens	175-179
12488138-3	2002	We report here that a mixture of hypochlorous acid (HOCl) and nitrite (NO 2 - ) induces nitration, oxidation, and chlorination of tyrosine residues in human SP-A and inhibits SP-A"s ability to aggregate lipids and bind mannose.	Tyrosine	130-138	surfactant protein A1	Homo sapiens	157-161
12488138-3	2002	We report here that a mixture of hypochlorous acid (HOCl) and nitrite (NO 2 - ) induces nitration, oxidation, and chlorination of tyrosine residues in human SP-A and inhibits SP-A"s ability to aggregate lipids and bind mannose.	Mannose	219-226	surfactant protein A1	Homo sapiens	175-179
12488138-5	2002	Moreover, both horseradish peroxidase and myeloperoxidase (MPO) can utilize NO 2 - and hydrogen peroxide (H 2 O 2 ) as substrates to catalyze tyrosine nitration in SP-A and inhibit its lipid aggregation function.	Hydrogen Peroxide	87-104	surfactant protein A1	Homo sapiens	164-168
12488138-5	2002	Moreover, both horseradish peroxidase and myeloperoxidase (MPO) can utilize NO 2 - and hydrogen peroxide (H 2 O 2 ) as substrates to catalyze tyrosine nitration in SP-A and inhibit its lipid aggregation function.	Tyrosine	142-150	surfactant protein A1	Homo sapiens	164-168
12612307-6	2003	SP-A was highly correlated with [A - a]DO(2), VC, and TLCO (p&lt;/=0.02), but other markers were not.	tlco	54-58	surfactant protein A1	Homo sapiens	0-4
12413892-4	2002	Here we report that SP-A treatment leads to rapid tyrosine-specific phosphorylation of several important proteins in lung epithelial cells including insulin receptor substrate-1 (IRS-1), an upstream activator of PI3K.	Tyrosine	50-58	surfactant protein A1	Homo sapiens	20-24
12421219-3	2002	CASE REPORT: A patient with mitomycin-associated hemolytic-uremic syndrome received SPA treatments after her ACE inhibitor, lisinopril, was held.	Mitomycin	28-37	surfactant protein A1	Homo sapiens	84-87
12421219-3	2002	CASE REPORT: A patient with mitomycin-associated hemolytic-uremic syndrome received SPA treatments after her ACE inhibitor, lisinopril, was held.	Lisinopril	124-134	surfactant protein A1	Homo sapiens	84-87
12421219-4	2002	Lisinopril was restarted before her 18th SPA treatment, and immediately after return of treated plasma she developed facial redness and hypotension, which resolved after the return stopped and recurred when restarted.	Lisinopril	0-10	surfactant protein A1	Homo sapiens	41-44
12244146-5	2002	Here we show that SP-A selectively enhances MR expression on human monocyte-derived macrophages, a process involving both the attached sugars and collagen-like domain of SP-A.	Sugars	135-141	surfactant protein A1	Homo sapiens	18-22
12244146-7	2002	Monocyte-derived macrophages on an SP-A substrate demonstrated enhanced pinocytosis of mannose BSA and phagocytosis of Mycobacterium tuberculosis lipoarabinomannan-coated microspheres.	Mannose	87-94	surfactant protein A1	Homo sapiens	35-39
12244146-8	2002	The newly expressed MR likely came from intracellular pools because: 1) up-regulation of the MR by SP-A occurred by 1 h, 2) new protein synthesis was not necessary for MR up-regulation, and 3) pinocytosis of mannose BSA via MR recycling was increased.	Mannose	208-215	surfactant protein A1	Homo sapiens	99-103
12114204-5	2002	PD-169316 and SB-203580, inhibitors of p38 MAPK, blocked the TNF-alpha-mediated inhibition of SP-A mRNA levels.	SB 203580	14-23	surfactant protein A1	Homo sapiens	94-98
12114204-7	2002	Anisomycin, an activator of p38 MAPK, increased p38 MAPK phosphorylation and decreased SP-A mRNA levels in a dose-dependent manner.	Anisomycin	0-10	surfactant protein A1	Homo sapiens	87-91
12060565-3	2002	We studied the effects of human SP-A on bleomycin-induced cytokine production and mRNA expression in THP-1 macrophage-like cells and obtained the following results.	Bleomycin	40-49	surfactant protein A1	Homo sapiens	32-36
12060565-2	2002	In the present study, we investigated the hypothesis that SP-A is involved in bleomycin-induced pulmonary fibrosis.	Bleomycin	78-87	surfactant protein A1	Homo sapiens	58-62
12060565-4	2002	1) Bleomycin-treated THP-1 cells increased tumor necrosis factor (TNF)-alpha, interleukin (IL)-8, and IL-1beta production in dose- and time-dependent patterns, as we have observed with SP-A.	Bleomycin	3-12	surfactant protein A1	Homo sapiens	185-189
12060565-7	2002	3) Although the bleomycin effect on cytokine production was not significantly affected by the presence of surfactant lipid, the additive and synergistic effect of SP-A-bleomycin on cytokine production was significantly reduced.	Bleomycin	168-177	surfactant protein A1	Homo sapiens	163-167
12060565-8	2002	We speculate that the elevated cytokine levels resulting from the bleomycin-SP-A synergism are responsible for bleomycin-induced pulmonary fibrosis and that surfactant lipids can help ameliorate pulmonary complications observed during bleomycin chemotherapy.	Bleomycin	66-75	surfactant protein A1	Homo sapiens	76-80
12060565-8	2002	We speculate that the elevated cytokine levels resulting from the bleomycin-SP-A synergism are responsible for bleomycin-induced pulmonary fibrosis and that surfactant lipids can help ameliorate pulmonary complications observed during bleomycin chemotherapy.	Bleomycin	111-120	surfactant protein A1	Homo sapiens	76-80
11943658-2	2002	Coincubation of AMs with human SP-A (25 microg/ml) and Klebsiella resulted in a 68% decrease in total colony forming units by 120 min compared with AMs infected with Klebsiella in the absence of SP-A, and this SP-A-mediated effect was abolished by preincubation with N(G)-monomethyl-L-arginine.	omega-N-Methylarginine	267-293	surfactant protein A1	Homo sapiens	31-35
12071842-2	2002	hSP-A has been shown to promote the uptake and the phagocytosis of pathogenic bacilli through the recognition and the binding of carbohydrate motifs on the invading pathogen surface.	Carbohydrates	129-141	surfactant protein A1	Homo sapiens	0-5
12071842-3	2002	Recently we identified lipomannan and mannosylated lipoarabinomannan (ManLAM), two major mycobacterial cell-wall lipoglycans, as potential ligands for binding of hSP-A.	lipomannan	23-33	surfactant protein A1	Homo sapiens	162-167
12071842-3	2002	Recently we identified lipomannan and mannosylated lipoarabinomannan (ManLAM), two major mycobacterial cell-wall lipoglycans, as potential ligands for binding of hSP-A.	lipoarabinomannan	51-68	surfactant protein A1	Homo sapiens	162-167
12071842-3	2002	Recently we identified lipomannan and mannosylated lipoarabinomannan (ManLAM), two major mycobacterial cell-wall lipoglycans, as potential ligands for binding of hSP-A.	manlam	70-76	surfactant protein A1	Homo sapiens	162-167
12071842-6	2002	Binding of ManLAM to immobilized hSP-A was consistent with the simplest one-to-one interaction model involving a single class of carbohydrate-binding site.	manlam	11-17	surfactant protein A1	Homo sapiens	33-38
12071842-6	2002	Binding of ManLAM to immobilized hSP-A was consistent with the simplest one-to-one interaction model involving a single class of carbohydrate-binding site.	Carbohydrates	129-141	surfactant protein A1	Homo sapiens	33-38
12071842-7	2002	This observation strongly suggests that the lipid moiety of ManLAM does not directly interact with hSP-A, but is rather responsible for the macromolecular organization of the lipoglycan, which may be necessary for efficient recognition of the terminal mannosyl epitopes.	manlam	60-66	surfactant protein A1	Homo sapiens	99-104
12040027-0	2002	Potential role of nuclear factor kappaB and reactive oxygen species in cAMP and cytokine regulation of surfactant protein-A gene expression in lung type II cells.	Reactive Oxygen Species	44-67	surfactant protein A1	Homo sapiens	103-123
11943658-3	2002	Incubation of transplant AMs with SP-A increased intracellular Ca(2+) concentration ([Ca(2+)](i)) by 70% and nitrite and nitrate (NO(x)) production by 45% (from 0.24 +/- 0.02 to 1.3 +/- 0.21 nmol small middle dot 10(6) AMs(-1).h(-1)).	Nitrites	109-116	surfactant protein A1	Homo sapiens	34-38
11943658-3	2002	Incubation of transplant AMs with SP-A increased intracellular Ca(2+) concentration ([Ca(2+)](i)) by 70% and nitrite and nitrate (NO(x)) production by 45% (from 0.24 +/- 0.02 to 1.3 +/- 0.21 nmol small middle dot 10(6) AMs(-1).h(-1)).	Nitrates	121-128	surfactant protein A1	Homo sapiens	34-38
11943658-4	2002	Preincubation with 1,2-bis(2-aminophenoxy)ethane-N,N,N",N"-tetraacetic acid-acetoxymethyl ester inhibited the increase in [Ca(2+)](i) and abrogated the SP-A-mediated Klebsiella phagocytosis and killing.	1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid acetoxymethyl ester	19-95	surfactant protein A1	Homo sapiens	152-156
11943658-7	2002	These findings indicate that SP-A mediates pathogen killing by AMs from transplant lungs by stimulating phagocytosis and production of reactive oxygen-nitrogen intermediates.	reactive oxygen-nitrogen	135-159	surfactant protein A1	Homo sapiens	29-33
12195567-0	2002	Alternative treatment of psoriasis with balneotherapy using Leopoldine spa water.	Water	75-80	surfactant protein A1	Homo sapiens	71-74
12195567-1	2002	BACKGROUND: Leopoldine spa water is a hypotonic water rich in sulphate that has been used occasionally for balneological treatments in psoriatics.	Water	27-32	surfactant protein A1	Homo sapiens	23-26
12195567-1	2002	BACKGROUND: Leopoldine spa water is a hypotonic water rich in sulphate that has been used occasionally for balneological treatments in psoriatics.	Sulfates	62-70	surfactant protein A1	Homo sapiens	23-26
12162458-0	2002	The role of nitric oxide in lung innate immunity: modulation by surfactant protein-A.	Nitric Oxide	12-24	surfactant protein A1	Homo sapiens	64-84
11948134-4	2002	In adenocarcinomas, trichostatin A up-regulated general differentiation markers (gelsolin, Mad, and p21/WAF1) and down-regulated markers of the type II pneumocyte progenitor cell lineage (MUC1 and SP-A), indicative of a more mature phenotype.	trichostatin A	20-34	surfactant protein A1	Homo sapiens	197-201
11834130-1	2002	Sephadex was derivatized consecutively with Staphylococcus Protein A (SpA) and cell-specific antibodies, and the binding of cells to the resulting material was examined.	sephadex	0-8	surfactant protein A1	Homo sapiens	70-73
11839531-2	2002	SP-A is involved in the formation of tubular myelin, the modulation of the surface tension-reducing properties of surfactant phospholipids, the metabolism of surfactant phospholipids, and local pulmonary host defense.	Phospholipids	125-138	surfactant protein A1	Homo sapiens	0-4
11839531-2	2002	SP-A is involved in the formation of tubular myelin, the modulation of the surface tension-reducing properties of surfactant phospholipids, the metabolism of surfactant phospholipids, and local pulmonary host defense.	Phospholipids	169-182	surfactant protein A1	Homo sapiens	0-4
11936520-4	2002	The authors found that serum SP-A and SP-D levels were significantly elevated in patients with IPF and systemic sclerosis compared to sarcoidosis, beryllium disease and normal controls, and that SP-D correlated with radiographic abnormalities in patients with IPF.	Beryllium	147-156	surfactant protein A1	Homo sapiens	29-33
11724772-9	2002	Coincubation of sTLR2 with SP-A significantly reduced the binding of sTLR2 to PGN.	stlr2	16-21	surfactant protein A1	Homo sapiens	27-31
11834130-2	2002	For comparison, cell binding to commercially obtained SpA-Sepharose was determined.	Sepharose	58-67	surfactant protein A1	Homo sapiens	54-57
11834130-3	2002	Sephadex G-10, carboxylated by reaction with glycine and activated subsequently with 1-ethyl-3-(3-dimethylaminopropyl)carbodi-imide/N-hydroxysuccinimide (NHS), was allowed to react with SpA.	sephadex	0-13	surfactant protein A1	Homo sapiens	186-189
11834130-3	2002	Sephadex G-10, carboxylated by reaction with glycine and activated subsequently with 1-ethyl-3-(3-dimethylaminopropyl)carbodi-imide/N-hydroxysuccinimide (NHS), was allowed to react with SpA.	Ethyldimethylaminopropyl Carbodiimide	85-131	surfactant protein A1	Homo sapiens	186-189
11834130-4	2002	Coupling of SpA to NHS-activated glycine-Sephadex appeared to be complete (immobilization capacity, approximately 300 microg of protein/ml of packed gel) when incubation was carried out at pH 4.0, in buffer of low ionic strength.	Glycine	33-40	surfactant protein A1	Homo sapiens	12-15
11834130-4	2002	Coupling of SpA to NHS-activated glycine-Sephadex appeared to be complete (immobilization capacity, approximately 300 microg of protein/ml of packed gel) when incubation was carried out at pH 4.0, in buffer of low ionic strength.	sephadex	41-49	surfactant protein A1	Homo sapiens	12-15
11834130-6	2002	After incubation with rabbit anti-(human red cell) antiserum, and upon mixing with human red blood cells, SpA-glycine-Sephadex G-10 could bind up to 5 x 10(8) red cells/ml of gel.	sephadex	118-131	surfactant protein A1	Homo sapiens	106-109
11834130-7	2002	Cell binding increased when the amount of antiserum, added to SpA-glycine-Sephadex G-10 for preparing the affinity gel, was increased from 0.5 to 5 microl/ml of gel.	sephadex	74-87	surfactant protein A1	Homo sapiens	62-65
11868369-4	2002	Surfactant proteins A and D (pulmonary collectins) function as host defense lectins and play important roles in innate immunity in the lung-Collectins including SP-A, SP-D and mannose-binding proteins can bind CD14.	Mannose	176-183	surfactant protein A1	Homo sapiens	0-27
11713256-1	2002	Surfactant protein-A (SP-A) gene expression is developmentally regulated in fetal lung type II cells and is enhanced by cAMP.	Cyclic AMP	120-124	surfactant protein A1	Homo sapiens	0-20
11713256-1	2002	Surfactant protein-A (SP-A) gene expression is developmentally regulated in fetal lung type II cells and is enhanced by cAMP.	Cyclic AMP	120-124	surfactant protein A1	Homo sapiens	22-26
11713256-2	2002	cAMP stimulation of SP-A gene expression is mediated by protein kinase A (PKA) phosphorylation of thyroid transcription factor 1 (TTF-1), expressed selectively in developing lung epithelium.	Cyclic AMP	0-4	surfactant protein A1	Homo sapiens	20-24
12562139-3	2002	Furthermore, clinical studies demonstrated that treatment with the SP (NK1 receptor) antagonist (SPA) aprepitant (also known as MK-0869) significantly improves depression symptoms and reduces the incidence of chemotherapy-induced nausea and vomiting.	Aprepitant	128-135	surfactant protein A1	Homo sapiens	97-100
11778926-3	2001	Today, SPA-based extracorporeal immunoadsorption relies on two rather different systems, namely, SPA-silica (Prosorba), and SPA-Sepharose (Immunosorba).	Silicon Dioxide	101-107	surfactant protein A1	Homo sapiens	7-10
11695915-0	2001	Thermal stability and DPPC/Ca2+ interactions of pulmonary surfactant SP-A from bulk-phase and monolayer IR spectroscopy.	1,2-Dipalmitoylphosphatidylcholine	22-26	surfactant protein A1	Homo sapiens	69-73
11695915-4	2001	The amide I contour of SP-A reveals two features at 1653 and 1636 cm(-1) arising from the collagen-like domain and a broad feature at 1645 cm(-1) suggested to arise from the carbohydrate recognition domain (CRD).	Amides	4-9	surfactant protein A1	Homo sapiens	23-27
11695915-4	2001	The amide I contour of SP-A reveals two features at 1653 and 1636 cm(-1) arising from the collagen-like domain and a broad feature at 1645 cm(-1) suggested to arise from the carbohydrate recognition domain (CRD).	Carbohydrates	174-186	surfactant protein A1	Homo sapiens	23-27
11695915-6	2001	Thermal denaturation of SP-A in the presence of either DPPC or Ca2+ ion reveals a sequence of events involving the initial melting of the collagen-like region, followed by formation of intermolecular extended forms.	1,2-Dipalmitoylphosphatidylcholine	55-59	surfactant protein A1	Homo sapiens	24-28
11695915-7	2001	Interestingly, these spectral changes were inhibited in the ternary system, showing that the combined presence of both DPPC and Ca2+ confers a remarkable thermal stability upon SP-A.	1,2-Dipalmitoylphosphatidylcholine	119-123	surfactant protein A1	Homo sapiens	177-181
11695915-9	2001	The IRRAS measurements indicated that incorporation of SP-A into preformed DPPC monolayers at a surface pressure of 10 mN/m induced a decrease in the average acyl chain tilt angle from 35 degrees to 28 degrees.	1,2-Dipalmitoylphosphatidylcholine	75-79	surfactant protein A1	Homo sapiens	55-59
11726395-5	2001	The effect of SP-A could be inhibited by high concentrations of mannose, but was not affected by the removal or addition of lipopolysaccharide (LPS).	Mannose	64-71	surfactant protein A1	Homo sapiens	14-18
11726395-6	2001	Finally, we observed that the SP-A-mediated increase in uptake of P. aeruginosa by THP-1 cells was optimal in a narrow (100 mM and 150 mM) range of NaCl concentrations.	Sodium Chloride	148-152	surfactant protein A1	Homo sapiens	30-34
11726395-7	2001	We conclude that SP-A enhances the THP-1 cell-mediated uptake of P. aeruginosa in a manner dependent on temperature, the concentration of SP-A, and the concentration of NaCl.	Sodium Chloride	169-173	surfactant protein A1	Homo sapiens	17-21
11714829-8	2001	This finding suggests that SP-A may share a common binding site for C1r and C1s or Clq.	(R)-chloroquine	83-86	surfactant protein A1	Homo sapiens	27-31
11778926-3	2001	Today, SPA-based extracorporeal immunoadsorption relies on two rather different systems, namely, SPA-silica (Prosorba), and SPA-Sepharose (Immunosorba).	Sepharose	128-137	surfactant protein A1	Homo sapiens	7-10
11778926-4	2001	Both systems are approved by the Food and Drug Administration for the core indications of rheumatoid arthritis and idiopathic thrombocytopenic purpura (SPA-silica) or hemophilia with inhibitors (SPA-Sepharose).	Sepharose	199-208	surfactant protein A1	Homo sapiens	195-198
11552737-6	2001	A approximately 35 kDa SP-A immunoreactive protein was detected in the tracheal tissues by immunoblot analysis and was shown to be modified by the addition of N-linked oligosaccharides.	n-linked oligosaccharides	159-184	surfactant protein A1	Homo sapiens	23-27
11552739-5	2001	The greatest increase in SP-A mRNA occurred with cAMP alone.	Cyclic AMP	49-53	surfactant protein A1	Homo sapiens	25-29
11486733-1	2001	Surfactant protein A (SP-A), an oligomeric glycoprotein, is a member of a group of proteins named collectins that contain collagen-like and Ca(2+)-dependent carbohydrate recognition domains.	Carbohydrates	157-169	surfactant protein A1	Homo sapiens	0-20
11486733-1	2001	Surfactant protein A (SP-A), an oligomeric glycoprotein, is a member of a group of proteins named collectins that contain collagen-like and Ca(2+)-dependent carbohydrate recognition domains.	Carbohydrates	157-169	surfactant protein A1	Homo sapiens	22-26
11486733-3	2001	This review summarizes SP-A/lipid interaction studies regarding the lipid system used (i.e., phospholipid vesicles, phospholipid monolayers, and lipids immobilized on silica or adsorbed on a solid support).	Phospholipids	116-128	surfactant protein A1	Homo sapiens	23-27
11486733-2	2001	SP-A interacts with a broad range of amphipathic lipids (glycerophospholipids, sphingophospholipids, glycosphingolipids, lipid A, and lipoglycans) that are present in surfactant or microbial membranes.	Glycerophospholipids	57-77	surfactant protein A1	Homo sapiens	0-4
11486733-3	2001	This review summarizes SP-A/lipid interaction studies regarding the lipid system used (i.e., phospholipid vesicles, phospholipid monolayers, and lipids immobilized on silica or adsorbed on a solid support).	Silicon Dioxide	167-173	surfactant protein A1	Homo sapiens	23-27
11486733-2	2001	SP-A interacts with a broad range of amphipathic lipids (glycerophospholipids, sphingophospholipids, glycosphingolipids, lipid A, and lipoglycans) that are present in surfactant or microbial membranes.	sphingophospholipids	79-99	surfactant protein A1	Homo sapiens	0-4
11486733-4	2001	The effect of calcium, ionic strength, and pH on the binding of SP-A to lipids and the subsequent lipid aggregation process is discussed.	Calcium	14-21	surfactant protein A1	Homo sapiens	64-68
11486733-8	2001	In addition, the interaction of SP-A with membranes might enhance the affinity of SP-A for terminal carbohydrates of glycolipids or glycoproteins on the surface of invading microorganisms.	Carbohydrates	100-113	surfactant protein A1	Homo sapiens	32-36
11486733-8	2001	In addition, the interaction of SP-A with membranes might enhance the affinity of SP-A for terminal carbohydrates of glycolipids or glycoproteins on the surface of invading microorganisms.	Carbohydrates	100-113	surfactant protein A1	Homo sapiens	82-86
11486733-2	2001	SP-A interacts with a broad range of amphipathic lipids (glycerophospholipids, sphingophospholipids, glycosphingolipids, lipid A, and lipoglycans) that are present in surfactant or microbial membranes.	Glycosphingolipids	101-119	surfactant protein A1	Homo sapiens	0-4
11486735-2	2001	Although research has shown that SP-A is both a calcium-dependent phospholipid-binding protein that affects surfactant structure and function and a lectin that opsonizes diverse microbial species, our understanding of the physiologically relevant roles of SP-A in the lung remains incomplete.	Calcium	48-55	surfactant protein A1	Homo sapiens	33-37
11486736-3	2001	SP-A and SP-D recognize and interact with glycoconjugates on the surface of microorganisms.	Glycoconjugates	42-57	surfactant protein A1	Homo sapiens	0-4
11486733-2	2001	SP-A interacts with a broad range of amphipathic lipids (glycerophospholipids, sphingophospholipids, glycosphingolipids, lipid A, and lipoglycans) that are present in surfactant or microbial membranes.	Lipid A	121-128	surfactant protein A1	Homo sapiens	0-4
11486733-3	2001	This review summarizes SP-A/lipid interaction studies regarding the lipid system used (i.e., phospholipid vesicles, phospholipid monolayers, and lipids immobilized on silica or adsorbed on a solid support).	Phospholipids	93-105	surfactant protein A1	Homo sapiens	23-27
11254556-1	2001	Surfactant proteins A (SP-A) and D (SP-D) are members of the collectin family of calcium-dependent lectins and are important pulmonary host defense molecules.	Calcium	81-88	surfactant protein A1	Homo sapiens	23-27
11369536-5	2001	The hydrophilic surfactant proteins SP-A and SP-D are members of a family of collagenous carbohydrate binding proteins, known as collectins, consisting of oligomers of trimeric subunits.	Carbohydrates	89-101	surfactant protein A1	Homo sapiens	36-40
11369537-3	2001	The N-terminal domain of SP-A is required for disulfide-dependent protein oligomerization, and for binding and aggregation of phospholipids, but there is no evidence that this domain directly interacts with lipid membranes.	Disulfides	46-55	surfactant protein A1	Homo sapiens	25-29
11369537-3	2001	The N-terminal domain of SP-A is required for disulfide-dependent protein oligomerization, and for binding and aggregation of phospholipids, but there is no evidence that this domain directly interacts with lipid membranes.	Phospholipids	126-139	surfactant protein A1	Homo sapiens	25-29
11294993-3	2001	Surfactant-apoprotein-A is expressed by the pneumocytes II in lung tissue and a portion of non-small cell lung carcinomas and has not yet been found to be expressed by other tumors when detected immunohistochemically by use of the monoclonal antibody PE-10.	INDOLINE, 1-(2-(2-PYRIDYL)ETHYL)-	251-256	surfactant protein A1	Homo sapiens	0-23
11294993-4	2001	We analyzed formalin-fixed, paraffin-embedded specimens of different malignancies with pulmonary location for the expression of SP-A by the use of PE-10 with other antibodies against additional epitopes such as the thyroid transcription factor-1.	Formaldehyde	12-20	surfactant protein A1	Homo sapiens	128-132
11161717-2	2001	Previously we have shown that activation of SPAR by SP-A binding initiates a signal through pathways that involve tyrosine phosphorylation, include IRS-1, and entail activation of phosphatidylinositol 3-kinase (PI3K).	Tyrosine	114-122	surfactant protein A1	Homo sapiens	52-56
11149893-2	2001	The function of SP-A in the alveolus is to facilitate the surface tension-lowering properties of surfactant phospholipids, regulate surfactant phospholipid synthesis, secretion, and recycling, and counteract the inhibitory effects of plasma proteins released during lung injury on surfactant function.	Phospholipids	108-121	surfactant protein A1	Homo sapiens	16-20
11160338-7	2001	However, other proteins that are structurally homologous to SP-A, mannose-binding lectin and complement protein 1q, did not.	Mannose	66-73	surfactant protein A1	Homo sapiens	60-64
11313189-9	2001	In samples with reproducibly detectable SP-D or SP-A, their carbohydrate binding capacity was zero.	Carbohydrates	60-72	surfactant protein A1	Homo sapiens	48-52
11174469-17	2001	A correlation (r = 0.83, P &lt;.001) was found be-tween the differences in MTAC creatinine between the first and last SPA during glucose-based PD and the difference in LVEGF between these observations.	Polysorbates	50-55	surfactant protein A1	Homo sapiens	118-121
11174469-17	2001	A correlation (r = 0.83, P &lt;.001) was found be-tween the differences in MTAC creatinine between the first and last SPA during glucose-based PD and the difference in LVEGF between these observations.	Tetradecyltrimethylammonium chloride	75-79	surfactant protein A1	Homo sapiens	118-121
11174469-17	2001	A correlation (r = 0.83, P &lt;.001) was found be-tween the differences in MTAC creatinine between the first and last SPA during glucose-based PD and the difference in LVEGF between these observations.	Creatinine	80-90	surfactant protein A1	Homo sapiens	118-121
11174469-17	2001	A correlation (r = 0.83, P &lt;.001) was found be-tween the differences in MTAC creatinine between the first and last SPA during glucose-based PD and the difference in LVEGF between these observations.	Glucose	129-136	surfactant protein A1	Homo sapiens	118-121
11133504-2	2001	Inhibition of coated-pit function by potassium depletion severely reduced both SP-A and SP-A-mediated lipid internalization.	Potassium	37-46	surfactant protein A1	Homo sapiens	79-83
11133504-2	2001	Inhibition of coated-pit function by potassium depletion severely reduced both SP-A and SP-A-mediated lipid internalization.	Potassium	37-46	surfactant protein A1	Homo sapiens	88-92
11598635-8	2001	Based on NMR and CD results, we suggest that the helices in Sp alpha 1-156 exhibit a looser (frayed) conformation, and that the helices convert to a tighter conformation upon association with its beta-partner.	Cadmium	17-19	surfactant protein A1	Homo sapiens	60-68
11149893-2	2001	The function of SP-A in the alveolus is to facilitate the surface tension-lowering properties of surfactant phospholipids, regulate surfactant phospholipid synthesis, secretion, and recycling, and counteract the inhibitory effects of plasma proteins released during lung injury on surfactant function.	Phospholipids	108-120	surfactant protein A1	Homo sapiens	16-20
11106621-10	2000	SP-A, combined with SP-B, induces a selective adsorption of DPPC from subphase vesicles into the surface film.	1,2-Dipalmitoylphosphatidylcholine	60-64	surfactant protein A1	Homo sapiens	0-4
10969075-5	2000	We now report that the hydrophilic surfactant proteins A (SP-A) and D (SP-D) directly protect surfactant phospholipids and macrophages from oxidative damage.	Phospholipids	105-118	surfactant protein A1	Homo sapiens	58-69
10969075-8	2000	The antioxidant activity of SP-A maps to the carboxyl-terminal domain of the protein, which, like SP-D, contains a C-type lectin carbohydrate recognition domain.	Carbohydrates	129-141	surfactant protein A1	Homo sapiens	28-32
10969075-9	2000	These results indicate that SP-A and SP-D, which are ubiquitous among air breathing organisms, could contribute to the protection of the lung from oxidative stresses due to atmospheric or supplemental oxygen, air pollutants, and lung inflammation.	Oxygen	201-207	surfactant protein A1	Homo sapiens	28-32
11053138-1	2000	Epifluorescence microscopy was used to investigate the interaction of pulmonary surfactant protein A (SP-A) with spread monolayers of porcine surfactant lipid extract (PSLE) containing 1 mol % fluorescent probe (NBD-PC) spread on a saline subphase (145 mM NaCl, 5 mM Tris-HCl, pH 6.9) containing 0, 0.13, or 0.16 microg/ml SP-A and 0, 1.64, or 5 mM CaCl(2).	Sodium Chloride	232-238	surfactant protein A1	Homo sapiens	70-100
11083772-3	2000	In the human monocytic cell line, THP-1, combining SP-A with lipid A or rough LPS further enhanced lipid A- or rough LPS-stimulated tumor necrosis factor alpha (TNF-alpha) mRNA levels, while SP-A-elicited increases in TNF-alpha mRNA levels were partially neutralized.	Lipid A	99-106	surfactant protein A1	Homo sapiens	51-55
11062136-7	2000	SP-A enhanced binding and uptake of fluorescently labeled RSV (RSV-FITC) by PBMC in a dose-dependent manner, with a maximal effect seen with 10 to 15 microg/ml SP-A as measured by both percent fluorescent monocytes and linear mean fluorescence (lmf) of individual cells.	PBMC	76-80	surfactant protein A1	Homo sapiens	0-4
11053138-1	2000	Epifluorescence microscopy was used to investigate the interaction of pulmonary surfactant protein A (SP-A) with spread monolayers of porcine surfactant lipid extract (PSLE) containing 1 mol % fluorescent probe (NBD-PC) spread on a saline subphase (145 mM NaCl, 5 mM Tris-HCl, pH 6.9) containing 0, 0.13, or 0.16 microg/ml SP-A and 0, 1.64, or 5 mM CaCl(2).	Sodium Chloride	232-238	surfactant protein A1	Homo sapiens	102-106
11053138-1	2000	Epifluorescence microscopy was used to investigate the interaction of pulmonary surfactant protein A (SP-A) with spread monolayers of porcine surfactant lipid extract (PSLE) containing 1 mol % fluorescent probe (NBD-PC) spread on a saline subphase (145 mM NaCl, 5 mM Tris-HCl, pH 6.9) containing 0, 0.13, or 0.16 microg/ml SP-A and 0, 1.64, or 5 mM CaCl(2).	Sodium Chloride	256-260	surfactant protein A1	Homo sapiens	70-100
11053138-1	2000	Epifluorescence microscopy was used to investigate the interaction of pulmonary surfactant protein A (SP-A) with spread monolayers of porcine surfactant lipid extract (PSLE) containing 1 mol % fluorescent probe (NBD-PC) spread on a saline subphase (145 mM NaCl, 5 mM Tris-HCl, pH 6.9) containing 0, 0.13, or 0.16 microg/ml SP-A and 0, 1.64, or 5 mM CaCl(2).	Sodium Chloride	256-260	surfactant protein A1	Homo sapiens	102-106
11053138-1	2000	Epifluorescence microscopy was used to investigate the interaction of pulmonary surfactant protein A (SP-A) with spread monolayers of porcine surfactant lipid extract (PSLE) containing 1 mol % fluorescent probe (NBD-PC) spread on a saline subphase (145 mM NaCl, 5 mM Tris-HCl, pH 6.9) containing 0, 0.13, or 0.16 microg/ml SP-A and 0, 1.64, or 5 mM CaCl(2).	Tris hydrochloride	267-275	surfactant protein A1	Homo sapiens	70-100
11053138-1	2000	Epifluorescence microscopy was used to investigate the interaction of pulmonary surfactant protein A (SP-A) with spread monolayers of porcine surfactant lipid extract (PSLE) containing 1 mol % fluorescent probe (NBD-PC) spread on a saline subphase (145 mM NaCl, 5 mM Tris-HCl, pH 6.9) containing 0, 0.13, or 0.16 microg/ml SP-A and 0, 1.64, or 5 mM CaCl(2).	Tris hydrochloride	267-275	surfactant protein A1	Homo sapiens	102-106
11053138-1	2000	Epifluorescence microscopy was used to investigate the interaction of pulmonary surfactant protein A (SP-A) with spread monolayers of porcine surfactant lipid extract (PSLE) containing 1 mol % fluorescent probe (NBD-PC) spread on a saline subphase (145 mM NaCl, 5 mM Tris-HCl, pH 6.9) containing 0, 0.13, or 0.16 microg/ml SP-A and 0, 1.64, or 5 mM CaCl(2).	cacl	349-353	surfactant protein A1	Homo sapiens	70-100
11053138-1	2000	Epifluorescence microscopy was used to investigate the interaction of pulmonary surfactant protein A (SP-A) with spread monolayers of porcine surfactant lipid extract (PSLE) containing 1 mol % fluorescent probe (NBD-PC) spread on a saline subphase (145 mM NaCl, 5 mM Tris-HCl, pH 6.9) containing 0, 0.13, or 0.16 microg/ml SP-A and 0, 1.64, or 5 mM CaCl(2).	cacl	349-353	surfactant protein A1	Homo sapiens	102-106
11053138-8	2000	PSLE films were spread on a subphase containing 0.16 microg/ml SP-A with covalently bound Texas Red (TR-SP-A).	Texas red	90-99	surfactant protein A1	Homo sapiens	63-67
11153579-7	2000	The levels of SP-A correlated with those of fucose in patients with bronchial asthma (r=0.849, p&lt;0.01).	Fucose	44-50	surfactant protein A1	Homo sapiens	14-18
11028547-6	2000	SP-A was purified from isolated surfactant using sequential butanol and octyl glucoside extractions.	Butanols	60-67	surfactant protein A1	Homo sapiens	0-4
11216568-3	2000	One SPA used 1.36% glucose; the other, 3.86% glucose.	Glucose	19-26	surfactant protein A1	Homo sapiens	4-7
11216568-6	2000	RESULTS: Median NUF in the 1.36% glucose SPA was -46 mL (range: -582 mL to 238 mL); in the 3.86% SPA, it was 554 mL (range: -274 mL to 1126 mL).	Glucose	33-40	surfactant protein A1	Homo sapiens	41-44
11001826-3	2000	SP-A and SP-D are large hydrophilic proteins, which play an important role in host defense, whereas the small hydrophobic peptides SP-B and SP-C interact with DPPC to generate and maintain a surface-active film.	1,2-Dipalmitoylphosphatidylcholine	159-163	surfactant protein A1	Homo sapiens	0-4
11028547-6	2000	SP-A was purified from isolated surfactant using sequential butanol and octyl glucoside extractions.	octyl-beta-D-glucoside	72-87	surfactant protein A1	Homo sapiens	0-4
11028547-10	2000	The SP-A effect on TNFalpha production could be mediated by a suppression in the LPS-induced increase in intracellular cGMP.	Cyclic GMP	119-123	surfactant protein A1	Homo sapiens	4-8
10864991-9	2000	CONCLUSION: Patients undergoing SPA column treatments, especially those with thrombocytopenia, may be at increased risk of bleeding as a result of the presence of a significant amount of heparin in their circulation during the entire period of SPA column treatment.	Heparin	187-194	surfactant protein A1	Homo sapiens	244-247
11030586-10	2000	We describe a model proposing that SP-A and SP-B create DPPC enriched domains which can readily be adsorbed to create a DPPC-rich monolayer at the interface.	1,2-Dipalmitoylphosphatidylcholine	56-60	surfactant protein A1	Homo sapiens	35-39
11030586-10	2000	We describe a model proposing that SP-A and SP-B create DPPC enriched domains which can readily be adsorbed to create a DPPC-rich monolayer at the interface.	1,2-Dipalmitoylphosphatidylcholine	120-124	surfactant protein A1	Homo sapiens	35-39
10914330-0	2000	Induction of AP-1 binding to intron 1 of SP-A1 and SP-A2 is implicated in the phorbol ester inhibition of human SP-A promoter activity.	Phorbol Esters	78-91	surfactant protein A1	Homo sapiens	41-46
10914330-1	2000	A deletional analysis of the SP-A1 promoter in NCI-H441 cells was performed to identify potential cis-acting elements involved in phorbol ester-mediated repression of human SP-A transcription.	Phorbol Esters	130-143	surfactant protein A1	Homo sapiens	29-34
10914330-2	2000	The phorbol ester TPA reduced SP-A1 and SP-A2 promoter activity to approximately 35% to 45% compared to that of control cells.	Phorbol Esters	4-17	surfactant protein A1	Homo sapiens	30-35
10914330-2	2000	The phorbol ester TPA reduced SP-A1 and SP-A2 promoter activity to approximately 35% to 45% compared to that of control cells.	Tetradecanoylphorbol Acetate	18-21	surfactant protein A1	Homo sapiens	30-35
10914330-3	2000	The inhibitory effect of TPA was significantly reduced upon removal of the region +64/+394 relative to the SP-A1 transcription start site.	Tetradecanoylphorbol Acetate	25-28	surfactant protein A1	Homo sapiens	107-112
10914330-4	2000	Using NCI-H441 nuclear proteins, electromobility shift assay analysis showed that the intron region +309/+329 of SP-A1 and the corresponding region of SP-A2 formed sequence-specific DNA/protein complexes that were induced by TPA exposure.	Tetradecanoylphorbol Acetate	225-228	surfactant protein A1	Homo sapiens	113-118
10914330-5	2000	The region +318/+324 of SP-A1 contains sequences similar to a consensus AP-1 binding site, TGACTGA (TCACTGA for SP-A2), which when mutated (TGAGAGT) prevented the formation of the TPA-induced DNA/protein complex.	Tetradecanoylphorbol Acetate	180-183	surfactant protein A1	Homo sapiens	24-29
10914330-7	2000	These results suggest that the binding of AP-1 or an AP-1--like factor to the first intron of SP-A1 and SP-A2 may be involved in the phorbol ester inhibition of human SP-A gene expression.	Phorbol Esters	133-146	surfactant protein A1	Homo sapiens	94-99
10864991-0	2000	Heparin-induced coagulopathy associated with staphylococcal protein A immunoadsorption treatment columns: an in vitro and in vivo analysis.	Heparin	0-7	surfactant protein A1	Homo sapiens	45-69
10864991-1	2000	BACKGROUND: The staphylococcal protein A (SPA) column used to treat refractory autoimmune and alloimmune thrombocytopenia and rheumatoid arthritis patients is primed with heparin to prevent possible fibrin clot formation when the patient"s plasma is passed through the column.	Heparin	171-178	surfactant protein A1	Homo sapiens	16-40
10828969-1	2000	Environmental factors of physiological relevance such as pH, calcium, ionic strength, and temperature can affect the state of self-aggregation of surfactant protein A (SP-A).	Calcium	61-68	surfactant protein A1	Homo sapiens	146-166
10828969-1	2000	Environmental factors of physiological relevance such as pH, calcium, ionic strength, and temperature can affect the state of self-aggregation of surfactant protein A (SP-A).	Calcium	61-68	surfactant protein A1	Homo sapiens	168-172
10828969-6	2000	Circular dichroism and fluorescence measurements of Ca(2+)-dependent SP-A aggregates indicated that those protein aggregates formed in the absence of NaCl are structurally different from those formed in its presence.	Sodium Chloride	150-154	surfactant protein A1	Homo sapiens	69-73
10828969-9	2000	The presence of both salts and Ca(2+) attenuated even more the effects of acidic media on SP-A self-aggregation.	Salts	21-26	surfactant protein A1	Homo sapiens	90-94
10828969-11	2000	At 20 degrees C, SP-A underwent self-aggregation at physiological but not at low ionic strength, in the presence of EDTA.	Edetic Acid	116-120	surfactant protein A1	Homo sapiens	17-21
10864991-1	2000	BACKGROUND: The staphylococcal protein A (SPA) column used to treat refractory autoimmune and alloimmune thrombocytopenia and rheumatoid arthritis patients is primed with heparin to prevent possible fibrin clot formation when the patient"s plasma is passed through the column.	Heparin	171-178	surfactant protein A1	Homo sapiens	42-45
10864991-3	2000	This observation led to in vivo and in vitro analysis of the kinetics of heparin elution from the SPA column.	Heparin	73-80	surfactant protein A1	Homo sapiens	98-101
10864991-5	2000	In addition, two in vitro analyses were performed with FFP for heparin elution from the SPA column.	Heparin	63-70	surfactant protein A1	Homo sapiens	88-91
10864991-6	2000	RESULTS: The in vivo studies showed the presence of 0.3 to 1.5 U per mL of heparin in patients" plasma at the end of the SPA column treatments that corresponded with the prolonged aPTTs.	Heparin	75-82	surfactant protein A1	Homo sapiens	121-124
10864991-9	2000	CONCLUSION: Patients undergoing SPA column treatments, especially those with thrombocytopenia, may be at increased risk of bleeding as a result of the presence of a significant amount of heparin in their circulation during the entire period of SPA column treatment.	Heparin	187-194	surfactant protein A1	Homo sapiens	32-35
10781434-0	2000	Carbon dioxide enhances nitration of surfactant protein A by activated alveolar macrophages.	Carbon Dioxide	0-14	surfactant protein A1	Homo sapiens	37-57
10781434-5	2000	Western blotting studies of immunoprecipitated SP-A indicated that CO(2) enhanced SP-A nitration by AMs and decreased carbonyl formation.	Carbon Dioxide	67-72	surfactant protein A1	Homo sapiens	47-51
10644694-8	2000	Selective removal of either the terminal mannose or the acyl residues esterifying the glycerol moiety of the ManLAM abrogates the interaction with hSP-A, further supporting the notion that the hSP-A recognition of the carbohydrate epitopes of the lipoglycans is dependent of the presence of the fatty acids.	Glycerol	86-94	surfactant protein A1	Homo sapiens	147-152
10781434-5	2000	Western blotting studies of immunoprecipitated SP-A indicated that CO(2) enhanced SP-A nitration by AMs and decreased carbonyl formation.	Carbon Dioxide	67-72	surfactant protein A1	Homo sapiens	82-86
10781434-6	2000	CO(2) (0-1.2 mM) also augmented peroxynitrite (0.5 mM)-induced SP-A nitration in a dose-dependent fashion.	Carbon Dioxide	0-5	surfactant protein A1	Homo sapiens	63-67
10781434-6	2000	CO(2) (0-1.2 mM) also augmented peroxynitrite (0.5 mM)-induced SP-A nitration in a dose-dependent fashion.	Peroxynitrous Acid	32-45	surfactant protein A1	Homo sapiens	63-67
10781434-7	2000	Peroxynitrite decreased the ability of SP-A to aggregate lipids, and this inhibition was augmented by 1.2 mM CO(2).	Peroxynitrous Acid	0-13	surfactant protein A1	Homo sapiens	39-43
10781434-7	2000	Peroxynitrite decreased the ability of SP-A to aggregate lipids, and this inhibition was augmented by 1.2 mM CO(2).	Carbon Dioxide	109-114	surfactant protein A1	Homo sapiens	39-43
10781434-8	2000	Mass spectrometry analysis of chymotryptic fragments of peroxynitrite-exposed SP-A showed nitration of two tyrosines (Tyr(164) and Tyr(166)) in the absence of CO(2) and three tyrosines (Tyr(164), Tyr(166), and Tyr(161)) in the presence of 1.2 mM CO(2).	Peroxynitrous Acid	56-69	surfactant protein A1	Homo sapiens	78-82
10781434-8	2000	Mass spectrometry analysis of chymotryptic fragments of peroxynitrite-exposed SP-A showed nitration of two tyrosines (Tyr(164) and Tyr(166)) in the absence of CO(2) and three tyrosines (Tyr(164), Tyr(166), and Tyr(161)) in the presence of 1.2 mM CO(2).	Tyrosine	107-116	surfactant protein A1	Homo sapiens	78-82
10781434-8	2000	Mass spectrometry analysis of chymotryptic fragments of peroxynitrite-exposed SP-A showed nitration of two tyrosines (Tyr(164) and Tyr(166)) in the absence of CO(2) and three tyrosines (Tyr(164), Tyr(166), and Tyr(161)) in the presence of 1.2 mM CO(2).	Tyrosine	118-121	surfactant protein A1	Homo sapiens	78-82
10781434-8	2000	Mass spectrometry analysis of chymotryptic fragments of peroxynitrite-exposed SP-A showed nitration of two tyrosines (Tyr(164) and Tyr(166)) in the absence of CO(2) and three tyrosines (Tyr(164), Tyr(166), and Tyr(161)) in the presence of 1.2 mM CO(2).	Tyrosine	131-134	surfactant protein A1	Homo sapiens	78-82
10781434-8	2000	Mass spectrometry analysis of chymotryptic fragments of peroxynitrite-exposed SP-A showed nitration of two tyrosines (Tyr(164) and Tyr(166)) in the absence of CO(2) and three tyrosines (Tyr(164), Tyr(166), and Tyr(161)) in the presence of 1.2 mM CO(2).	Tyrosine	175-184	surfactant protein A1	Homo sapiens	78-82
10781434-8	2000	Mass spectrometry analysis of chymotryptic fragments of peroxynitrite-exposed SP-A showed nitration of two tyrosines (Tyr(164) and Tyr(166)) in the absence of CO(2) and three tyrosines (Tyr(164), Tyr(166), and Tyr(161)) in the presence of 1.2 mM CO(2).	Tyrosine	131-134	surfactant protein A1	Homo sapiens	78-82
10781434-8	2000	Mass spectrometry analysis of chymotryptic fragments of peroxynitrite-exposed SP-A showed nitration of two tyrosines (Tyr(164) and Tyr(166)) in the absence of CO(2) and three tyrosines (Tyr(164), Tyr(166), and Tyr(161)) in the presence of 1.2 mM CO(2).	Tyrosine	131-134	surfactant protein A1	Homo sapiens	78-82
10781434-8	2000	Mass spectrometry analysis of chymotryptic fragments of peroxynitrite-exposed SP-A showed nitration of two tyrosines (Tyr(164) and Tyr(166)) in the absence of CO(2) and three tyrosines (Tyr(164), Tyr(166), and Tyr(161)) in the presence of 1.2 mM CO(2).	Tyrosine	131-134	surfactant protein A1	Homo sapiens	78-82
10781434-8	2000	Mass spectrometry analysis of chymotryptic fragments of peroxynitrite-exposed SP-A showed nitration of two tyrosines (Tyr(164) and Tyr(166)) in the absence of CO(2) and three tyrosines (Tyr(164), Tyr(166), and Tyr(161)) in the presence of 1.2 mM CO(2).	Carbon Dioxide	246-251	surfactant protein A1	Homo sapiens	78-82
10781434-9	2000	These findings indicate that physiological levels of peroxynitrite, produced by activated AMs, nitrate SP-A and that CO(2) increased nitration, at least partially, by enhancing enzymatic nitric oxide production.	Peroxynitrous Acid	53-66	surfactant protein A1	Homo sapiens	103-107
10710531-6	2000	Although, as shown by confocal laser scanning microscopy, after a 10-min uptake period at 37 degrees C, most of the fluorescein isothiocyanate-labeled SP-A and rhodamine-phosphatidylethanolamine-labeled lipids colocalized within the cells, after an additional 10 min of resecretion, both the strength of the fluorescence signals and the extent of colocalization had markedly decreased.	Fluorescein-5-isothiocyanate	116-142	surfactant protein A1	Homo sapiens	151-155
10666335-4	2000	The phosphatidylinositol 3-kinase (PI3K) inhibitor LY294002 rescued surfactant secretion from inhibition by SP-A.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	51-59	surfactant protein A1	Homo sapiens	108-112
10666335-9	2000	In addition, the tyrosine-specific protein kinase inhibitors genistein and herbimycin A blocked the action of SP-A on surfactant secretion.	Genistein	61-70	surfactant protein A1	Homo sapiens	110-114
10666335-9	2000	In addition, the tyrosine-specific protein kinase inhibitors genistein and herbimycin A blocked the action of SP-A on surfactant secretion.	herbimycin	75-87	surfactant protein A1	Homo sapiens	110-114
10666335-10	2000	We conclude that SP-A signals to regulate surfactant secretion through SPAR, via pathways that involve tyrosine phosphorylation, include IRS-1, and entail activation of PI3K.	Tyrosine	103-111	surfactant protein A1	Homo sapiens	17-21
10732762-4	2000	Surfactant protein A was induced in NCI-H441 cells by conditioned medium and dexamethasone and, to a much lesser extent, by oncostatin M or IL-6.	Dexamethasone	77-90	surfactant protein A1	Homo sapiens	0-20
10732762-5	2000	Induction of alkaline phosphatase and surfactant protein A were both dexamethasone-dependent, though some induction of surfactant protein A was obtained with interferon-alpha in the absence of dexamethasone.	Dexamethasone	69-82	surfactant protein A1	Homo sapiens	38-58
10696064-6	2000	The increase in SP-A mRNA was evident within 4 to 6 h. IL-1alpha increased the SP-A concentration in alveolar epithelial cells and in the culture medium within 20 h. In contrast, at 27 to 30 d of gestation and in newborns, IL-1alpha decreased SP-C, -B, and -A mRNA by means of 64 to 67%, 48 to 59%, and 12 to 15%, respectively.	sp-c	243-247	surfactant protein A1	Homo sapiens	16-20
10696064-6	2000	The increase in SP-A mRNA was evident within 4 to 6 h. IL-1alpha increased the SP-A concentration in alveolar epithelial cells and in the culture medium within 20 h. In contrast, at 27 to 30 d of gestation and in newborns, IL-1alpha decreased SP-C, -B, and -A mRNA by means of 64 to 67%, 48 to 59%, and 12 to 15%, respectively.	sp-c	243-247	surfactant protein A1	Homo sapiens	79-83
10644694-8	2000	Selective removal of either the terminal mannose or the acyl residues esterifying the glycerol moiety of the ManLAM abrogates the interaction with hSP-A, further supporting the notion that the hSP-A recognition of the carbohydrate epitopes of the lipoglycans is dependent of the presence of the fatty acids.	manlam	109-115	surfactant protein A1	Homo sapiens	147-152
10644694-8	2000	Selective removal of either the terminal mannose or the acyl residues esterifying the glycerol moiety of the ManLAM abrogates the interaction with hSP-A, further supporting the notion that the hSP-A recognition of the carbohydrate epitopes of the lipoglycans is dependent of the presence of the fatty acids.	Carbohydrates	218-230	surfactant protein A1	Homo sapiens	147-152
10644694-8	2000	Selective removal of either the terminal mannose or the acyl residues esterifying the glycerol moiety of the ManLAM abrogates the interaction with hSP-A, further supporting the notion that the hSP-A recognition of the carbohydrate epitopes of the lipoglycans is dependent of the presence of the fatty acids.	Fatty Acids	295-306	surfactant protein A1	Homo sapiens	147-152
10584204-8	1999	Protein A (SpA)-induced NADPH oxidase activation in the membrane fraction was observed even in the absence of the substrate NADPH.	NADP	24-29	surfactant protein A1	Homo sapiens	11-14
10645896-3	2000	The effects of a modified natural porcine surfactant, Curosurf, and the major surfactant protein A were evaluated on resting and stimulated cAMP levels of human monocytes.	Cyclic AMP	140-144	surfactant protein A1	Homo sapiens	78-98
10733174-4	2000	SP-A binds to RSV G-protein in a concentration-dependent manner that is inhibitable by both ethylenediamine tetraacetic acid (EDTA) and mannan, indicating that binding is through the carbohydrate recognition domain of the SP-A and a carbohydrate moiety of the G-protein.	Edetic Acid	92-124	surfactant protein A1	Homo sapiens	0-4
10733174-4	2000	SP-A binds to RSV G-protein in a concentration-dependent manner that is inhibitable by both ethylenediamine tetraacetic acid (EDTA) and mannan, indicating that binding is through the carbohydrate recognition domain of the SP-A and a carbohydrate moiety of the G-protein.	Edetic Acid	126-130	surfactant protein A1	Homo sapiens	0-4
10733174-4	2000	SP-A binds to RSV G-protein in a concentration-dependent manner that is inhibitable by both ethylenediamine tetraacetic acid (EDTA) and mannan, indicating that binding is through the carbohydrate recognition domain of the SP-A and a carbohydrate moiety of the G-protein.	Mannans	136-142	surfactant protein A1	Homo sapiens	0-4
10733174-4	2000	SP-A binds to RSV G-protein in a concentration-dependent manner that is inhibitable by both ethylenediamine tetraacetic acid (EDTA) and mannan, indicating that binding is through the carbohydrate recognition domain of the SP-A and a carbohydrate moiety of the G-protein.	Carbohydrates	183-195	surfactant protein A1	Homo sapiens	0-4
10733174-4	2000	SP-A binds to RSV G-protein in a concentration-dependent manner that is inhibitable by both ethylenediamine tetraacetic acid (EDTA) and mannan, indicating that binding is through the carbohydrate recognition domain of the SP-A and a carbohydrate moiety of the G-protein.	Carbohydrates	183-195	surfactant protein A1	Homo sapiens	222-226
10733174-4	2000	SP-A binds to RSV G-protein in a concentration-dependent manner that is inhibitable by both ethylenediamine tetraacetic acid (EDTA) and mannan, indicating that binding is through the carbohydrate recognition domain of the SP-A and a carbohydrate moiety of the G-protein.	Carbohydrates	233-245	surfactant protein A1	Homo sapiens	0-4
10733174-4	2000	SP-A binds to RSV G-protein in a concentration-dependent manner that is inhibitable by both ethylenediamine tetraacetic acid (EDTA) and mannan, indicating that binding is through the carbohydrate recognition domain of the SP-A and a carbohydrate moiety of the G-protein.	Carbohydrates	233-245	surfactant protein A1	Homo sapiens	222-226
10662499-1	2000	A hydrophilic matrix of periodate-oxidized dextran was used as a double-sided linker to covalently immobilize Staphylococcus aureus protein A (SpA) molecules onto a poly-L-lysine-modified piezoelectric crystal surface to improve their stability, activity, and binding specificity with human immunoglobulin G (IgG) in flow injection assays.	metaperiodate	24-33	surfactant protein A1	Homo sapiens	143-146
10662499-1	2000	A hydrophilic matrix of periodate-oxidized dextran was used as a double-sided linker to covalently immobilize Staphylococcus aureus protein A (SpA) molecules onto a poly-L-lysine-modified piezoelectric crystal surface to improve their stability, activity, and binding specificity with human immunoglobulin G (IgG) in flow injection assays.	Dextrans	43-50	surfactant protein A1	Homo sapiens	143-146
10662499-1	2000	A hydrophilic matrix of periodate-oxidized dextran was used as a double-sided linker to covalently immobilize Staphylococcus aureus protein A (SpA) molecules onto a poly-L-lysine-modified piezoelectric crystal surface to improve their stability, activity, and binding specificity with human immunoglobulin G (IgG) in flow injection assays.	Lysine	165-178	surfactant protein A1	Homo sapiens	143-146
10558959-3	1999	SP-A was shown to bind to the F (fusion) glycoprotein but not to the viral G (attachment) glycoprotein, and binding was completely abrogated in the presence of EDTA.	Edetic Acid	160-164	surfactant protein A1	Homo sapiens	0-4
10558959-5	1999	SP-A also neutralized RSV in a calcium dependent fashion.	Calcium	31-38	surfactant protein A1	Homo sapiens	0-4
10577504-3	1999	The main role of SP-A and SP-D is to interact directly with carbohydrate on the surface of microbial pathogens, thereby initiating a variety of effector mechanisms.	Carbohydrates	60-72	surfactant protein A1	Homo sapiens	17-21
10598320-0	1999	Calcium-dependent degradation of surfactant protein A by activated neutrophils due to serine proteases.	Calcium	0-7	surfactant protein A1	Homo sapiens	33-53
10526225-0	1999	Interaction of pulmonary surfactant protein A with phospholipid liposomes: a kinetic study on head group and fatty acid specificity.	Phospholipids	51-63	surfactant protein A1	Homo sapiens	15-45
10526225-0	1999	Interaction of pulmonary surfactant protein A with phospholipid liposomes: a kinetic study on head group and fatty acid specificity.	Fatty Acids	109-119	surfactant protein A1	Homo sapiens	15-45
10526225-4	1999	K(d)=5 microM is obtained for the complex between SP-A and dipalmitoylphosphatidylcholine (DPPC) liposomes.	1,2-Dipalmitoylphosphatidylcholine	59-89	surfactant protein A1	Homo sapiens	50-54
10526225-4	1999	K(d)=5 microM is obtained for the complex between SP-A and dipalmitoylphosphatidylcholine (DPPC) liposomes.	1,2-Dipalmitoylphosphatidylcholine	91-95	surfactant protein A1	Homo sapiens	50-54
10526225-6	1999	With palmitoyloleoylphosphatidylcholine (POPC), the complex formation proceeds at half the rate, compared to DPPC, leading to a lower final equilibrium level of SP-A lipid interaction.	1-palmitoyl-2-oleoylphosphatidylcholine	5-39	surfactant protein A1	Homo sapiens	161-165
10526225-6	1999	With palmitoyloleoylphosphatidylcholine (POPC), the complex formation proceeds at half the rate, compared to DPPC, leading to a lower final equilibrium level of SP-A lipid interaction.	1-palmitoyl-2-oleoylphosphatidylcholine	41-45	surfactant protein A1	Homo sapiens	161-165
10526225-6	1999	With palmitoyloleoylphosphatidylcholine (POPC), the complex formation proceeds at half the rate, compared to DPPC, leading to a lower final equilibrium level of SP-A lipid interaction.	1,2-Dipalmitoylphosphatidylcholine	109-113	surfactant protein A1	Homo sapiens	161-165
10526225-9	1999	Thus both headgroup and fatty acid composition determine SP-A phospholipid interaction.	Fatty Acids	24-34	surfactant protein A1	Homo sapiens	57-61
10526225-9	1999	Thus both headgroup and fatty acid composition determine SP-A phospholipid interaction.	Phospholipids	62-74	surfactant protein A1	Homo sapiens	57-61
10598320-10	1999	Activated leukocytes cause surfactant dysfunction in vitro by serine protease-mediated degradation of SP-A, which occurs only in the presence of EDTA, and is prevented by addition of calcium.	Edetic Acid	145-149	surfactant protein A1	Homo sapiens	102-106
10598320-10	1999	Activated leukocytes cause surfactant dysfunction in vitro by serine protease-mediated degradation of SP-A, which occurs only in the presence of EDTA, and is prevented by addition of calcium.	Calcium	183-190	surfactant protein A1	Homo sapiens	102-106
10465757-0	1999	Interactions of pulmonary surfactant protein A with phospholipid monolayers change with pH.	Phospholipids	52-64	surfactant protein A1	Homo sapiens	16-46
10465757-1	1999	The interaction of pulmonary surfactant protein A (SP-A) labeled with Texas Red (TR-SP-A) with monolayers containing zwitterionic and acidic phospholipids has been studied at pH 7.4 and 4.5 using epifluorescence microscopy.	Texas red	70-79	surfactant protein A1	Homo sapiens	19-49
10465757-1	1999	The interaction of pulmonary surfactant protein A (SP-A) labeled with Texas Red (TR-SP-A) with monolayers containing zwitterionic and acidic phospholipids has been studied at pH 7.4 and 4.5 using epifluorescence microscopy.	Texas red	70-79	surfactant protein A1	Homo sapiens	51-55
10465757-1	1999	The interaction of pulmonary surfactant protein A (SP-A) labeled with Texas Red (TR-SP-A) with monolayers containing zwitterionic and acidic phospholipids has been studied at pH 7.4 and 4.5 using epifluorescence microscopy.	Phospholipids	141-154	surfactant protein A1	Homo sapiens	19-49
10465757-1	1999	The interaction of pulmonary surfactant protein A (SP-A) labeled with Texas Red (TR-SP-A) with monolayers containing zwitterionic and acidic phospholipids has been studied at pH 7.4 and 4.5 using epifluorescence microscopy.	Phospholipids	141-154	surfactant protein A1	Homo sapiens	51-55
10465757-2	1999	At pH 7.4, TR-SP-A expanded the pi-A isotherms of film of dipalmitoylphosphatidylcholine (DPPC).	1,2-Dipalmitoylphosphatidylcholine	58-88	surfactant protein A1	Homo sapiens	14-18
10465757-2	1999	At pH 7.4, TR-SP-A expanded the pi-A isotherms of film of dipalmitoylphosphatidylcholine (DPPC).	1,2-Dipalmitoylphosphatidylcholine	90-94	surfactant protein A1	Homo sapiens	14-18
10465757-4	1999	At pH 4.5, TR-SP-A expanded DPPC monolayers to a slightly lower extent than at pH 7.4.	1,2-Dipalmitoylphosphatidylcholine	28-32	surfactant protein A1	Homo sapiens	14-18
10465757-6	1999	Films of DPPC/dipalmitoylphosphatidylglycerol (DPPG) 7:3 mol/mol were somewhat expanded by TR-SP-A at pH 7.4.	1,2-Dipalmitoylphosphatidylcholine	9-13	surfactant protein A1	Homo sapiens	94-98
10465757-6	1999	Films of DPPC/dipalmitoylphosphatidylglycerol (DPPG) 7:3 mol/mol were somewhat expanded by TR-SP-A at pH 7.4.	1,2-dipalmitoylphosphatidylglycerol	14-45	surfactant protein A1	Homo sapiens	94-98
10465757-6	1999	Films of DPPC/dipalmitoylphosphatidylglycerol (DPPG) 7:3 mol/mol were somewhat expanded by TR-SP-A at pH 7.4.	1,2-dipalmitoylphosphatidylglycerol	47-51	surfactant protein A1	Homo sapiens	94-98
10533675-6	1999	In contrast, the glutathione precursor N-acetyl-l-cysteine (NAC) prevented PDTC-dependent increase in GSSG/GSH ratio, inhibition of SP-A and -B mRNAs, and induction of apoJ.	Glutathione	17-28	surfactant protein A1	Homo sapiens	132-143
10533675-0	1999	Antagonistic effects of pyrrolidine dithiocarbamate and N-acetyl-L-cysteine on surfactant protein A and B mRNAs.	pyrrolidine dithiocarbamic acid	24-51	surfactant protein A1	Homo sapiens	79-105
10533675-6	1999	In contrast, the glutathione precursor N-acetyl-l-cysteine (NAC) prevented PDTC-dependent increase in GSSG/GSH ratio, inhibition of SP-A and -B mRNAs, and induction of apoJ.	Acetylcysteine	39-58	surfactant protein A1	Homo sapiens	132-143
10533675-0	1999	Antagonistic effects of pyrrolidine dithiocarbamate and N-acetyl-L-cysteine on surfactant protein A and B mRNAs.	Acetylcysteine	56-75	surfactant protein A1	Homo sapiens	79-105
10533675-6	1999	In contrast, the glutathione precursor N-acetyl-l-cysteine (NAC) prevented PDTC-dependent increase in GSSG/GSH ratio, inhibition of SP-A and -B mRNAs, and induction of apoJ.	Acetylcysteine	60-63	surfactant protein A1	Homo sapiens	132-143
10533675-3	1999	In the current work, increased levels of oxidized glutathione (GSSG) are demonstrated at doses of pyrrolidine dithiocarbamate (PDTC) which decrease SP-A and SP-B mRNAs, suggesting that cellular oxidation reduces surfactant protein expression.	Glutathione	50-61	surfactant protein A1	Homo sapiens	148-152
10533675-7	1999	Insufficiency of SP-A and -B, which occurs in inflammatory lung diseases, may result from the exposure of the pulmonary epithelium to oxidant stress and may be reversed by the antioxidant NAC.	Acetylcysteine	188-191	surfactant protein A1	Homo sapiens	17-28
10533675-3	1999	In the current work, increased levels of oxidized glutathione (GSSG) are demonstrated at doses of pyrrolidine dithiocarbamate (PDTC) which decrease SP-A and SP-B mRNAs, suggesting that cellular oxidation reduces surfactant protein expression.	Glutathione Disulfide	63-67	surfactant protein A1	Homo sapiens	148-152
10497393-4	1999	Both PL and SPs (SP-A and SP-D) decrease in bronchoalveolar lavage fluid in smokers.	Sodium phenolsulfonate	12-15	surfactant protein A1	Homo sapiens	17-21
10533675-3	1999	In the current work, increased levels of oxidized glutathione (GSSG) are demonstrated at doses of pyrrolidine dithiocarbamate (PDTC) which decrease SP-A and SP-B mRNAs, suggesting that cellular oxidation reduces surfactant protein expression.	pyrrolidine dithiocarbamic acid	98-125	surfactant protein A1	Homo sapiens	148-152
10533675-3	1999	In the current work, increased levels of oxidized glutathione (GSSG) are demonstrated at doses of pyrrolidine dithiocarbamate (PDTC) which decrease SP-A and SP-B mRNAs, suggesting that cellular oxidation reduces surfactant protein expression.	pyrrolidine dithiocarbamic acid	127-131	surfactant protein A1	Homo sapiens	148-152
10533675-4	1999	Similarly, reduction of SP-A and SP-B mRNA levels following accumulation of GSSG induced by glutathione reductase inhibitor 1,3-bis-(2-chloroethyl)-1-nitrosourea (BCNU), supports the hypothesis that surfactant protein synthesis is reduced in response to oxidation of pulmonary epithelial glutathione.	Carmustine	124-161	surfactant protein A1	Homo sapiens	24-28
10533675-4	1999	Similarly, reduction of SP-A and SP-B mRNA levels following accumulation of GSSG induced by glutathione reductase inhibitor 1,3-bis-(2-chloroethyl)-1-nitrosourea (BCNU), supports the hypothesis that surfactant protein synthesis is reduced in response to oxidation of pulmonary epithelial glutathione.	Carmustine	163-167	surfactant protein A1	Homo sapiens	24-28
10533675-4	1999	Similarly, reduction of SP-A and SP-B mRNA levels following accumulation of GSSG induced by glutathione reductase inhibitor 1,3-bis-(2-chloroethyl)-1-nitrosourea (BCNU), supports the hypothesis that surfactant protein synthesis is reduced in response to oxidation of pulmonary epithelial glutathione.	Glutathione	92-103	surfactant protein A1	Homo sapiens	24-28
10362715-1	1999	The synthetic glucocorticoid dexamethasone has a major inhibitory effect on human surfactant protein A1 (SP-A1) and SP-A2 gene expression that occurs at both the transcriptional and posttranscriptional levels.	Dexamethasone	29-42	surfactant protein A1	Homo sapiens	82-103
10384140-8	1999	In addition, SP-A directly bound to recombinant soluble CD14 (rsCD14).	rscd14	62-68	surfactant protein A1	Homo sapiens	13-17
10384140-9	1999	When rsCD14 was preincubated with SP-A, the binding of rsCD14 to smooth LPS was significantly reduced but the association of rsCD14 with rough LPS was augmented.	rscd14	5-11	surfactant protein A1	Homo sapiens	34-38
10384140-9	1999	When rsCD14 was preincubated with SP-A, the binding of rsCD14 to smooth LPS was significantly reduced but the association of rsCD14 with rough LPS was augmented.	rscd14	55-61	surfactant protein A1	Homo sapiens	34-38
10384140-9	1999	When rsCD14 was preincubated with SP-A, the binding of rsCD14 to smooth LPS was significantly reduced but the association of rsCD14 with rough LPS was augmented.	rscd14	55-61	surfactant protein A1	Homo sapiens	34-38
10362715-1	1999	The synthetic glucocorticoid dexamethasone has a major inhibitory effect on human surfactant protein A1 (SP-A1) and SP-A2 gene expression that occurs at both the transcriptional and posttranscriptional levels.	Dexamethasone	29-42	surfactant protein A1	Homo sapiens	105-110
10362715-2	1999	Toward the identification of cis-acting elements that may be involved in the dexamethasone regulation of SP-A mRNA stability, chimeric chloramphenicol acetyltransferase (CAT) constructs that contained various portions of SP-A1 or SP-A2 cDNA in place of the native CAT 3"-untranslated region (UTR) were transiently transfected into the lung adenocarcinoma cell line NCI-H441.	Dexamethasone	77-90	surfactant protein A1	Homo sapiens	105-109
10362715-4	1999	Moreover, the inhibitory response seen with dexamethasone was greater for the 3"-UTR derived from the SP-A1 allele 6A3 than with the 3"-UTR derived from either the SP-A1 allele 6A2 or SP-A2 allele 1A0, indicating differential regulation between SP-A genes and/or alleles.	Dexamethasone	44-57	surfactant protein A1	Homo sapiens	102-107
10362715-4	1999	Moreover, the inhibitory response seen with dexamethasone was greater for the 3"-UTR derived from the SP-A1 allele 6A3 than with the 3"-UTR derived from either the SP-A1 allele 6A2 or SP-A2 allele 1A0, indicating differential regulation between SP-A genes and/or alleles.	Dexamethasone	44-57	surfactant protein A1	Homo sapiens	164-169
10362715-4	1999	Moreover, the inhibitory response seen with dexamethasone was greater for the 3"-UTR derived from the SP-A1 allele 6A3 than with the 3"-UTR derived from either the SP-A1 allele 6A2 or SP-A2 allele 1A0, indicating differential regulation between SP-A genes and/or alleles.	Dexamethasone	44-57	surfactant protein A1	Homo sapiens	102-106
10229660-3	1999	In this study, a deletional analysis of the SP-A1 promoter was performed in order to identify cis-acting elements that mediate dexamethasone responsiveness in NCI-H441 cells.	Dexamethasone	127-140	surfactant protein A1	Homo sapiens	44-49
10353843-0	1999	Introduction of mannose binding protein-type phosphatidylinositol recognition into pulmonary surfactant protein A.	Mannose	16-23	surfactant protein A1	Homo sapiens	83-113
10353843-0	1999	Introduction of mannose binding protein-type phosphatidylinositol recognition into pulmonary surfactant protein A.	Phosphatidylinositols	45-65	surfactant protein A1	Homo sapiens	83-113
10353843-3	1999	SP-A binds to dipalmitoyl phosphatidylcholine (DPPC) and galactosylceramide (GalCer) and MBP-A binds to phosphatidylinositol (PI).	1,2-Dipalmitoylphosphatidylcholine	14-45	surfactant protein A1	Homo sapiens	0-4
10353843-3	1999	SP-A binds to dipalmitoyl phosphatidylcholine (DPPC) and galactosylceramide (GalCer) and MBP-A binds to phosphatidylinositol (PI).	1,2-Dipalmitoylphosphatidylcholine	47-51	surfactant protein A1	Homo sapiens	0-4
10353843-3	1999	SP-A binds to dipalmitoyl phosphatidylcholine (DPPC) and galactosylceramide (GalCer) and MBP-A binds to phosphatidylinositol (PI).	Galactosylceramides	57-75	surfactant protein A1	Homo sapiens	0-4
10353843-3	1999	SP-A binds to dipalmitoyl phosphatidylcholine (DPPC) and galactosylceramide (GalCer) and MBP-A binds to phosphatidylinositol (PI).	Galactosylceramides	77-83	surfactant protein A1	Homo sapiens	0-4
10353843-8	1999	The synthetic peptide GTPVNYTNWYRG completely blocked the binding of mAbs to human SP-A.	gtpvnytnwyrg	22-34	surfactant protein A1	Homo sapiens	83-87
10229660-4	1999	The region -32/+63 relative to the start of SP-A1 transcription mediated both basal promoter activity and dexamethasone repression of transcription.	Dexamethasone	106-119	surfactant protein A1	Homo sapiens	44-49
10101009-5	1999	We have shown that soluble gp-340 binds SP-A in a calcium-dependent manner independent of the lectin activity of SP-A.	Calcium	50-57	surfactant protein A1	Homo sapiens	40-44
9843927-11	1998	The uptake of [35S]SP-A was blocked at 4 degrees C and was promoted by addition of unlabeled SP-A at 37 degrees C. These findings support a pathway of extracellular routing of SP-A prior to its accumulation in LBs in cultured type II cells.	Sulfur-35	15-18	surfactant protein A1	Homo sapiens	93-97
9813267-3	1998	Functional mapping of SP-A using directed mutagenesis has identified domains which interact with surfactant phospholipids, alveolar type II cells and microbes.	Phospholipids	108-121	surfactant protein A1	Homo sapiens	22-26
9843839-2	1998	Human SP-A was nitrated by incubation with tetranitromethane at pH 8.0 or synthetic peroxynitrite (ONOO-) at pH 7.4, which resulted in significant nitration of tyrosines in its carbohydrate recognition domain [0.63 +/- 0.001 (SE) and 1.25 +/- 0.02 mol nitrotyrosine/mol monomeric SP-A, respectively; n = 3 samples].	Tetranitromethane	43-60	surfactant protein A1	Homo sapiens	6-10
9843839-2	1998	Human SP-A was nitrated by incubation with tetranitromethane at pH 8.0 or synthetic peroxynitrite (ONOO-) at pH 7.4, which resulted in significant nitration of tyrosines in its carbohydrate recognition domain [0.63 +/- 0.001 (SE) and 1.25 +/- 0.02 mol nitrotyrosine/mol monomeric SP-A, respectively; n = 3 samples].	Peroxynitrous Acid	84-97	surfactant protein A1	Homo sapiens	6-10
9843839-2	1998	Human SP-A was nitrated by incubation with tetranitromethane at pH 8.0 or synthetic peroxynitrite (ONOO-) at pH 7.4, which resulted in significant nitration of tyrosines in its carbohydrate recognition domain [0.63 +/- 0.001 (SE) and 1.25 +/- 0.02 mol nitrotyrosine/mol monomeric SP-A, respectively; n = 3 samples].	oxido nitrite	99-104	surfactant protein A1	Homo sapiens	6-10
9843839-2	1998	Human SP-A was nitrated by incubation with tetranitromethane at pH 8.0 or synthetic peroxynitrite (ONOO-) at pH 7.4, which resulted in significant nitration of tyrosines in its carbohydrate recognition domain [0.63 +/- 0.001 (SE) and 1.25 +/- 0.02 mol nitrotyrosine/mol monomeric SP-A, respectively; n = 3 samples].	Tyrosine	160-169	surfactant protein A1	Homo sapiens	6-10
9843839-2	1998	Human SP-A was nitrated by incubation with tetranitromethane at pH 8.0 or synthetic peroxynitrite (ONOO-) at pH 7.4, which resulted in significant nitration of tyrosines in its carbohydrate recognition domain [0.63 +/- 0.001 (SE) and 1.25 +/- 0.02 mol nitrotyrosine/mol monomeric SP-A, respectively; n = 3 samples].	Tyrosine	160-169	surfactant protein A1	Homo sapiens	280-284
9843839-2	1998	Human SP-A was nitrated by incubation with tetranitromethane at pH 8.0 or synthetic peroxynitrite (ONOO-) at pH 7.4, which resulted in significant nitration of tyrosines in its carbohydrate recognition domain [0.63 +/- 0.001 (SE) and 1.25 +/- 0.02 mol nitrotyrosine/mol monomeric SP-A, respectively; n = 3 samples].	Carbohydrates	177-189	surfactant protein A1	Homo sapiens	6-10
9843839-2	1998	Human SP-A was nitrated by incubation with tetranitromethane at pH 8.0 or synthetic peroxynitrite (ONOO-) at pH 7.4, which resulted in significant nitration of tyrosines in its carbohydrate recognition domain [0.63 +/- 0.001 (SE) and 1.25 +/- 0.02 mol nitrotyrosine/mol monomeric SP-A, respectively; n = 3 samples].	3-nitrotyrosine	252-265	surfactant protein A1	Homo sapiens	6-10
9813383-5	1998	The concentrations of SP-A and SP-D in BAL fluids from patients with idiopathic pulmonary fibrosis (IPF) and interstitial pneumonia with collagen vascular diseases (IPCD) are rather lower than those in healthy controls and the SP-A/phospholipid ratio may be a useful marker of survival prediction.	Phospholipids	232-244	surfactant protein A1	Homo sapiens	22-26
9839935-5	1998	Both SP-A and SP-D are further purified by gel-filtration on Superose-6.	superose	61-69	surfactant protein A1	Homo sapiens	5-9
9724531-0	1998	Calcium-triggered selective intermembrane exchange of phospholipids by the lung surfactant protein SP-A.	Calcium	0-7	surfactant protein A1	Homo sapiens	99-103
9724531-0	1998	Calcium-triggered selective intermembrane exchange of phospholipids by the lung surfactant protein SP-A.	Phospholipids	54-67	surfactant protein A1	Homo sapiens	99-103
9724531-1	1998	It is shown that human lung surfactant protein (SP-A) mediates selective exchange of phospholipid probes with unlabeled phospholipid in excess vesicles in the presence of calcium and NaCl.	Phospholipids	85-97	surfactant protein A1	Homo sapiens	48-52
9724531-1	1998	It is shown that human lung surfactant protein (SP-A) mediates selective exchange of phospholipid probes with unlabeled phospholipid in excess vesicles in the presence of calcium and NaCl.	Phospholipids	120-132	surfactant protein A1	Homo sapiens	48-52
9724531-1	1998	It is shown that human lung surfactant protein (SP-A) mediates selective exchange of phospholipid probes with unlabeled phospholipid in excess vesicles in the presence of calcium and NaCl.	Calcium	171-178	surfactant protein A1	Homo sapiens	48-52
9724531-1	1998	It is shown that human lung surfactant protein (SP-A) mediates selective exchange of phospholipid probes with unlabeled phospholipid in excess vesicles in the presence of calcium and NaCl.	Sodium Chloride	183-187	surfactant protein A1	Homo sapiens	48-52
9724531-3	1998	Individual steps preceding the exchange are dissected by a combination of protocols, and the results are operationally interpreted in terms of a model where a calcium-dependent change in SP-A triggers aggregation of vesicles followed by probe exchange between the vesicles in contact through SP-A.	Calcium	159-166	surfactant protein A1	Homo sapiens	187-191
9724531-3	1998	Individual steps preceding the exchange are dissected by a combination of protocols, and the results are operationally interpreted in terms of a model where a calcium-dependent change in SP-A triggers aggregation of vesicles followed by probe exchange between the vesicles in contact through SP-A.	Calcium	159-166	surfactant protein A1	Homo sapiens	292-296
9724531-5	1998	The binding of SP-A to vesicles and the aggregation of vesicles are rapid, and the aggregation is rapidly reversed by EGTA; i.e., both the forward and reverse aggregation reactions are complete in about 1 min.	Egtazic Acid	118-122	surfactant protein A1	Homo sapiens	15-19
9724531-8	1998	SP-A binding to vesicles does not show an absolute specificity for the phospholipid structure, but the time course of the subsequent changes does.	Phospholipids	71-83	surfactant protein A1	Homo sapiens	0-4
9724531-9	1998	The results suggest that SP-A contacts between phospholipid interfaces could mediate the exchange of phospholipid species (trafficking and sorting) between lung surfactant pools in the hypophase and all accessible phospholipid interfaces of the alveolar space.	Phospholipids	47-59	surfactant protein A1	Homo sapiens	25-29
9724531-9	1998	The results suggest that SP-A contacts between phospholipid interfaces could mediate the exchange of phospholipid species (trafficking and sorting) between lung surfactant pools in the hypophase and all accessible phospholipid interfaces of the alveolar space.	Phospholipids	101-113	surfactant protein A1	Homo sapiens	25-29
9724531-9	1998	The results suggest that SP-A contacts between phospholipid interfaces could mediate the exchange of phospholipid species (trafficking and sorting) between lung surfactant pools in the hypophase and all accessible phospholipid interfaces of the alveolar space.	Phospholipids	101-113	surfactant protein A1	Homo sapiens	25-29
9758900-0	1998	Suppressive effects of SP-A on ionomycin-induced IL-8 production and release by eosinophils.	Ionomycin	31-40	surfactant protein A1	Homo sapiens	23-27
9700129-0	1998	Inhibitory effect of pulmonary surfactant proteins A and D on allergen-induced lymphocyte proliferation and histamine release in children with asthma.	Histamine	108-117	surfactant protein A1	Homo sapiens	31-58
9700129-3	1998	The results show that SP-A and SP-D were able to reduce the incorporation of [3H]thymidine into PBMC in a dose-dependent manner.	3h]thymidine	78-90	surfactant protein A1	Homo sapiens	22-26
9700129-3	1998	The results show that SP-A and SP-D were able to reduce the incorporation of [3H]thymidine into PBMC in a dose-dependent manner.	PBMC	96-100	surfactant protein A1	Homo sapiens	22-26
9700129-5	1998	This effect was abolished by the presence of 100 mM mannose (for SP-A) or maltose (for SP-D) in the culture medium, which suggested that the CRD regions of SP-A and SP-D may interact with the carbohydrate structures on the surface molecules of lymphocytes.	Mannose	52-59	surfactant protein A1	Homo sapiens	65-69
9700129-5	1998	This effect was abolished by the presence of 100 mM mannose (for SP-A) or maltose (for SP-D) in the culture medium, which suggested that the CRD regions of SP-A and SP-D may interact with the carbohydrate structures on the surface molecules of lymphocytes.	Mannose	52-59	surfactant protein A1	Homo sapiens	156-160
9700129-5	1998	This effect was abolished by the presence of 100 mM mannose (for SP-A) or maltose (for SP-D) in the culture medium, which suggested that the CRD regions of SP-A and SP-D may interact with the carbohydrate structures on the surface molecules of lymphocytes.	Maltose	74-81	surfactant protein A1	Homo sapiens	156-160
9700129-5	1998	This effect was abolished by the presence of 100 mM mannose (for SP-A) or maltose (for SP-D) in the culture medium, which suggested that the CRD regions of SP-A and SP-D may interact with the carbohydrate structures on the surface molecules of lymphocytes.	Carbohydrates	192-204	surfactant protein A1	Homo sapiens	65-69
9700129-5	1998	This effect was abolished by the presence of 100 mM mannose (for SP-A) or maltose (for SP-D) in the culture medium, which suggested that the CRD regions of SP-A and SP-D may interact with the carbohydrate structures on the surface molecules of lymphocytes.	Carbohydrates	192-204	surfactant protein A1	Homo sapiens	156-160
9700129-7	1998	SP-A and SP-D were also found to inhibit allergen-induced histamine release, in a dose-dependent manner, in the diluted whole blood of asthmatic children.	Histamine	58-67	surfactant protein A1	Homo sapiens	0-4
9700129-8	1998	We conclude that both SP-A and SP-D can inhibit histamine release in the early phase of allergen provocation and suppress lymphocyte proliferation in the late phase of bronchial inflammation, the two essential steps in the development of asthmatic symptoms.	Histamine	48-57	surfactant protein A1	Homo sapiens	22-26
9777404-8	1998	SP-A and SP-D stimulate chemotaxis of phagocytes and once bound to the phagocytes, the production of oxygen radicals can be induced.	Reactive Oxygen Species	101-116	surfactant protein A1	Homo sapiens	0-4
9777406-2	1998	Recognition of the pathogens is, in most cases, mediated by the Ca+2-dependent binding of the C-type lectin domains of SP-A, or SP-D, to carbohydrate structures on the surface of the microorganisms.	Carbohydrates	137-149	surfactant protein A1	Homo sapiens	119-123
9671381-0	1998	Nitric oxide decreases surfactant protein A gene expression in H441 cells.	Nitric Oxide	0-12	surfactant protein A1	Homo sapiens	23-43
9688933-5	1998	A2R inhibited cell association of 125I-SP-A to type II cells plated on Transwell membranes as well as those plated on plastic dishes and also inhibited the SP-A-stimulated incorporation of phosphatidylcholine liposomes into type II cells.	Phosphatidylcholines	189-208	surfactant protein A1	Homo sapiens	156-160
9688933-9	1998	Under nonreducing conditions, the mass of the SP-A and A2R binding protein was approximately 210 kDa, indicating that the SP-A receptor is composed of disulfide-linked subunits.	Disulfides	151-160	surfactant protein A1	Homo sapiens	46-50
9688933-9	1998	Under nonreducing conditions, the mass of the SP-A and A2R binding protein was approximately 210 kDa, indicating that the SP-A receptor is composed of disulfide-linked subunits.	Disulfides	151-160	surfactant protein A1	Homo sapiens	122-126
9671381-1	1998	OBJECTIVE: To study the effects of nitric oxide (NO) on surfactant protein A (SP-A) gene expression.	Nitric Oxide	35-47	surfactant protein A1	Homo sapiens	56-76
9671381-1	1998	OBJECTIVE: To study the effects of nitric oxide (NO) on surfactant protein A (SP-A) gene expression.	Nitric Oxide	35-47	surfactant protein A1	Homo sapiens	78-82
9486201-5	1998	Dexamethasone inhibited all of the SP-A1 and SP-A2 mRNA transcripts to the same extent, by approximately 70%, whereas insulin inhibited all SP-A mRNA transcripts by approximately 60%.	Dexamethasone	0-13	surfactant protein A1	Homo sapiens	35-39
9605120-3	1998	For example, SpA reacts with the Fabs of most human Igs using heavy chains from the VH3 gene family (VH3+).	FAB protocol	33-37	surfactant protein A1	Homo sapiens	13-16
9612289-5	1998	Studying in greater detail the interaction of SP-A with VLDLs, we found that the binding is time and concentration dependent; is inhibited by unlabeled lipoproteins, phospholipids, and antibodies to SP-A; is increased by Ca2+; and is unaffected by methyl alpha-D-mannopyranoside.	Phospholipids	166-179	surfactant protein A1	Homo sapiens	46-50
9612289-5	1998	Studying in greater detail the interaction of SP-A with VLDLs, we found that the binding is time and concentration dependent; is inhibited by unlabeled lipoproteins, phospholipids, and antibodies to SP-A; is increased by Ca2+; and is unaffected by methyl alpha-D-mannopyranoside.	alpha-D-Mannose	255-278	surfactant protein A1	Homo sapiens	46-50
9575872-6	1998	Tyrphostin AG-1478 also decreased SP-A content and SP-A mRNA levels in cultured fetal lung explants.	Tyrphostins	0-10	surfactant protein A1	Homo sapiens	34-38
9575872-9	1998	Furthermore, exposure to genistein also decreases SP-A expression and blocks the effects of EGF in human fetal lung tissue without inhibiting EGF-receptor tyrosine phosphorylation.	Genistein	25-34	surfactant protein A1	Homo sapiens	50-54
9575874-2	1998	We characterized the effects of cortisol and all trans-retinoic acid (RA) on SP-A and SP-B gene expression in H441 cells, a human pulmonary adenocarcinoma cell line.	Hydrocortisone	32-40	surfactant protein A1	Homo sapiens	77-81
9575874-2	1998	We characterized the effects of cortisol and all trans-retinoic acid (RA) on SP-A and SP-B gene expression in H441 cells, a human pulmonary adenocarcinoma cell line.	Tretinoin	49-68	surfactant protein A1	Homo sapiens	77-81
9575874-2	1998	We characterized the effects of cortisol and all trans-retinoic acid (RA) on SP-A and SP-B gene expression in H441 cells, a human pulmonary adenocarcinoma cell line.	Tretinoin	70-72	surfactant protein A1	Homo sapiens	77-81
9606179-2	1998	In vivo, SP-A probably binds to a wide range of inhaled materials via the interaction of surface carbohydrates with the lectin domains of SP-A and mediates their interaction with cells as part of a natural defense system.	Carbohydrates	97-110	surfactant protein A1	Homo sapiens	9-13
9606179-5	1998	Sucrose density gradient centrifugation was employed to determine molecular weights of SP-A oligomers.	Sucrose	0-7	surfactant protein A1	Homo sapiens	87-91
9606179-8	1998	This is true for both the water- and lipid-soluble fractions of SP-A.	Water	26-31	surfactant protein A1	Homo sapiens	64-68
9490653-3	1998	SP-A belongs to the family of collagenous C-type lectins along with mannose binding protein (MBP) and SP-D, both of which have also been mapped to the long arm of chromosome 10.	Mannose	68-75	surfactant protein A1	Homo sapiens	0-4
9530169-2	1998	Incubation of tissues in 70% O2 resulted in a 133% increase in SP-A mRNA transcription rate compared with control tissues.	Oxygen	29-31	surfactant protein A1	Homo sapiens	63-67
9530169-3	1998	The SP-A mRNA half-life was increased by 54% in lung tissues cultured in 70% O2 vs. control tissues.	Oxygen	77-79	surfactant protein A1	Homo sapiens	4-8
9530169-4	1998	Western blot analysis indicated a threefold increase in SP-A in the 70% O2 condition, demonstrating that O2 regulation of SP-A mRNA levels results in corresponding changes in SP-A levels.	Oxygen	72-74	surfactant protein A1	Homo sapiens	56-60
9530169-4	1998	Western blot analysis indicated a threefold increase in SP-A in the 70% O2 condition, demonstrating that O2 regulation of SP-A mRNA levels results in corresponding changes in SP-A levels.	Oxygen	72-74	surfactant protein A1	Homo sapiens	122-126
9530169-4	1998	Western blot analysis indicated a threefold increase in SP-A in the 70% O2 condition, demonstrating that O2 regulation of SP-A mRNA levels results in corresponding changes in SP-A levels.	Oxygen	72-74	surfactant protein A1	Homo sapiens	122-126
9530169-4	1998	Western blot analysis indicated a threefold increase in SP-A in the 70% O2 condition, demonstrating that O2 regulation of SP-A mRNA levels results in corresponding changes in SP-A levels.	Oxygen	105-107	surfactant protein A1	Homo sapiens	56-60
9530169-4	1998	Western blot analysis indicated a threefold increase in SP-A in the 70% O2 condition, demonstrating that O2 regulation of SP-A mRNA levels results in corresponding changes in SP-A levels.	Oxygen	105-107	surfactant protein A1	Homo sapiens	122-126
9530169-4	1998	Western blot analysis indicated a threefold increase in SP-A in the 70% O2 condition, demonstrating that O2 regulation of SP-A mRNA levels results in corresponding changes in SP-A levels.	Oxygen	105-107	surfactant protein A1	Homo sapiens	122-126
9530169-6	1998	Transcripts of both the SP-A1 and SP-A2 genes were increased approximately 100% in tissues maintained in 70% O2 compared with control tissues.	Oxygen	109-111	surfactant protein A1	Homo sapiens	24-29
9530169-7	1998	These data demonstrate that O2 regulates human SP-A mRNA levels by both transcriptional and posttranscriptional mechanisms.	Oxygen	28-30	surfactant protein A1	Homo sapiens	47-51
9476887-7	1998	Although AP lavage generally contained more non-thiol-dependent SP-A aggregates and low Mr isoforms, the two-dimensional immunochemical staining patterns varied between patients and right and left lung.	Sulfhydryl Compounds	48-53	surfactant protein A1	Homo sapiens	64-68
9689918-6	1998	(d) SP-A1 alleles are inhibited to a greater degree by dexamethasone than SP-A2 alleles.	Dexamethasone	55-68	surfactant protein A1	Homo sapiens	4-9
9689918-7	1998	The relative effect of cAMP and IFN gamma on SP-A1 and SP-A2 mRNA varied widely among explants.	Cyclic AMP	23-27	surfactant protein A1	Homo sapiens	45-50
9488702-2	1998	In previous studies, tandem mutagenesis of Glu195 and Arg197 of surfactant protein A (SP-A) has implicated both residues as critical participants in the interaction of the molecule with alveolar type II cells and phospholipids.	Phospholipids	213-226	surfactant protein A1	Homo sapiens	64-84
9488702-2	1998	In previous studies, tandem mutagenesis of Glu195 and Arg197 of surfactant protein A (SP-A) has implicated both residues as critical participants in the interaction of the molecule with alveolar type II cells and phospholipids.	Phospholipids	213-226	surfactant protein A1	Homo sapiens	86-90
9548588-0	1998	Interaction of pulmonary surfactant protein A with dipalmitoylphosphatidylcholine and cholesterol at the air/water interface.	1,2-Dipalmitoylphosphatidylcholine	51-81	surfactant protein A1	Homo sapiens	15-45
9548588-0	1998	Interaction of pulmonary surfactant protein A with dipalmitoylphosphatidylcholine and cholesterol at the air/water interface.	Cholesterol	86-97	surfactant protein A1	Homo sapiens	15-45
9548588-0	1998	Interaction of pulmonary surfactant protein A with dipalmitoylphosphatidylcholine and cholesterol at the air/water interface.	Water	109-114	surfactant protein A1	Homo sapiens	15-45
9548588-1	1998	Interaction of pulmonary surfactant protein A (SP-A) with pure and binary mixed dipalmitoylphosphatidylcholine (DPPC) and cholesterol (3.5 wt%) at the air/saline, 1.5 mM CaCl2 interface was investigated using a rhomboid surface balance at 37 degrees C. Surface tension-area isotherms were measured to access the surface active properties of the monolayers.	1,2-Dipalmitoylphosphatidylcholine	80-110	surfactant protein A1	Homo sapiens	47-51
9548588-1	1998	Interaction of pulmonary surfactant protein A (SP-A) with pure and binary mixed dipalmitoylphosphatidylcholine (DPPC) and cholesterol (3.5 wt%) at the air/saline, 1.5 mM CaCl2 interface was investigated using a rhomboid surface balance at 37 degrees C. Surface tension-area isotherms were measured to access the surface active properties of the monolayers.	1,2-Dipalmitoylphosphatidylcholine	112-116	surfactant protein A1	Homo sapiens	47-51
9548588-1	1998	Interaction of pulmonary surfactant protein A (SP-A) with pure and binary mixed dipalmitoylphosphatidylcholine (DPPC) and cholesterol (3.5 wt%) at the air/saline, 1.5 mM CaCl2 interface was investigated using a rhomboid surface balance at 37 degrees C. Surface tension-area isotherms were measured to access the surface active properties of the monolayers.	Cholesterol	122-133	surfactant protein A1	Homo sapiens	15-45
9548588-1	1998	Interaction of pulmonary surfactant protein A (SP-A) with pure and binary mixed dipalmitoylphosphatidylcholine (DPPC) and cholesterol (3.5 wt%) at the air/saline, 1.5 mM CaCl2 interface was investigated using a rhomboid surface balance at 37 degrees C. Surface tension-area isotherms were measured to access the surface active properties of the monolayers.	Cholesterol	122-133	surfactant protein A1	Homo sapiens	47-51
9548588-3	1998	The results showed that SP-A can interact with the polar head groups of DPPC monolayers and aggregate DPPC molecules.	1,2-Dipalmitoylphosphatidylcholine	72-76	surfactant protein A1	Homo sapiens	24-28
9548588-3	1998	The results showed that SP-A can interact with the polar head groups of DPPC monolayers and aggregate DPPC molecules.	1,2-Dipalmitoylphosphatidylcholine	102-106	surfactant protein A1	Homo sapiens	24-28
9548588-4	1998	SP-A decreased the surface area reduction required for DPPC monolayers to achieve near zero surface tension from 30 to 25% of the area at equilibrium.	1,2-Dipalmitoylphosphatidylcholine	55-59	surfactant protein A1	Homo sapiens	0-4
9548588-5	1998	SP-A also reduced the collapse surface tension of pure cholesterol from 27 to 23 mN/m.	Cholesterol	55-66	surfactant protein A1	Homo sapiens	0-4
9548588-8	1998	Although SP-A could not promote the squeeze-out of cholesterol from homogeneous mixed monolayers, it facilitated that of cholesterol domains especially when SP-A had first interacted with DPPC.	Cholesterol	121-132	surfactant protein A1	Homo sapiens	9-13
9548588-8	1998	Although SP-A could not promote the squeeze-out of cholesterol from homogeneous mixed monolayers, it facilitated that of cholesterol domains especially when SP-A had first interacted with DPPC.	1,2-Dipalmitoylphosphatidylcholine	188-192	surfactant protein A1	Homo sapiens	9-13
9548588-9	1998	These results indicate that pulmonary surfactant protein A facilitates the squeeze-out of cholesterol domains from mixed monolayers by condensing DPPC and limiting lateral interactions of DPPC with cholesterol domains.	Cholesterol	90-101	surfactant protein A1	Homo sapiens	28-58
9548588-9	1998	These results indicate that pulmonary surfactant protein A facilitates the squeeze-out of cholesterol domains from mixed monolayers by condensing DPPC and limiting lateral interactions of DPPC with cholesterol domains.	1,2-Dipalmitoylphosphatidylcholine	146-150	surfactant protein A1	Homo sapiens	28-58
9548588-9	1998	These results indicate that pulmonary surfactant protein A facilitates the squeeze-out of cholesterol domains from mixed monolayers by condensing DPPC and limiting lateral interactions of DPPC with cholesterol domains.	1,2-Dipalmitoylphosphatidylcholine	188-192	surfactant protein A1	Homo sapiens	28-58
9548588-9	1998	These results indicate that pulmonary surfactant protein A facilitates the squeeze-out of cholesterol domains from mixed monolayers by condensing DPPC and limiting lateral interactions of DPPC with cholesterol domains.	Cholesterol	198-209	surfactant protein A1	Homo sapiens	28-58
9486201-0	1998	Differential regulation of SP-A1 and SP-A2 genes by cAMP, glucocorticoids, and insulin.	Cyclic AMP	52-56	surfactant protein A1	Homo sapiens	27-32
9486201-5	1998	Dexamethasone inhibited all of the SP-A1 and SP-A2 mRNA transcripts to the same extent, by approximately 70%, whereas insulin inhibited all SP-A mRNA transcripts by approximately 60%.	Dexamethasone	0-13	surfactant protein A1	Homo sapiens	35-40
9486201-6	1998	The ratio of SP-A1 to SP-A2 mRNA in dexamethasone- or insulin-treated explants was the same as the ratio observed in controls.	Dexamethasone	36-49	surfactant protein A1	Homo sapiens	13-18
9486201-9	1998	Dexamethasone inhibited SP-A1 mRNA levels in the cell line by 60%, whereas SP-A2 mRNA levels were not significantly affected.	Dexamethasone	0-13	surfactant protein A1	Homo sapiens	24-29
9486215-2	1998	The proinflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) and the phorbol ester 12-O-tetradecanoyl phorbol-13-acetate (TPA) inhibit expression of surfactant-associated proteins A and B (SP-A and SP-B), both important for normal surfactant function.	Phorbol Esters	77-90	surfactant protein A1	Homo sapiens	197-201
9486215-2	1998	The proinflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) and the phorbol ester 12-O-tetradecanoyl phorbol-13-acetate (TPA) inhibit expression of surfactant-associated proteins A and B (SP-A and SP-B), both important for normal surfactant function.	Tetradecanoylphorbol Acetate	91-128	surfactant protein A1	Homo sapiens	197-201
9486215-2	1998	The proinflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) and the phorbol ester 12-O-tetradecanoyl phorbol-13-acetate (TPA) inhibit expression of surfactant-associated proteins A and B (SP-A and SP-B), both important for normal surfactant function.	Tetradecanoylphorbol Acetate	130-133	surfactant protein A1	Homo sapiens	197-201
9617742-5	1998	SP-A values correlated significantly with CC10 and phospholipid values in BAL fluids.	Phospholipids	51-63	surfactant protein A1	Homo sapiens	0-4
9448836-4	1998	The fucosyltransferase catalyses the transfer of [3H]fucose, from GDP-[3H]fucose, onto the sugar chains of a glycoprotein acceptor noncovalently bound to a scintillant-impregnated microsphere (SPA bead).	[3h]fucose	49-59	surfactant protein A1	Homo sapiens	193-196
9448836-4	1998	The fucosyltransferase catalyses the transfer of [3H]fucose, from GDP-[3H]fucose, onto the sugar chains of a glycoprotein acceptor noncovalently bound to a scintillant-impregnated microsphere (SPA bead).	gdp-[3h]fucose	66-80	surfactant protein A1	Homo sapiens	193-196
9448836-4	1998	The fucosyltransferase catalyses the transfer of [3H]fucose, from GDP-[3H]fucose, onto the sugar chains of a glycoprotein acceptor noncovalently bound to a scintillant-impregnated microsphere (SPA bead).	Sugars	91-96	surfactant protein A1	Homo sapiens	193-196
9640079-2	1997	Aspirin therapy will reduce platelet activation both by its negative effect on platelet aggregation (SPA) and by inhibition of granule release which liberates such mediators as platelet factor 4 (PF4) and plasminogen activator inhibitor 1 (PAI-1).	Aspirin	0-7	surfactant protein A1	Homo sapiens	101-104
9389540-2	1997	Surfactant protein-A (SP-A) gene transcription in human fetal lung in culture is stimulated by glucocorticoids and cAMP; cAMP also enhances the rate of type II cell differentiation.	Cyclic AMP	115-119	surfactant protein A1	Homo sapiens	0-20
9389540-2	1997	Surfactant protein-A (SP-A) gene transcription in human fetal lung in culture is stimulated by glucocorticoids and cAMP; cAMP also enhances the rate of type II cell differentiation.	Cyclic AMP	115-119	surfactant protein A1	Homo sapiens	22-26
9409554-8	1997	The expression of mRNAs encoding SP-A, SP-B, and SP-C were regulated in the cultured cells by glucocorticoids and cyclic AMP in a manner similar to that observed in fetal lung tissue in organ culture.	Cyclic AMP	114-124	surfactant protein A1	Homo sapiens	33-37
9640079-12	1997	Aspirin did not satisfactorily reduce the level of PF4, although it strongly inhibited SPA.	Aspirin	0-7	surfactant protein A1	Homo sapiens	87-90
9294011-0	1997	Transcriptional regulation of surfactant proteins SP-A and SP-B by phorbol ester.	Phorbol Esters	67-80	surfactant protein A1	Homo sapiens	50-54
9367408-3	1997	Purified SP-A and SP-D, isolated from human bronchoalveolar lavage fluid, bound to the 3wcf allergens and purified allergens, gp55 and gp45, in a carbohydrate-specific and calcium-dependent manner.	Carbohydrates	146-158	surfactant protein A1	Homo sapiens	9-13
9367408-3	1997	Purified SP-A and SP-D, isolated from human bronchoalveolar lavage fluid, bound to the 3wcf allergens and purified allergens, gp55 and gp45, in a carbohydrate-specific and calcium-dependent manner.	Calcium	172-179	surfactant protein A1	Homo sapiens	9-13
9367408-4	1997	Both SP-A and SP-D did not bind to deglycosylated allergens, suggesting that the ability of SP-A and SP-D to bind certain allergens is mediated through their carbohydrate recognition domains, interacting with the carbohydrate residues on the allergen.	Carbohydrates	158-170	surfactant protein A1	Homo sapiens	92-96
9367408-4	1997	Both SP-A and SP-D did not bind to deglycosylated allergens, suggesting that the ability of SP-A and SP-D to bind certain allergens is mediated through their carbohydrate recognition domains, interacting with the carbohydrate residues on the allergen.	Carbohydrates	213-225	surfactant protein A1	Homo sapiens	5-9
9367408-4	1997	Both SP-A and SP-D did not bind to deglycosylated allergens, suggesting that the ability of SP-A and SP-D to bind certain allergens is mediated through their carbohydrate recognition domains, interacting with the carbohydrate residues on the allergen.	Carbohydrates	213-225	surfactant protein A1	Homo sapiens	92-96
9367408-6	1997	The view that SP-A and SP-D play a protective role against airborne allergens is further supported by the demonstration of their ability to inhibit A. fumigatus allergen-induced histamine release from allergic patients" basophils.	Histamine	178-187	surfactant protein A1	Homo sapiens	14-18
9357859-4	1997	Incubation of cells with NH4Cl reduced the degradation of SP-A to a similar extent (to 33% of control values) in resting and primed tissue macrophages.	Ammonium Chloride	25-30	surfactant protein A1	Homo sapiens	58-62
9294011-1	1997	Phorbol esters such as 12-O-tetradecanoylphorbol-13-acetate (TPA) activate protein kinase C and have been previously shown to down-regulate surfactant proteins SP-A and SP-B in H441 adenocarcinoma cells.	Phorbol Esters	0-14	surfactant protein A1	Homo sapiens	160-164
9294011-1	1997	Phorbol esters such as 12-O-tetradecanoylphorbol-13-acetate (TPA) activate protein kinase C and have been previously shown to down-regulate surfactant proteins SP-A and SP-B in H441 adenocarcinoma cells.	Tetradecanoylphorbol Acetate	23-59	surfactant protein A1	Homo sapiens	160-164
9294011-1	1997	Phorbol esters such as 12-O-tetradecanoylphorbol-13-acetate (TPA) activate protein kinase C and have been previously shown to down-regulate surfactant proteins SP-A and SP-B in H441 adenocarcinoma cells.	Tetradecanoylphorbol Acetate	61-64	surfactant protein A1	Homo sapiens	160-164
9294011-3	1997	In H441 cells, TPA (10 nM) treatment for 24 h decreased SP-A mRNA content to approximately 5% of control cells, with half-maximal effect at approximately 0.5 nM, and reduced SP-A gene transcription rate to 28% of control after 8 h exposure.	Tetradecanoylphorbol Acetate	15-18	surfactant protein A1	Homo sapiens	56-60
9294011-3	1997	In H441 cells, TPA (10 nM) treatment for 24 h decreased SP-A mRNA content to approximately 5% of control cells, with half-maximal effect at approximately 0.5 nM, and reduced SP-A gene transcription rate to 28% of control after 8 h exposure.	Tetradecanoylphorbol Acetate	15-18	surfactant protein A1	Homo sapiens	174-178
9294011-5	1997	In cultured human fetal lung explants, TPA decreased SP-A and SP-B protein and mRNA in a time- and dose-dependent fashion, with half-maximal effect on mRNAs at approximately 3 nM and approximately 50% inhibition after 24 h of exposure, and similarly reduced SP-A and SP-B gene transcription (approximately 55% of control at 8-24 h).	Tetradecanoylphorbol Acetate	39-42	surfactant protein A1	Homo sapiens	53-57
9294011-5	1997	In cultured human fetal lung explants, TPA decreased SP-A and SP-B protein and mRNA in a time- and dose-dependent fashion, with half-maximal effect on mRNAs at approximately 3 nM and approximately 50% inhibition after 24 h of exposure, and similarly reduced SP-A and SP-B gene transcription (approximately 55% of control at 8-24 h).	Tetradecanoylphorbol Acetate	39-42	surfactant protein A1	Homo sapiens	258-262
9294011-6	1997	We conclude that TPA acts primarily at the level of gene transcription to down-regulate both SP-A and SP-B in H441 and fetal lung cells, and we speculate that inflammatory and other agents that act through PKC may modulate expression of the surfactant proteins and alter surfactant function in vivo.	Tetradecanoylphorbol Acetate	17-20	surfactant protein A1	Homo sapiens	93-97
9188699-9	1997	Sequencing of both native rat SP-A and human SP-A also revealed isoforms with disulfide-forming NH2-terminal extensions.	Disulfides	78-87	surfactant protein A1	Homo sapiens	45-49
10072808-4	1997	RESULTS: In 19 VSD patients with CPB, SatPC/TPL was significantly decreased from 48% to 34% (t = 2.737, P &lt; 0.05), SatPC/TP decreased from 64 to 33 mg/g (t = 3.011, P &lt; 0.01), and SP-A from 23 to 11mg/g (t = 2.987, P &lt; 0.01).	cpb	33-36	surfactant protein A1	Homo sapiens	186-190
10072808-4	1997	RESULTS: In 19 VSD patients with CPB, SatPC/TPL was significantly decreased from 48% to 34% (t = 2.737, P &lt; 0.05), SatPC/TP decreased from 64 to 33 mg/g (t = 3.011, P &lt; 0.01), and SP-A from 23 to 11mg/g (t = 2.987, P &lt; 0.01).	satpc	38-43	surfactant protein A1	Homo sapiens	186-190
9176265-4	1997	125I-labeled SP-A bound BCG in a Ca(2+)-, carbohydrate-, and dose-dependent manner.	Carbohydrates	42-54	surfactant protein A1	Homo sapiens	13-17
9227523-2	1997	Surfactant-associated protein A (SP-A) from various sources (human alveolar proteinosis, rat and recombinant rat) was found to upregulate nitric oxide production by alveolar macrophages in a concentration- and time-dependent manner, whereas type II cells were unresponsive to SP-A.	Nitric Oxide	138-150	surfactant protein A1	Homo sapiens	0-31
9227523-2	1997	Surfactant-associated protein A (SP-A) from various sources (human alveolar proteinosis, rat and recombinant rat) was found to upregulate nitric oxide production by alveolar macrophages in a concentration- and time-dependent manner, whereas type II cells were unresponsive to SP-A.	Nitric Oxide	138-150	surfactant protein A1	Homo sapiens	33-37
9032407-7	1997	The rendered SpA binding of the Fc variant Fc(3(1)), is concluded to result from the introduced dipeptide substitution (R435H, F436Y).	Dipeptides	96-105	surfactant protein A1	Homo sapiens	13-16
9130640-3	1997	In the present study, we investigated the opsonic activities of SP-A and SP-D for phagocytosis of fluorescein isothiocyanate (FITC)-labeled influenza A (H3N2) virus by rat alveolar macrophages using flow cytometry.	Fluorescein-5-isothiocyanate	126-130	surfactant protein A1	Homo sapiens	64-68
9130640-7	1997	These results indicate that SP-A mediates internalization of FITC-labeled influenza A (H3N2) virus by alveolar macrophages.	Fluorescein-5-isothiocyanate	61-65	surfactant protein A1	Homo sapiens	28-32
9130640-8	1997	Removal of the carbohydrate moiety of SP-A by N-glycosidase F treatment or cleavage of its sialic acid residues by neuraminidase abolished the enhancement of the phagocytosis of FITC-labeled influenza A virus by alveolar macrophages.	Carbohydrates	15-27	surfactant protein A1	Homo sapiens	38-42
9130640-8	1997	Removal of the carbohydrate moiety of SP-A by N-glycosidase F treatment or cleavage of its sialic acid residues by neuraminidase abolished the enhancement of the phagocytosis of FITC-labeled influenza A virus by alveolar macrophages.	N-Acetylneuraminic Acid	91-102	surfactant protein A1	Homo sapiens	38-42
9130640-8	1997	Removal of the carbohydrate moiety of SP-A by N-glycosidase F treatment or cleavage of its sialic acid residues by neuraminidase abolished the enhancement of the phagocytosis of FITC-labeled influenza A virus by alveolar macrophages.	Fluorescein-5-isothiocyanate	178-182	surfactant protein A1	Homo sapiens	38-42
9130640-10	1997	In contrast, SP-D neither enhanced the association of FITC-labeled influenza A virus with alveolar macrophages nor affected the opsonic activity of SP-A for FITC-labeled influenza A (H3N2) virus at the SP-D concentrations tested.	Fluorescein-5-isothiocyanate	157-161	surfactant protein A1	Homo sapiens	148-152
9130640-11	1997	It is concluded that SP-A acts via its sialic acid residues as an opsonin in the phagocytosis of influenza A virus by alveolar macrophages.	N-Acetylneuraminic Acid	39-50	surfactant protein A1	Homo sapiens	21-25
9108235-5	1997	SP-A and SP-D also bind lipids and SP-A is involved in organization of alveolar surfactant phospholipids.	Phospholipids	91-104	surfactant protein A1	Homo sapiens	0-4
9108235-5	1997	SP-A and SP-D also bind lipids and SP-A is involved in organization of alveolar surfactant phospholipids.	Phospholipids	91-104	surfactant protein A1	Homo sapiens	35-39
9128293-2	1997	We have previously shown that SP-B mRNA is increased whereas SP-A and SP-C mRNA are decreased by all-trans-retinoic acid (RA) in a dose-dependent manner in human fetal lung explants.	Tretinoin	97-120	surfactant protein A1	Homo sapiens	61-65
9128293-2	1997	We have previously shown that SP-B mRNA is increased whereas SP-A and SP-C mRNA are decreased by all-trans-retinoic acid (RA) in a dose-dependent manner in human fetal lung explants.	Tretinoin	122-124	surfactant protein A1	Homo sapiens	61-65
9128293-7	1997	Human fetal lung explants were treated with 9-cis-RA for 6 d. 9-cis-RA did not significantly increase SP-B mRNA levels, significantly inhibited SP-A mRNA levels at all concentrations tested, and significantly inhibited SP-C mRNA levels at 10(-6) M in the human fetal lung explants.	Tretinoin	62-70	surfactant protein A1	Homo sapiens	144-148
9130640-3	1997	In the present study, we investigated the opsonic activities of SP-A and SP-D for phagocytosis of fluorescein isothiocyanate (FITC)-labeled influenza A (H3N2) virus by rat alveolar macrophages using flow cytometry.	Fluorescein-5-isothiocyanate	98-124	surfactant protein A1	Homo sapiens	64-68
9045627-0	1997	Molecular cloning, mapping to human chromosome 1 q21-q23, and cell binding characteristics of Spalpha, a new member of the scavenger receptor cysteine-rich (SRCR) family of proteins.	Cysteine	142-150	surfactant protein A1	Homo sapiens	94-101
9045627-3	1997	Spalpha has the same domain organization as the extracellular region of CD5 and CD6 and is composed of three SRCR (scavenger receptor cysteine rich) domains.	Cysteine	134-142	surfactant protein A1	Homo sapiens	0-7
9060993-6	1997	The inhibitory effect of genistein on SP-A content was reversible.	Genistein	25-34	surfactant protein A1	Homo sapiens	38-42
9124386-0	1997	SP-A enhances phagocytosis of Klebsiella by interaction with capsular polysaccharides and alveolar macrophages.	Polysaccharides	70-85	surfactant protein A1	Homo sapiens	0-4
9124386-4	1997	Furthermore, binding of capsular polysaccharide of K21a to immobilized SP-A was inhibited by mannan but not by lipopolysaccharide and K2 capsular polysaccharide.	Polysaccharides	33-47	surfactant protein A1	Homo sapiens	71-75
9124386-4	1997	Furthermore, binding of capsular polysaccharide of K21a to immobilized SP-A was inhibited by mannan but not by lipopolysaccharide and K2 capsular polysaccharide.	Mannans	93-99	surfactant protein A1	Homo sapiens	71-75
9124386-7	1997	The enhanced binding of K21a by macrophages pretreated with SP-A was inhibited by mannan, suggesting that binding is mediated by the mannose receptor on macrophages.	Mannans	82-88	surfactant protein A1	Homo sapiens	60-64
9124386-8	1997	We conclude that SP-A increases phagocytosis of the Klebsiella by two mechanisms, one of which is by serving as an opsonin, which binds to the capsular polysaccharides of the bacteria and potentially to SP-A receptors on the macrophages, and the other by activating the macrophages, resulting in increased activity of the mannose receptor.	Polysaccharides	152-167	surfactant protein A1	Homo sapiens	17-21
9039518-3	1997	The SP-A/ ALB was initially low in both RDS groups and increased to levels measured in the non-RDS group by age 48 h. Multiple regression analysis showed that SP-BC/ALB, postnatal age, SM count, SM count/SP-A plus SP-BC, and surfactant therapy were independently associated with the severity of RDS as assessed by ventilatory index (r = 0.75, P &lt; 0.0001; number of samples = 256).	sp-bc	159-164	surfactant protein A1	Homo sapiens	4-8
9014347-0	1997	Cochliobolic acid, a novel metabolite produced by Cochliobolus lunatus, inhibits binding of TGF-alpha to the EGF receptor in a SPA assay.	cochliobolic acid	0-17	surfactant protein A1	Homo sapiens	127-130
8994517-0	1996	Effect of contact avoidance or treatment with oral prednisolone on bronchoalveolar lavage surfactant protein A levels in subjects with farmer"s lung.	Prednisolone	51-63	surfactant protein A1	Homo sapiens	90-110
8969273-6	1996	Dexamethasone treatment during culture increased SP-D mRNA and protein about 2-fold with maximal response after 1 to 3 days" exposure to 100 nM steroid; under the same conditions SP-A mRNA content is inhibited.	Dexamethasone	0-13	surfactant protein A1	Homo sapiens	179-183
9392439-0	1997	Surfactant protein-A receptor-mediated inhibition of calcium signaling in alveolar type II cells.	Calcium	53-60	surfactant protein A1	Homo sapiens	0-20
9392439-12	1997	Type II cells incubated in Ca2+-free medium plus SP-A show diminished Ca2+ release responses to TG or ATP, suggesting that the action of SP-A to prevent secretagog initiated increases in [Ca2+]i may reflect its ability to block Ca2+ release from cytoplasmic Ca stores.	Adenosine Triphosphate	102-105	surfactant protein A1	Homo sapiens	49-53
8918587-1	1996	Human lung surfactant proteins A (SP-A) and D (SP-D) are both collagenous C-type lectins which appear to mediate antimicrobial activity by binding to carbohydrates on micro-organisms and to receptors on phagocytic cells.	Carbohydrates	150-163	surfactant protein A1	Homo sapiens	11-32
8914938-1	1996	Previous studies have shown that exposure of human surfactant protein A (SP-A) to nitrating agents [peroxynitrite (ONOO-); tetranitromethane (TNM; pH 8)] leads to nitrotyrosine formation.	Peroxynitrous Acid	100-113	surfactant protein A1	Homo sapiens	51-71
8914938-1	1996	Previous studies have shown that exposure of human surfactant protein A (SP-A) to nitrating agents [peroxynitrite (ONOO-); tetranitromethane (TNM; pH 8)] leads to nitrotyrosine formation.	Peroxynitrous Acid	100-113	surfactant protein A1	Homo sapiens	73-77
8914938-1	1996	Previous studies have shown that exposure of human surfactant protein A (SP-A) to nitrating agents [peroxynitrite (ONOO-); tetranitromethane (TNM; pH 8)] leads to nitrotyrosine formation.	onoo-)	115-121	surfactant protein A1	Homo sapiens	51-71
8914938-1	1996	Previous studies have shown that exposure of human surfactant protein A (SP-A) to nitrating agents [peroxynitrite (ONOO-); tetranitromethane (TNM; pH 8)] leads to nitrotyrosine formation.	onoo-)	115-121	surfactant protein A1	Homo sapiens	73-77
8914938-1	1996	Previous studies have shown that exposure of human surfactant protein A (SP-A) to nitrating agents [peroxynitrite (ONOO-); tetranitromethane (TNM; pH 8)] leads to nitrotyrosine formation.	Tetranitromethane	123-140	surfactant protein A1	Homo sapiens	51-71
8914938-1	1996	Previous studies have shown that exposure of human surfactant protein A (SP-A) to nitrating agents [peroxynitrite (ONOO-); tetranitromethane (TNM; pH 8)] leads to nitrotyrosine formation.	Tetranitromethane	123-140	surfactant protein A1	Homo sapiens	73-77
8914938-1	1996	Previous studies have shown that exposure of human surfactant protein A (SP-A) to nitrating agents [peroxynitrite (ONOO-); tetranitromethane (TNM; pH 8)] leads to nitrotyrosine formation.	Tetranitromethane	142-145	surfactant protein A1	Homo sapiens	51-71
8914938-1	1996	Previous studies have shown that exposure of human surfactant protein A (SP-A) to nitrating agents [peroxynitrite (ONOO-); tetranitromethane (TNM; pH 8)] leads to nitrotyrosine formation.	Tetranitromethane	142-145	surfactant protein A1	Homo sapiens	73-77
8914938-1	1996	Previous studies have shown that exposure of human surfactant protein A (SP-A) to nitrating agents [peroxynitrite (ONOO-); tetranitromethane (TNM; pH 8)] leads to nitrotyrosine formation.	3-nitrotyrosine	163-176	surfactant protein A1	Homo sapiens	51-71
8914938-1	1996	Previous studies have shown that exposure of human surfactant protein A (SP-A) to nitrating agents [peroxynitrite (ONOO-); tetranitromethane (TNM; pH 8)] leads to nitrotyrosine formation.	3-nitrotyrosine	163-176	surfactant protein A1	Homo sapiens	73-77
8914938-3	1996	Herein, human SP-A, dissolved in Hepes buffer, was incubated with two boluses each of 0.5 mM ONOO- (pH 7.4) or 0.5 mM TNM (pH 8.0) for 15 min.	HEPES	33-38	surfactant protein A1	Homo sapiens	14-18
8914938-3	1996	Herein, human SP-A, dissolved in Hepes buffer, was incubated with two boluses each of 0.5 mM ONOO- (pH 7.4) or 0.5 mM TNM (pH 8.0) for 15 min.	onoo	93-97	surfactant protein A1	Homo sapiens	14-18
8914938-6	1996	The major nitrated peptide on both TNM- and (ONOO-)-exposed SP-A was the tryptic fragment Tyr161-Arg179 (YNTYAYVGLTEGPSPGDFR), located in the SP-A carbohydrate recognition domain.	onoo-)	45-51	surfactant protein A1	Homo sapiens	60-64
8914938-6	1996	The major nitrated peptide on both TNM- and (ONOO-)-exposed SP-A was the tryptic fragment Tyr161-Arg179 (YNTYAYVGLTEGPSPGDFR), located in the SP-A carbohydrate recognition domain.	Carbohydrates	147-159	surfactant protein A1	Homo sapiens	60-64
8914938-8	1996	A second lesser nitrated peptide corresponding to tryptic fragment Asn217-Arg222 (NCLYSR) was also found on TNM- and (ONOO-)-modified SP-A.	Peptides	25-32	surfactant protein A1	Homo sapiens	134-138
8914938-8	1996	A second lesser nitrated peptide corresponding to tryptic fragment Asn217-Arg222 (NCLYSR) was also found on TNM- and (ONOO-)-modified SP-A.	onoo	118-122	surfactant protein A1	Homo sapiens	134-138
8918587-1	1996	Human lung surfactant proteins A (SP-A) and D (SP-D) are both collagenous C-type lectins which appear to mediate antimicrobial activity by binding to carbohydrates on micro-organisms and to receptors on phagocytic cells.	Carbohydrates	150-163	surfactant protein A1	Homo sapiens	34-45
8918587-2	1996	Purified native SP-A and SP-D, isolated from human bronchoalveolar lavage fluid, were found to bind to whole mite extracts (Dermatophagoides pteronyssinus) and the purified allergen Der p I, in a carbohydrate-specific and calcium-dependent manner.	Carbohydrates	196-208	surfactant protein A1	Homo sapiens	16-20
8918587-2	1996	Purified native SP-A and SP-D, isolated from human bronchoalveolar lavage fluid, were found to bind to whole mite extracts (Dermatophagoides pteronyssinus) and the purified allergen Der p I, in a carbohydrate-specific and calcium-dependent manner.	Calcium	222-229	surfactant protein A1	Homo sapiens	16-20
8993356-7	1996	In this capacity, PspA might expand the breath of protection elicited by a vaccine composed of only a few polysaccharide-protein conjugates representing capsule types most commonly associated with infectious pneumococci.	Polysaccharides	106-120	surfactant protein A1	Homo sapiens	18-22
8806782-0	1996	Nitration of surfactant protein A (SP-A) tyrosine residues results in decreased mannose binding ability.	Tyrosine	41-49	surfactant protein A1	Homo sapiens	13-33
8806782-5	1996	On the other hand, an increase in the .NO/O2.- value resulted in nitration of SP-A tyrosine residues, located in the carbohydrate recognition domain (CRD), and decreased the ability of SP-A to aggregate lipids and bind mannose, two functions that require an intact CRD.	Superoxides	42-44	surfactant protein A1	Homo sapiens	78-82
8806782-5	1996	On the other hand, an increase in the .NO/O2.- value resulted in nitration of SP-A tyrosine residues, located in the carbohydrate recognition domain (CRD), and decreased the ability of SP-A to aggregate lipids and bind mannose, two functions that require an intact CRD.	Superoxides	42-44	surfactant protein A1	Homo sapiens	185-189
8897910-3	1996	By contrast, the human genome contains two similar genes, hSP-A1 and hSP-A2, which are differentially regulated during development and differentially regulated by adenosine 3",5"-cyclic monophosphate (cAMP) and glucocorticoid treatment of human fetal lung in culture.	Cyclic AMP	163-199	surfactant protein A1	Homo sapiens	58-64
8897910-3	1996	By contrast, the human genome contains two similar genes, hSP-A1 and hSP-A2, which are differentially regulated during development and differentially regulated by adenosine 3",5"-cyclic monophosphate (cAMP) and glucocorticoid treatment of human fetal lung in culture.	Cyclic AMP	201-205	surfactant protein A1	Homo sapiens	58-64
8806782-0	1996	Nitration of surfactant protein A (SP-A) tyrosine residues results in decreased mannose binding ability.	Tyrosine	41-49	surfactant protein A1	Homo sapiens	35-39
8806782-5	1996	On the other hand, an increase in the .NO/O2.- value resulted in nitration of SP-A tyrosine residues, located in the carbohydrate recognition domain (CRD), and decreased the ability of SP-A to aggregate lipids and bind mannose, two functions that require an intact CRD.	Tyrosine	83-91	surfactant protein A1	Homo sapiens	78-82
8806782-0	1996	Nitration of surfactant protein A (SP-A) tyrosine residues results in decreased mannose binding ability.	Mannose	80-87	surfactant protein A1	Homo sapiens	13-33
8806782-5	1996	On the other hand, an increase in the .NO/O2.- value resulted in nitration of SP-A tyrosine residues, located in the carbohydrate recognition domain (CRD), and decreased the ability of SP-A to aggregate lipids and bind mannose, two functions that require an intact CRD.	Carbohydrates	117-129	surfactant protein A1	Homo sapiens	78-82
8806782-5	1996	On the other hand, an increase in the .NO/O2.- value resulted in nitration of SP-A tyrosine residues, located in the carbohydrate recognition domain (CRD), and decreased the ability of SP-A to aggregate lipids and bind mannose, two functions that require an intact CRD.	Mannose	219-226	surfactant protein A1	Homo sapiens	78-82
8806782-0	1996	Nitration of surfactant protein A (SP-A) tyrosine residues results in decreased mannose binding ability.	Mannose	80-87	surfactant protein A1	Homo sapiens	35-39
8806782-5	1996	On the other hand, an increase in the .NO/O2.- value resulted in nitration of SP-A tyrosine residues, located in the carbohydrate recognition domain (CRD), and decreased the ability of SP-A to aggregate lipids and bind mannose, two functions that require an intact CRD.	Mannose	219-226	surfactant protein A1	Homo sapiens	185-189
8872089-4	1996	This study investigated the effect of oxidation (via radioiodination and exposure to H2O2) on the structural and functional characteristics of SP-A.	Hydrogen Peroxide	85-89	surfactant protein A1	Homo sapiens	143-147
8806782-6	1996	SP-A was also nitrated to a large extent following exposure to 3-morpholinosydnonimine (SIN-1) or tetranitromethane at pH 8.	linsidomine	63-86	surfactant protein A1	Homo sapiens	0-4
8806782-6	1996	SP-A was also nitrated to a large extent following exposure to 3-morpholinosydnonimine (SIN-1) or tetranitromethane at pH 8.	Tetranitromethane	98-115	surfactant protein A1	Homo sapiens	0-4
8806782-11	1996	However, ONOO., formed by the reaction of .NO and O2.-, nitrates SP-A leading to decreased ability to aggregate lipids and bind mannose.	onoo	9-13	surfactant protein A1	Homo sapiens	65-69
8806782-11	1996	However, ONOO., formed by the reaction of .NO and O2.-, nitrates SP-A leading to decreased ability to aggregate lipids and bind mannose.	Superoxides	50-52	surfactant protein A1	Homo sapiens	65-69
8806782-11	1996	However, ONOO., formed by the reaction of .NO and O2.-, nitrates SP-A leading to decreased ability to aggregate lipids and bind mannose.	Nitrates	56-64	surfactant protein A1	Homo sapiens	65-69
8806782-11	1996	However, ONOO., formed by the reaction of .NO and O2.-, nitrates SP-A leading to decreased ability to aggregate lipids and bind mannose.	Mannose	128-135	surfactant protein A1	Homo sapiens	65-69
8984701-3	1996	METHODS: A double blind, placebo controlled study was performed to determine the change in pulmonary ventilation of premature infants with RDS as a result of dexamethasone treatment, and to evaluate the effect of dexamethasone on the levels of surfactant-associated proteins A (SP-A) and D (SP-D) in the tracheal fluid from 34 premature infants with RDS and 29 control subjects.	Dexamethasone	213-226	surfactant protein A1	Homo sapiens	244-276
8984701-7	1996	There was an inverse correlation between PCO2 values and SP-A concentrations.	pco2	41-45	surfactant protein A1	Homo sapiens	57-61
8984701-8	1996	CONCLUSIONS: These results suggest that early use of dexamethasone can improve pulmonary status and also increase SP-A and SP-D levels in the tracheal fluid in premature infants with RDS.	Dexamethasone	53-66	surfactant protein A1	Homo sapiens	114-118
8770068-1	1996	The human has two genes encoding surfactant protein-A (SP-A), termed SP-A1 and SP-A2; the SP-A2 gene is more highly regulated by cAMP and during fetal development than is SP-A1.	Cyclic AMP	129-133	surfactant protein A1	Homo sapiens	33-53
8770068-1	1996	The human has two genes encoding surfactant protein-A (SP-A), termed SP-A1 and SP-A2; the SP-A2 gene is more highly regulated by cAMP and during fetal development than is SP-A1.	Cyclic AMP	129-133	surfactant protein A1	Homo sapiens	55-59
8770068-10	1996	These findings indicate that CRESP-A2 serves an important role in mediating basal and cAMP-inducible expression of the human SP-A2 gene in type II cells, that the fetal lung nuclear proteins bound to CRESP-A2 differ from those bound to the canonical palindromic CRE, and that changes in the complex of nuclear proteins bound to CRESP-A2 accompany induction of SP-A gene expression.	Cyclic AMP	86-90	surfactant protein A1	Homo sapiens	32-36
8760386-5	1996	We investigated the abilities of both SP-A oligomers to regulate phospholipid secretion and to bind to alveolar type II cells.	Phospholipids	65-77	surfactant protein A1	Homo sapiens	38-42
8760386-13	1996	This study demonstrates that the multimerized form of human SP-A oligomer exhibits the following attributes: (1) the reduced capacity to regulate phospholipid secretion from type II cells, and (2) lower affinity to bind to type II cells, and that the integrity of a flower-bouquet-like octadecameric structure of SP-A oligomer is important for the expression of full activity of this protein, indicating the importance of the oligomeric structure of mammalian lectins with collagenous domains.	Phospholipids	146-158	surfactant protein A1	Homo sapiens	60-64
8872089-5	1996	Radioiodinated SP-A, stored at 4 degrees C, retained carbohydrate binding activity after labeling.	Carbohydrates	53-65	surfactant protein A1	Homo sapiens	15-19
8872089-6	1996	After 10 days storage, the radioiodinated SP-A was indistinguishable on SDS-PAGE from freshly radioiodinated SP-A, but sedimentation coefficient and Stokes radius values changed dramatically, indicating SP-A depolymerization.	Sodium Dodecyl Sulfate	72-75	surfactant protein A1	Homo sapiens	42-46
8872089-9	1996	Consequently, the effect of prolonged incubation with H2O2 upon SP-A was investigated, with similar results.	Hydrogen Peroxide	54-58	surfactant protein A1	Homo sapiens	64-68
8652189-15	1996	From these data we conclude that there exists an abnormal multimerized form of SP-A oligomer in the alveoli of patients with PAP, and that this unusual subpopulation of SP-A oligomer exhibits abnormal function on phospholipid membrane organization.	Phospholipids	213-225	surfactant protein A1	Homo sapiens	169-173
8698480-1	1996	Serotype b-specific polysaccharide antigen (SPA) was extracted from whole cells of Actinobacillus actinomycetemcomitans Y4 by autoclaving and purified by chromatography on DEAE-Sephadex A-25 and Sephacryl S-300.	DEAE-sephadex A-25	172-190	surfactant protein A1	Homo sapiens	9-42
8698480-1	1996	Serotype b-specific polysaccharide antigen (SPA) was extracted from whole cells of Actinobacillus actinomycetemcomitans Y4 by autoclaving and purified by chromatography on DEAE-Sephadex A-25 and Sephacryl S-300.	DEAE-sephadex A-25	172-190	surfactant protein A1	Homo sapiens	44-47
8698480-1	1996	Serotype b-specific polysaccharide antigen (SPA) was extracted from whole cells of Actinobacillus actinomycetemcomitans Y4 by autoclaving and purified by chromatography on DEAE-Sephadex A-25 and Sephacryl S-300.	sephacryl s-300	195-210	surfactant protein A1	Homo sapiens	9-42
8698480-1	1996	Serotype b-specific polysaccharide antigen (SPA) was extracted from whole cells of Actinobacillus actinomycetemcomitans Y4 by autoclaving and purified by chromatography on DEAE-Sephadex A-25 and Sephacryl S-300.	sephacryl s-300	195-210	surfactant protein A1	Homo sapiens	44-47
8870120-8	1996	Peroxynitrite added to surfactant in vitro is capable of decreasing the surface activity, inducing lipid peroxidation, decreasing the function of surfactant proteins, SP-A and SP-B, and inducing protein-associated nitro-tyrosine.	Peroxynitrous Acid	0-13	surfactant protein A1	Homo sapiens	167-171
8652605-8	1996	SP-A increased the association of liposomes containing DPPC with the membrane by 2-fold more than that containing 1-palmitoyl-2-linoleoyl-phosphatidylcholine (PLPC).	1,2-Dipalmitoylphosphatidylcholine	55-59	surfactant protein A1	Homo sapiens	0-4
8652605-9	1996	SP-A induced aggregation of phospholipid liposomes containing PLPC as well as those containing DPPC, but the final turbidity of DPPC liposomes aggregated by SP-A was only by 15% greater than that of PLPC liposomes.	Phospholipids	28-40	surfactant protein A1	Homo sapiens	0-4
8652605-1	1996	Pulmonary surfactant protein A (SP-A) augments the uptake of phospholipid liposomes containing dipalmitoylphosphatidylcholine (DPPC) by alveolar type II cells.	Phospholipids	61-73	surfactant protein A1	Homo sapiens	0-30
8652605-1	1996	Pulmonary surfactant protein A (SP-A) augments the uptake of phospholipid liposomes containing dipalmitoylphosphatidylcholine (DPPC) by alveolar type II cells.	Phospholipids	61-73	surfactant protein A1	Homo sapiens	32-36
8652605-9	1996	SP-A induced aggregation of phospholipid liposomes containing PLPC as well as those containing DPPC, but the final turbidity of DPPC liposomes aggregated by SP-A was only by 15% greater than that of PLPC liposomes.	1,2-Dipalmitoylphosphatidylcholine	95-99	surfactant protein A1	Homo sapiens	0-4
8652605-1	1996	Pulmonary surfactant protein A (SP-A) augments the uptake of phospholipid liposomes containing dipalmitoylphosphatidylcholine (DPPC) by alveolar type II cells.	1,2-Dipalmitoylphosphatidylcholine	95-125	surfactant protein A1	Homo sapiens	0-30
8652605-9	1996	SP-A induced aggregation of phospholipid liposomes containing PLPC as well as those containing DPPC, but the final turbidity of DPPC liposomes aggregated by SP-A was only by 15% greater than that of PLPC liposomes.	1,2-Dipalmitoylphosphatidylcholine	128-132	surfactant protein A1	Homo sapiens	157-161
8652605-1	1996	Pulmonary surfactant protein A (SP-A) augments the uptake of phospholipid liposomes containing dipalmitoylphosphatidylcholine (DPPC) by alveolar type II cells.	1,2-Dipalmitoylphosphatidylcholine	95-125	surfactant protein A1	Homo sapiens	32-36
8845173-8	1996	PC attachment by SP-A was calcium- and mannose-dependent as SP-A-mediated attachment was significantly reduced in the presence of EGTA and mannose to 13.1 +/- 1.6% and 19.3 +/- 2.6%, respectively (P&lt;0.05).	Calcium	26-33	surfactant protein A1	Homo sapiens	17-21
8652605-1	1996	Pulmonary surfactant protein A (SP-A) augments the uptake of phospholipid liposomes containing dipalmitoylphosphatidylcholine (DPPC) by alveolar type II cells.	1,2-Dipalmitoylphosphatidylcholine	127-131	surfactant protein A1	Homo sapiens	0-30
8652605-1	1996	Pulmonary surfactant protein A (SP-A) augments the uptake of phospholipid liposomes containing dipalmitoylphosphatidylcholine (DPPC) by alveolar type II cells.	1,2-Dipalmitoylphosphatidylcholine	127-131	surfactant protein A1	Homo sapiens	32-36
8652605-3	1996	In the present study we investigated the SP-A-mediated interaction of phospholipids with plasma membrane isolated from alveolar type II cells.	Phospholipids	70-83	surfactant protein A1	Homo sapiens	41-45
8652605-4	1996	SP-A increased the amount of liposomes containing radiolabeled DPPC associated with type II cell plasma membrane by 4-fold compared to the control without SP-A when analyzed by sucrose density gradient centrifugation.	1,2-Dipalmitoylphosphatidylcholine	63-67	surfactant protein A1	Homo sapiens	0-4
8652605-4	1996	SP-A increased the amount of liposomes containing radiolabeled DPPC associated with type II cell plasma membrane by 4-fold compared to the control without SP-A when analyzed by sucrose density gradient centrifugation.	Sucrose	177-184	surfactant protein A1	Homo sapiens	0-4
8652605-7	1996	When type II cell plasma membrane and liposomes containing [14C]DPPC and [3H]triolein were coincubated with or without SP-A, analysis on sucrose density gradients revealed that the profiles of [14C]DPPC and [3H]triolein in each fraction were almost identical with or without SP-A, indicating that SP-A mediates the binding of liposomes to plasma membrane but not transfer of DPPC.	Carbon-14	194-197	surfactant protein A1	Homo sapiens	119-123
8652605-7	1996	When type II cell plasma membrane and liposomes containing [14C]DPPC and [3H]triolein were coincubated with or without SP-A, analysis on sucrose density gradients revealed that the profiles of [14C]DPPC and [3H]triolein in each fraction were almost identical with or without SP-A, indicating that SP-A mediates the binding of liposomes to plasma membrane but not transfer of DPPC.	1,2-Dipalmitoylphosphatidylcholine	198-202	surfactant protein A1	Homo sapiens	119-123
8652605-7	1996	When type II cell plasma membrane and liposomes containing [14C]DPPC and [3H]triolein were coincubated with or without SP-A, analysis on sucrose density gradients revealed that the profiles of [14C]DPPC and [3H]triolein in each fraction were almost identical with or without SP-A, indicating that SP-A mediates the binding of liposomes to plasma membrane but not transfer of DPPC.	1,2-Dipalmitoylphosphatidylcholine	198-202	surfactant protein A1	Homo sapiens	119-123
8619616-0	1996	Calcium dependent association of surfactant protein A with pulmonary surfactant: application to simple surfactant protein A purification.	Calcium	0-7	surfactant protein A1	Homo sapiens	33-53
8619616-0	1996	Calcium dependent association of surfactant protein A with pulmonary surfactant: application to simple surfactant protein A purification.	Calcium	0-7	surfactant protein A1	Homo sapiens	103-123
8619616-4	1996	Following the Ca2+ buffer wash, the surfactant pellet is washed in buffer containing EGTA and Mg2+ which releases the bound SP-A in almost pure form.	Egtazic Acid	85-89	surfactant protein A1	Homo sapiens	124-128
8619616-4	1996	Following the Ca2+ buffer wash, the surfactant pellet is washed in buffer containing EGTA and Mg2+ which releases the bound SP-A in almost pure form.	magnesium ion	94-98	surfactant protein A1	Homo sapiens	124-128
8619616-5	1996	Subsequent chromatography of the SP-A on Sephacryl S-500 yields homogeneous preparations of the protein.	sephacryl S 500	41-56	surfactant protein A1	Homo sapiens	33-37
8845173-8	1996	PC attachment by SP-A was calcium- and mannose-dependent as SP-A-mediated attachment was significantly reduced in the presence of EGTA and mannose to 13.1 +/- 1.6% and 19.3 +/- 2.6%, respectively (P&lt;0.05).	Calcium	26-33	surfactant protein A1	Homo sapiens	60-64
8845173-8	1996	PC attachment by SP-A was calcium- and mannose-dependent as SP-A-mediated attachment was significantly reduced in the presence of EGTA and mannose to 13.1 +/- 1.6% and 19.3 +/- 2.6%, respectively (P&lt;0.05).	Mannose	39-46	surfactant protein A1	Homo sapiens	17-21
8845173-8	1996	PC attachment by SP-A was calcium- and mannose-dependent as SP-A-mediated attachment was significantly reduced in the presence of EGTA and mannose to 13.1 +/- 1.6% and 19.3 +/- 2.6%, respectively (P&lt;0.05).	Mannose	39-46	surfactant protein A1	Homo sapiens	60-64
8845173-8	1996	PC attachment by SP-A was calcium- and mannose-dependent as SP-A-mediated attachment was significantly reduced in the presence of EGTA and mannose to 13.1 +/- 1.6% and 19.3 +/- 2.6%, respectively (P&lt;0.05).	Egtazic Acid	130-134	surfactant protein A1	Homo sapiens	17-21
8845173-8	1996	PC attachment by SP-A was calcium- and mannose-dependent as SP-A-mediated attachment was significantly reduced in the presence of EGTA and mannose to 13.1 +/- 1.6% and 19.3 +/- 2.6%, respectively (P&lt;0.05).	Egtazic Acid	130-134	surfactant protein A1	Homo sapiens	60-64
8845173-8	1996	PC attachment by SP-A was calcium- and mannose-dependent as SP-A-mediated attachment was significantly reduced in the presence of EGTA and mannose to 13.1 +/- 1.6% and 19.3 +/- 2.6%, respectively (P&lt;0.05).	Mannose	139-146	surfactant protein A1	Homo sapiens	17-21
8845173-8	1996	PC attachment by SP-A was calcium- and mannose-dependent as SP-A-mediated attachment was significantly reduced in the presence of EGTA and mannose to 13.1 +/- 1.6% and 19.3 +/- 2.6%, respectively (P&lt;0.05).	Mannose	139-146	surfactant protein A1	Homo sapiens	60-64
8779998-2	1996	SP-A was treated with various concentrations of tetranitromethane (TNM) at pH 6, 7.4, 8, or 10.	Tetranitromethane	48-65	surfactant protein A1	Homo sapiens	0-4
8779998-2	1996	SP-A was treated with various concentrations of tetranitromethane (TNM) at pH 6, 7.4, 8, or 10.	Tetranitromethane	67-70	surfactant protein A1	Homo sapiens	0-4
8779998-4	1996	Exposure of SP-A to TNM (0.1-1 mM) at pH 7.4 or 8 for 30 min resulted in dose-and pH-dependent increases in nitrotyrosine, detected by Western blotting, enzyme-linked immunosorbent assay, and direct amino acid analysis.	3-nitrotyrosine	108-121	surfactant protein A1	Homo sapiens	12-16
8779998-6	1996	In contrast, SP-A exposed to 1 mM TNM at pH 6 had background levels of nitrotyrosine and exhibited normal lipid aggregation properties.	3-nitrotyrosine	71-84	surfactant protein A1	Homo sapiens	13-17
8779998-7	1996	TNM, but not a hydroxyl radical-generating system, resulted in a pH-dependent loss of SP-A fluorescence, suggesting that tryptophan also may have been nitrated.	Tryptophan	121-131	surfactant protein A1	Homo sapiens	86-90
8779998-10	1996	We conclude that tyrosine nitration selectively inhibits the SP-A-mediated lipid aggregation without affecting its ability to bind lipids.	Tyrosine	17-25	surfactant protein A1	Homo sapiens	61-65
8552433-9	1995	Prenatal DEX improved the surface activity of surfactant isolated from airway specimens and tended to increase the ratio of surfactant protein A to phosphatidylcholine among recipients of exogenous surfactant.	Dexamethasone	9-12	surfactant protein A1	Homo sapiens	124-144
8838078-4	1996	Hydrophilic surfactant apoproteins (SP-A and SP-D) that are members of C-type lectin superfamily, interact with phospholipids and glycolipids and modulate host defense functions in the lung.	Phospholipids	112-125	surfactant protein A1	Homo sapiens	36-40
8838078-5	1996	SP-A also plays an important role in regulating phospholipid homeostasis in the alveolar spaces.	Phospholipids	48-60	surfactant protein A1	Homo sapiens	0-4
8835192-1	1995	Using immunohistochemical (IH) staining for epithelial membrane antigen (EMA), keratin, Leu-7, Ca 19-9, secretory component (SC) and surfactant protein A (SPA) on formalin-fixed, paraffin-embedded autopsy cases of stillbirth and early neonatal death, the normal profile of IH-positive cells in the airway of the developing fetal lung was clarified.	Formaldehyde	163-171	surfactant protein A1	Homo sapiens	133-153
8541330-9	1995	Only silica-treated lungs maintained elevated levels of surfactant phospholipids and SP-A throughout the course of the experiment.	Silicon Dioxide	5-11	surfactant protein A1	Homo sapiens	85-89
7782337-5	1995	The indicated mutations have previously been shown to change the carbohydrate binding specificity of surfactant protein A and mannose-binding protein from mannose &gt; galactose to the converse.	Carbohydrates	65-77	surfactant protein A1	Homo sapiens	101-121
7647097-0	1995	Epitope mapping for monoclonal antibody against human surfactant protein A (SP-A) that alters receptor binding of SP-A and the SP-A-dependent regulation of phospholipid secretion by alveolar type II cells.	Phospholipids	156-168	surfactant protein A1	Homo sapiens	54-74
7647097-0	1995	Epitope mapping for monoclonal antibody against human surfactant protein A (SP-A) that alters receptor binding of SP-A and the SP-A-dependent regulation of phospholipid secretion by alveolar type II cells.	Phospholipids	156-168	surfactant protein A1	Homo sapiens	76-80
7647097-2	1995	SP-A has been shown to function as an inhibitor of phospholipid secretion by primary culture of alveolar type II cells via cell surface receptor(s) for SP-A.	Phospholipids	51-63	surfactant protein A1	Homo sapiens	0-4
7647097-2	1995	SP-A has been shown to function as an inhibitor of phospholipid secretion by primary culture of alveolar type II cells via cell surface receptor(s) for SP-A.	Phospholipids	51-63	surfactant protein A1	Homo sapiens	152-156
7626019-6	1995	However, rat, dog and normal human SP-A isolated by a novel method, involving extraction from pulmonary surfactant by using n-octyl beta-D-glucopyranoside and subsequent purification by cation-exchange chromatography, were able to elicit an oxidative burst in rat as well as normal human alveolar macrophages.	octyl-beta-D-glucoside	124-154	surfactant protein A1	Homo sapiens	35-39
7633738-5	1995	Using Cox"s proportional hazard model, we found that SP-A/PL modeled continuously was associated with survival time (p = 0.002).	Phospholipids	58-60	surfactant protein A1	Homo sapiens	53-57
7782337-5	1995	The indicated mutations have previously been shown to change the carbohydrate binding specificity of surfactant protein A and mannose-binding protein from mannose &gt; galactose to the converse.	Mannose	126-133	surfactant protein A1	Homo sapiens	101-121
7782337-5	1995	The indicated mutations have previously been shown to change the carbohydrate binding specificity of surfactant protein A and mannose-binding protein from mannose &gt; galactose to the converse.	Mannose	155-162	surfactant protein A1	Homo sapiens	101-121
7782337-5	1995	The indicated mutations have previously been shown to change the carbohydrate binding specificity of surfactant protein A and mannose-binding protein from mannose &gt; galactose to the converse.	Galactose	168-177	surfactant protein A1	Homo sapiens	101-121
7762680-8	1995	Phosphatidylcholine was rapidly degraded by macrophages and the degradation occurred both in the presence and absence of SP-A.	Phosphatidylcholines	0-19	surfactant protein A1	Homo sapiens	121-125
7742011-4	1995	We found that retinoic acid interferes, in a dose-dependent fashion, with the expression of epithelial genes that are found in distal segments of the fetal lung (surfactant-associated proteins SP-A, SP-B, and SP-C).	Tretinoin	14-27	surfactant protein A1	Homo sapiens	193-197
10155709-1	1995	Studies were conducted to evaluate the potential cause for release of covalently bound Staphylococcal protein A (SpA) from a silica based extracorporeal immunoadsorbent matrix.	Silicon Dioxide	125-131	surfactant protein A1	Homo sapiens	87-111
7762796-0	1995	Use of factorial experimental design to delineate the strong calcium- and pH-dependent changes in binding of human surfactant protein-A to neutral glycosphingolipids--a model for studies of protein-carbohydrate interactions.	Calcium	61-68	surfactant protein A1	Homo sapiens	115-135
7762796-0	1995	Use of factorial experimental design to delineate the strong calcium- and pH-dependent changes in binding of human surfactant protein-A to neutral glycosphingolipids--a model for studies of protein-carbohydrate interactions.	Glycosphingolipids	147-165	surfactant protein A1	Homo sapiens	115-135
7762796-0	1995	Use of factorial experimental design to delineate the strong calcium- and pH-dependent changes in binding of human surfactant protein-A to neutral glycosphingolipids--a model for studies of protein-carbohydrate interactions.	Carbohydrates	198-210	surfactant protein A1	Homo sapiens	115-135
7762796-8	1995	To evaluate the pH- and calcium-dependent binding of SP-A to neutral glycosphingolipids we employed a microtiter plate technique and performed a series of full factorial design experiments using lactosylceramide, galactosylceramide, and gangliotetraosylceramide and native nonderivatized SP-A.	Calcium	24-31	surfactant protein A1	Homo sapiens	53-57
7762796-8	1995	To evaluate the pH- and calcium-dependent binding of SP-A to neutral glycosphingolipids we employed a microtiter plate technique and performed a series of full factorial design experiments using lactosylceramide, galactosylceramide, and gangliotetraosylceramide and native nonderivatized SP-A.	Glycosphingolipids	69-87	surfactant protein A1	Homo sapiens	53-57
7762796-8	1995	To evaluate the pH- and calcium-dependent binding of SP-A to neutral glycosphingolipids we employed a microtiter plate technique and performed a series of full factorial design experiments using lactosylceramide, galactosylceramide, and gangliotetraosylceramide and native nonderivatized SP-A.	G(A1) ganglioside	237-261	surfactant protein A1	Homo sapiens	53-57
7762796-10	1995	At pH 7.4 and at 5 mM Ca concentration the binding affinity of SP-A followed the order galactosylceramide &gt; lactosylceramide &gt; gangliotetraosylceramide.	Galactosylceramides	87-105	surfactant protein A1	Homo sapiens	63-67
7762796-10	1995	At pH 7.4 and at 5 mM Ca concentration the binding affinity of SP-A followed the order galactosylceramide &gt; lactosylceramide &gt; gangliotetraosylceramide.	CDw17 antigen	89-105	surfactant protein A1	Homo sapiens	63-67
7762796-10	1995	At pH 7.4 and at 5 mM Ca concentration the binding affinity of SP-A followed the order galactosylceramide &gt; lactosylceramide &gt; gangliotetraosylceramide.	G(A1) ganglioside	133-157	surfactant protein A1	Homo sapiens	63-67
7762796-11	1995	However, this was close to optimal conditions for binding of SP-A to lactosylceramide and at minimum for binding to gangliotetraosylceramide.	CDw17 antigen	69-85	surfactant protein A1	Homo sapiens	61-65
7762796-12	1995	Binding of SP-A to galactosylceramide was relatively insensitive to pH but increased significantly with increasing Ca concentrations.	Galactosylceramides	19-37	surfactant protein A1	Homo sapiens	11-15
10155709-1	1995	Studies were conducted to evaluate the potential cause for release of covalently bound Staphylococcal protein A (SpA) from a silica based extracorporeal immunoadsorbent matrix.	Silicon Dioxide	125-131	surfactant protein A1	Homo sapiens	113-116
7840221-10	1995	Lipid A, the hydrophobic component of LPS, however, inhibited the SP-A-LPS interaction and also caused a partial reversal of the binding.	Lipid A	0-7	surfactant protein A1	Homo sapiens	66-70
7703285-0	1995	Surfactant protein A-polylysine conjugates for delivery of DNA to airway cells in culture.	Polylysine	21-31	surfactant protein A1	Homo sapiens	0-20
7703285-1	1995	Surfactant protein A (SP-A) was modified by covalent linkage with polylysine of average M(r) 21 kD ([Lys]21kD-SP-A) and utilized to transfect human airway epithelial cells (H441) in vitro.	Polylysine	66-76	surfactant protein A1	Homo sapiens	0-20
7703285-1	1995	Surfactant protein A (SP-A) was modified by covalent linkage with polylysine of average M(r) 21 kD ([Lys]21kD-SP-A) and utilized to transfect human airway epithelial cells (H441) in vitro.	Polylysine	66-76	surfactant protein A1	Homo sapiens	22-26
7703285-1	1995	Surfactant protein A (SP-A) was modified by covalent linkage with polylysine of average M(r) 21 kD ([Lys]21kD-SP-A) and utilized to transfect human airway epithelial cells (H441) in vitro.	Lysine	101-104	surfactant protein A1	Homo sapiens	0-20
7703285-1	1995	Surfactant protein A (SP-A) was modified by covalent linkage with polylysine of average M(r) 21 kD ([Lys]21kD-SP-A) and utilized to transfect human airway epithelial cells (H441) in vitro.	Lysine	101-104	surfactant protein A1	Homo sapiens	22-26
7703285-1	1995	Surfactant protein A (SP-A) was modified by covalent linkage with polylysine of average M(r) 21 kD ([Lys]21kD-SP-A) and utilized to transfect human airway epithelial cells (H441) in vitro.	Lysine	101-104	surfactant protein A1	Homo sapiens	110-114
7703285-2	1995	Transfection of H441 cells was more efficient with [Lys]21kD-SP-A than with polylysine-DNA or unmodified SP-A-DNA complexes.	Lysine	52-55	surfactant protein A1	Homo sapiens	61-65
7703285-3	1995	Transfection with [Lys]21kD-SP-A was effective at a protein-to-DNA molar ratio of 400:1 and in the presence of an exogenous surfactant preparation, Survanta.	Lysine	19-22	surfactant protein A1	Homo sapiens	28-32
7703285-4	1995	Transfection with [Lys]21kD-SP-A was reduced in the presence of unmodified SP-A consistent with the concept of a receptor mediated uptake of protein-DNA complexes.	Lysine	19-22	surfactant protein A1	Homo sapiens	28-32
7703285-4	1995	Transfection with [Lys]21kD-SP-A was reduced in the presence of unmodified SP-A consistent with the concept of a receptor mediated uptake of protein-DNA complexes.	Lysine	19-22	surfactant protein A1	Homo sapiens	75-79
7703285-5	1995	Increased transfection efficiency correlated with decreasing diameter of the [Lys]21kD-SP-A-DNA complexes, and these complexes bound to the cell surface and pseudopodia of H441 cells.	Lysine	78-81	surfactant protein A1	Homo sapiens	87-91
7703285-7	1995	Cotransfection by [Lys]21kD-SP-A-DNA and [Lys]10kD-SP-B resulted in an additive level of reporter gene (CAT) expression.	Lysine	19-22	surfactant protein A1	Homo sapiens	28-32
7525589-1	1994	Pulmonary surfactant protein A (SP-A) contains 4 domains: a disulfide forming amino terminus, a collagen-like region, a neck region, and a carbohydrate recognition region.	Disulfides	60-69	surfactant protein A1	Homo sapiens	0-30
7700729-6	1995	The inhibitory effects of plasma on DLSE were significantly less when SP-A was added to DLSE (5:1, phospholipid:SP-A, wt:wt).	Phospholipids	99-111	surfactant protein A1	Homo sapiens	70-74
7525589-1	1994	Pulmonary surfactant protein A (SP-A) contains 4 domains: a disulfide forming amino terminus, a collagen-like region, a neck region, and a carbohydrate recognition region.	Disulfides	60-69	surfactant protein A1	Homo sapiens	32-36
7525589-1	1994	Pulmonary surfactant protein A (SP-A) contains 4 domains: a disulfide forming amino terminus, a collagen-like region, a neck region, and a carbohydrate recognition region.	Carbohydrates	139-151	surfactant protein A1	Homo sapiens	0-30
7525589-1	1994	Pulmonary surfactant protein A (SP-A) contains 4 domains: a disulfide forming amino terminus, a collagen-like region, a neck region, and a carbohydrate recognition region.	Carbohydrates	139-151	surfactant protein A1	Homo sapiens	32-36
7525589-3	1994	SP-A also inhibits lipid secretion and enhances the uptake of phospholipid by alveolar type II cells.	Phospholipids	62-74	surfactant protein A1	Homo sapiens	0-4
7525589-9	1994	Antibody 1D6 completely blocked the binding of SP-A to dipalmitoylphosphatidylcholine and galactosylceramide and liposome aggregation.	1,2-Dipalmitoylphosphatidylcholine	55-85	surfactant protein A1	Homo sapiens	47-51
7525589-9	1994	Antibody 1D6 completely blocked the binding of SP-A to dipalmitoylphosphatidylcholine and galactosylceramide and liposome aggregation.	Galactosylceramides	90-108	surfactant protein A1	Homo sapiens	47-51
7977768-7	1994	SP-A binds to the C1q receptor (C1qR) on monocytes, since its binding was inhibited by C1q and the SP-A-enhanced association of S. aureus with these cells was completely abolished when monocytes were adherent to surfaces coated with C1q or anti-C1qR monoclonal antibody.	C10Ph	18-21	surfactant protein A1	Homo sapiens	0-4
7977768-7	1994	SP-A binds to the C1q receptor (C1qR) on monocytes, since its binding was inhibited by C1q and the SP-A-enhanced association of S. aureus with these cells was completely abolished when monocytes were adherent to surfaces coated with C1q or anti-C1qR monoclonal antibody.	C10Ph	18-21	surfactant protein A1	Homo sapiens	99-103
7977768-7	1994	SP-A binds to the C1q receptor (C1qR) on monocytes, since its binding was inhibited by C1q and the SP-A-enhanced association of S. aureus with these cells was completely abolished when monocytes were adherent to surfaces coated with C1q or anti-C1qR monoclonal antibody.	C10Ph	32-35	surfactant protein A1	Homo sapiens	0-4
7977768-7	1994	SP-A binds to the C1q receptor (C1qR) on monocytes, since its binding was inhibited by C1q and the SP-A-enhanced association of S. aureus with these cells was completely abolished when monocytes were adherent to surfaces coated with C1q or anti-C1qR monoclonal antibody.	C10Ph	32-35	surfactant protein A1	Homo sapiens	99-103
7977768-8	1994	Furthermore, the binding of SP-A to monocytes results in an increased intracellular concentration of adenosine 3",5"-cyclic monophosphate.	Cyclic AMP	101-137	surfactant protein A1	Homo sapiens	28-32
8024567-2	1994	The density of SpA in dipalmitoylphosphatidic acid (DPPA) monolayers is determined from ultraviolet spectroscopy.	dipalmitoylphosphatidic acid	22-50	surfactant protein A1	Homo sapiens	15-18
7943339-4	1994	The inhibitory effects of DPPC and Survanta were altered in mixtures that contained SP-A.	colfosceril palmitate	26-30	surfactant protein A1	Homo sapiens	84-88
7943339-6	1994	These findings suggest that surfactant phospholipids cause a suppression of mitogen-induced lymphocyte proliferation, which is reversed somewhat by addition of SP-A.	Phospholipids	39-52	surfactant protein A1	Homo sapiens	160-164
7808837-9	1994	DEX transiently increased the concentration of surfactant protein-A in epithelial lining fluid but had no effect on surface activity of the sedimentable surfactant complex or on concentrations of phosphatidylcholine, IL-1 beta, lactoferrin, or myeloperoxidase.	Dexamethasone	0-3	surfactant protein A1	Homo sapiens	47-67
8089481-4	1994	In contrast, stimulation with SPA containing S. aureus or SPA-Sepharose resulted in biased expression of VH3 containing IgM.	Sepharose	62-71	surfactant protein A1	Homo sapiens	58-61
7943250-0	1994	Concurrent generation of nitric oxide and superoxide damages surfactant protein A.	Nitric Oxide	25-37	surfactant protein A1	Homo sapiens	61-81
7943250-0	1994	Concurrent generation of nitric oxide and superoxide damages surfactant protein A.	Superoxides	42-52	surfactant protein A1	Homo sapiens	61-81
7943250-3	1994	The simultaneous generation of .NO and superoxide by 3-morpholinosydnonimine (SIN-1, 0.1-2 mM) resulted in oxidation of dihydrorhodamine, a marker of peroxynitrite production, and a dose-dependent decrease in the ability of SP-A to enhance lipid aggregation.	Superoxides	39-49	surfactant protein A1	Homo sapiens	224-228
7943250-3	1994	The simultaneous generation of .NO and superoxide by 3-morpholinosydnonimine (SIN-1, 0.1-2 mM) resulted in oxidation of dihydrorhodamine, a marker of peroxynitrite production, and a dose-dependent decrease in the ability of SP-A to enhance lipid aggregation.	linsidomine	53-76	surfactant protein A1	Homo sapiens	224-228
7943250-3	1994	The simultaneous generation of .NO and superoxide by 3-morpholinosydnonimine (SIN-1, 0.1-2 mM) resulted in oxidation of dihydrorhodamine, a marker of peroxynitrite production, and a dose-dependent decrease in the ability of SP-A to enhance lipid aggregation.	dihydrorhodamine 123	120-136	surfactant protein A1	Homo sapiens	224-228
7943250-3	1994	The simultaneous generation of .NO and superoxide by 3-morpholinosydnonimine (SIN-1, 0.1-2 mM) resulted in oxidation of dihydrorhodamine, a marker of peroxynitrite production, and a dose-dependent decrease in the ability of SP-A to enhance lipid aggregation.	Peroxynitrous Acid	150-163	surfactant protein A1	Homo sapiens	224-228
7943250-4	1994	Western blot analysis of SIN-1 exposed SP-A samples, overlaid with a polyclonal antibody against nitrotyrosine, were consistent with nitration of SP-A tyrosine residues.	3-nitrotyrosine	97-110	surfactant protein A1	Homo sapiens	146-150
7943250-4	1994	Western blot analysis of SIN-1 exposed SP-A samples, overlaid with a polyclonal antibody against nitrotyrosine, were consistent with nitration of SP-A tyrosine residues.	Tyrosine	102-110	surfactant protein A1	Homo sapiens	146-150
7943250-7	1994	We concluded that peroxynitrite, but not .NO or superoxide and hydrogen peroxide, in concentrations likely to be encountered in vivo, caused nitrotyrosine formation and decreased the ability of SP-A to aggregate lipids.	Peroxynitrous Acid	18-31	surfactant protein A1	Homo sapiens	194-198
8024567-2	1994	The density of SpA in dipalmitoylphosphatidic acid (DPPA) monolayers is determined from ultraviolet spectroscopy.	dipalmitoylphosphatidic acid	52-56	surfactant protein A1	Homo sapiens	15-18
8024567-3	1994	The influence of calcium on the SpA concentration in the monolayer is also investigated.	Calcium	17-24	surfactant protein A1	Homo sapiens	32-35
8024567-4	1994	The spectroscopic results indicate that the incorporation of SpA in the monolayer is influenced by the calcium concentration in the subphase, and more than 90% of adsorbed protein is excluded from the monolayer when calcium concentration is in the order of millimoles.	Calcium	103-110	surfactant protein A1	Homo sapiens	61-64
8024567-4	1994	The spectroscopic results indicate that the incorporation of SpA in the monolayer is influenced by the calcium concentration in the subphase, and more than 90% of adsorbed protein is excluded from the monolayer when calcium concentration is in the order of millimoles.	Calcium	216-223	surfactant protein A1	Homo sapiens	61-64
8198539-4	1994	Both SP-D and SP-A have been shown to enhance oxygen radical production by alveolar macrophages.	Reactive Oxygen Species	46-60	surfactant protein A1	Homo sapiens	14-18
8185601-0	1994	Characterization of modified staphylococcal protein A containing phospholipid monolayer on both solution and slide surfaces.	Phospholipids	65-77	surfactant protein A1	Homo sapiens	29-53
8185601-1	1994	A method is described for incorporation of water-soluble protein Staphylococcal protein A (SpA) into phospholipid monolayer using covalent protein-lipid conjugates in detergent solution.	Water	43-48	surfactant protein A1	Homo sapiens	65-89
8185601-1	1994	A method is described for incorporation of water-soluble protein Staphylococcal protein A (SpA) into phospholipid monolayer using covalent protein-lipid conjugates in detergent solution.	Water	43-48	surfactant protein A1	Homo sapiens	91-94
8185601-1	1994	A method is described for incorporation of water-soluble protein Staphylococcal protein A (SpA) into phospholipid monolayer using covalent protein-lipid conjugates in detergent solution.	Phospholipids	101-113	surfactant protein A1	Homo sapiens	65-89
8185601-1	1994	A method is described for incorporation of water-soluble protein Staphylococcal protein A (SpA) into phospholipid monolayer using covalent protein-lipid conjugates in detergent solution.	Phospholipids	101-113	surfactant protein A1	Homo sapiens	91-94
8004321-6	1994	We found a direct relationship between CHOL and DSP (rs = 0.84, p &lt; 0.001), SP-A and CHOL (rs = 0.40, p &lt; 0.025), and between SP-A and DSP (rs = 0.44, p &lt; 0.025).	Cholesterol	88-92	surfactant protein A1	Homo sapiens	79-83
8205397-3	1994	Maximal tissue reactivity to anti-SP-A antibodies was found in the synovium of 55 rheumatoid patients exhibiting classical histopathological appearances of RA, in a pattern of immunostaining identical to that obtained with ML30, an antibody to mycobacterial heat shock protein 65kDa which, in turn, cross-reacted with SP-A in dot blot testing.	Radium	156-158	surfactant protein A1	Homo sapiens	34-38
8131621-0	1994	Structural and functional alterations of surfactant protein A by peroxynitrite.	Peroxynitrous Acid	65-78	surfactant protein A1	Homo sapiens	41-61
8179013-1	1994	Expression of the surfactant protein A (SP-A) gene is lung specific, developmentally induced, and regulated by adenosine 3",5"-cyclic monophosphate (cAMP) and glucocorticoids.	Cyclic AMP	111-147	surfactant protein A1	Homo sapiens	18-38
8179013-1	1994	Expression of the surfactant protein A (SP-A) gene is lung specific, developmentally induced, and regulated by adenosine 3",5"-cyclic monophosphate (cAMP) and glucocorticoids.	Cyclic AMP	111-147	surfactant protein A1	Homo sapiens	40-44
8179013-1	1994	Expression of the surfactant protein A (SP-A) gene is lung specific, developmentally induced, and regulated by adenosine 3",5"-cyclic monophosphate (cAMP) and glucocorticoids.	Cyclic AMP	149-153	surfactant protein A1	Homo sapiens	18-38
8179013-1	1994	Expression of the surfactant protein A (SP-A) gene is lung specific, developmentally induced, and regulated by adenosine 3",5"-cyclic monophosphate (cAMP) and glucocorticoids.	Cyclic AMP	149-153	surfactant protein A1	Homo sapiens	40-44
8179013-11	1994	In the present study, primer extension was used to assess the relative levels of expression of the SP-A1 and SP-A2 genes in human adult lung tissue and in fetal lung tissues maintained in organ culture in the absence or presence of dibutyryl (DB)cAMP (1 mM) and dexamethasone (Dex, 10(-4) M).	Dexamethasone	262-275	surfactant protein A1	Homo sapiens	99-104
8179013-11	1994	In the present study, primer extension was used to assess the relative levels of expression of the SP-A1 and SP-A2 genes in human adult lung tissue and in fetal lung tissues maintained in organ culture in the absence or presence of dibutyryl (DB)cAMP (1 mM) and dexamethasone (Dex, 10(-4) M).	Dexamethasone	262-275	surfactant protein A1	Homo sapiens	109-114
8179013-11	1994	In the present study, primer extension was used to assess the relative levels of expression of the SP-A1 and SP-A2 genes in human adult lung tissue and in fetal lung tissues maintained in organ culture in the absence or presence of dibutyryl (DB)cAMP (1 mM) and dexamethasone (Dex, 10(-4) M).	Dexamethasone	277-280	surfactant protein A1	Homo sapiens	99-104
8179013-11	1994	In the present study, primer extension was used to assess the relative levels of expression of the SP-A1 and SP-A2 genes in human adult lung tissue and in fetal lung tissues maintained in organ culture in the absence or presence of dibutyryl (DB)cAMP (1 mM) and dexamethasone (Dex, 10(-4) M).	Dexamethasone	277-280	surfactant protein A1	Homo sapiens	109-114
8179012-15	1994	10): L367-L374, 1994], we report that the SP-A1 and SP-A2 genes are differentially regulated during development and by adenosine 3",5"-cyclic monophosphate and glucocorticoids in human fetal lung in culture.	Cyclic AMP	119-155	surfactant protein A1	Homo sapiens	42-47
8179013-0	1994	Human SP-A1 and SP-A2 genes are differentially regulated during development and by cAMP and glucocorticoids.	Cyclic AMP	83-87	surfactant protein A1	Homo sapiens	6-11
8179013-0	1994	Human SP-A1 and SP-A2 genes are differentially regulated during development and by cAMP and glucocorticoids.	Cyclic AMP	83-87	surfactant protein A1	Homo sapiens	16-21
8351444-4	1993	Methacholine (MCh) or isoproterenol (ISP), added to the medium at the beginning of period II, reduced the ratio of SP-A concentration in period II to that in period I, compared to samples without treatment.	Methacholine Chloride	0-12	surfactant protein A1	Homo sapiens	115-119
8305484-5	1994	Immunochemistry of paraffin sections of fetal membranes, revealed the presence of both SP-A and SP-D in the amniotic epithelium and chorio-decidual layers.	Paraffin	19-27	surfactant protein A1	Homo sapiens	87-91
8404646-6	1993	Retinoic acid reduced SP-A protein levels in a concentration-dependent manner [analysis of variance (ANOVA), P &lt; 0.01].	Tretinoin	0-13	surfactant protein A1	Homo sapiens	22-26
8404646-10	1993	Retinoic acid reduced SP-A mRNA levels in a concentration-dependent manner (ANOVA, P &lt; 0.02) and reduced SP-C mRNA levels at 3 microM.	Tretinoin	0-13	surfactant protein A1	Homo sapiens	22-26
8364413-0	1993	Calcium and dithiothreitol dependent conformational changes in beta-sheet structure of collagenase resistant fragment of human surfactant protein A.	Calcium	0-7	surfactant protein A1	Homo sapiens	127-147
8364413-0	1993	Calcium and dithiothreitol dependent conformational changes in beta-sheet structure of collagenase resistant fragment of human surfactant protein A.	Dithiothreitol	12-26	surfactant protein A1	Homo sapiens	127-147
8364413-6	1993	One of the functions of SP-A, enhancement of phospholipid uptake by alveolar type II cells, was abolished by the addition of 2-mercaptoethanol.	Phospholipids	45-57	surfactant protein A1	Homo sapiens	24-28
8364413-6	1993	One of the functions of SP-A, enhancement of phospholipid uptake by alveolar type II cells, was abolished by the addition of 2-mercaptoethanol.	Mercaptoethanol	125-142	surfactant protein A1	Homo sapiens	24-28
8119925-2	1994	Pulmonary surfactant protein A (SP-A) regulates the uptake and secretion of phospholipid by alveolar type II cells and is an important component of surfactant lipid aggregates.	Phospholipids	76-88	surfactant protein A1	Homo sapiens	0-30
8119925-2	1994	Pulmonary surfactant protein A (SP-A) regulates the uptake and secretion of phospholipid by alveolar type II cells and is an important component of surfactant lipid aggregates.	Phospholipids	76-88	surfactant protein A1	Homo sapiens	32-36
8119925-4	1994	Synthesis of the wild type SP-A in insect cells resulted in a form of the protein in which proline residues were not hydroxylated and that is denoted SP-Ahyp.	Proline	91-98	surfactant protein A1	Homo sapiens	27-31
8119925-9	1994	Furthermore, recombinant SP-A is able to inhibit the secretion of phospholipid from isolated type II cells and to aggregate lipid vesicles independent of the presence of N-linked carbohydrate or the site of glycosylation.	Phospholipids	66-78	surfactant protein A1	Homo sapiens	25-29
8119925-9	1994	Furthermore, recombinant SP-A is able to inhibit the secretion of phospholipid from isolated type II cells and to aggregate lipid vesicles independent of the presence of N-linked carbohydrate or the site of glycosylation.	n-linked carbohydrate	170-191	surfactant protein A1	Homo sapiens	25-29
8162991-2	1994	Two of these, SP-A and SP-D, are large and water-soluble, while SP-B and SP-C are small and very hydrophobic.	Water	43-48	surfactant protein A1	Homo sapiens	14-18
8162991-3	1994	SP-A is an 18-mer of 26 kDa polypeptide chains and contains N-linked oligosaccharides.	n-linked oligosaccharides	60-85	surfactant protein A1	Homo sapiens	0-4
8280055-0	1993	Tryptophan fluorescence study on the interaction of pulmonary surfactant protein A with phospholipid vesicles.	Tryptophan	0-10	surfactant protein A1	Homo sapiens	52-82
8280055-2	1993	After excitation at either 275 or 295 nm, the fluorescence emission spectrum of both proteins was characterized by two maxima at about 326 and 337 nm, indicating heterogeneity in the emission of the two tryptophan residues of SP-A, and also revealing a partially buried character for these fluorophores.	Tryptophan	203-213	surfactant protein A1	Homo sapiens	226-230
8280055-3	1993	Interaction of both human and porcine SP-A with various phospholipid vesicles resulted in an increase in the fluorescence emission of tryptophan without any shift in the emission wavelength maxima.	Phospholipids	56-68	surfactant protein A1	Homo sapiens	38-42
8280055-3	1993	Interaction of both human and porcine SP-A with various phospholipid vesicles resulted in an increase in the fluorescence emission of tryptophan without any shift in the emission wavelength maxima.	Tryptophan	134-144	surfactant protein A1	Homo sapiens	38-42
8280055-5	1993	Intrinsic fluorescence of SP-A was almost completely unaffected in the presence of egg phosphatidylcholine (egg-PC).	(3-Hexadecanoyloxy-2-nonadecanoyloxypropyl) 2-(trimethylazaniumyl)ethyl phosphate	108-114	surfactant protein A1	Homo sapiens	26-30
8280055-6	1993	In addition, we demonstrated a shielding of the tryptophan fluorescence from quenching by acrylamide on interaction of porcine SP-A with DPPC, DPPG or LPC.	Tryptophan	48-58	surfactant protein A1	Homo sapiens	127-131
8280055-6	1993	In addition, we demonstrated a shielding of the tryptophan fluorescence from quenching by acrylamide on interaction of porcine SP-A with DPPC, DPPG or LPC.	Acrylamide	90-100	surfactant protein A1	Homo sapiens	127-131
8280055-6	1993	In addition, we demonstrated a shielding of the tryptophan fluorescence from quenching by acrylamide on interaction of porcine SP-A with DPPC, DPPG or LPC.	1,2-Dipalmitoylphosphatidylcholine	137-141	surfactant protein A1	Homo sapiens	127-131
8280055-6	1993	In addition, we demonstrated a shielding of the tryptophan fluorescence from quenching by acrylamide on interaction of porcine SP-A with DPPC, DPPG or LPC.	1,2-dipalmitoylphosphatidylglycerol	143-147	surfactant protein A1	Homo sapiens	127-131
8280055-6	1993	In addition, we demonstrated a shielding of the tryptophan fluorescence from quenching by acrylamide on interaction of porcine SP-A with DPPC, DPPG or LPC.	lpc	151-154	surfactant protein A1	Homo sapiens	127-131
8280055-8	1993	In the case of human SP-A, shielding was only observed on interaction with DPPC.	1,2-Dipalmitoylphosphatidylcholine	75-79	surfactant protein A1	Homo sapiens	21-25
8280055-9	1993	From the intrinsic fluorescence measurements as well as from the quenching experiments, we concluded that the interaction of some phospholipid vesicles with SP-A produces a conformational change on the protein molecule and that the interaction of SP-A with DPPC is stronger than with other phospholipids.	Phospholipids	130-142	surfactant protein A1	Homo sapiens	157-161
8280055-9	1993	From the intrinsic fluorescence measurements as well as from the quenching experiments, we concluded that the interaction of some phospholipid vesicles with SP-A produces a conformational change on the protein molecule and that the interaction of SP-A with DPPC is stronger than with other phospholipids.	Phospholipids	130-142	surfactant protein A1	Homo sapiens	247-251
8280055-9	1993	From the intrinsic fluorescence measurements as well as from the quenching experiments, we concluded that the interaction of some phospholipid vesicles with SP-A produces a conformational change on the protein molecule and that the interaction of SP-A with DPPC is stronger than with other phospholipids.	1,2-Dipalmitoylphosphatidylcholine	257-261	surfactant protein A1	Homo sapiens	247-251
8280055-9	1993	From the intrinsic fluorescence measurements as well as from the quenching experiments, we concluded that the interaction of some phospholipid vesicles with SP-A produces a conformational change on the protein molecule and that the interaction of SP-A with DPPC is stronger than with other phospholipids.	Phospholipids	290-303	surfactant protein A1	Homo sapiens	157-161
8280055-9	1993	From the intrinsic fluorescence measurements as well as from the quenching experiments, we concluded that the interaction of some phospholipid vesicles with SP-A produces a conformational change on the protein molecule and that the interaction of SP-A with DPPC is stronger than with other phospholipids.	Phospholipids	290-303	surfactant protein A1	Homo sapiens	247-251
8280055-11	1993	Physiological ionic strength was found to be required for the interaction of SP-A with negatively charged vesicles of either DPPG or DPPC/DPPG (7:3, w/w).	1,2-dipalmitoylphosphatidylglycerol	125-129	surfactant protein A1	Homo sapiens	77-81
8280055-11	1993	Physiological ionic strength was found to be required for the interaction of SP-A with negatively charged vesicles of either DPPG or DPPC/DPPG (7:3, w/w).	1,2-Dipalmitoylphosphatidylcholine	133-137	surfactant protein A1	Homo sapiens	77-81
8280055-11	1993	Physiological ionic strength was found to be required for the interaction of SP-A with negatively charged vesicles of either DPPG or DPPC/DPPG (7:3, w/w).	1,2-dipalmitoylphosphatidylglycerol	138-142	surfactant protein A1	Homo sapiens	77-81
8280055-13	1993	The increase in intrinsic fluorescence of SP-A in the presence of DPPC vesicles was much stronger when the vesicles were in the gel state than when they were in the liquid-crystalline state.	1,2-Dipalmitoylphosphatidylcholine	66-70	surfactant protein A1	Homo sapiens	42-46
8280055-16	1993	These results strongly indicate that the interaction of SP-A with phospholipid vesicles requires the lipids to be in the gel phase.	Phospholipids	66-78	surfactant protein A1	Homo sapiens	56-60
8368326-7	1993	The isoproterenol-stimulated secretion of [3H]tocopherol and of 14C-labeled phospholipids by type II cells is inhibited by surfactant protein A.	Isoproterenol	4-17	surfactant protein A1	Homo sapiens	123-143
8368326-7	1993	The isoproterenol-stimulated secretion of [3H]tocopherol and of 14C-labeled phospholipids by type II cells is inhibited by surfactant protein A.	[3h]tocopherol	42-56	surfactant protein A1	Homo sapiens	123-143
8368326-7	1993	The isoproterenol-stimulated secretion of [3H]tocopherol and of 14C-labeled phospholipids by type II cells is inhibited by surfactant protein A.	Carbon-14	64-67	surfactant protein A1	Homo sapiens	123-143
8368326-7	1993	The isoproterenol-stimulated secretion of [3H]tocopherol and of 14C-labeled phospholipids by type II cells is inhibited by surfactant protein A.	Phospholipids	76-89	surfactant protein A1	Homo sapiens	123-143
8368329-0	1993	Pulmonary surfactant protein A-mediated uptake of phosphatidylcholine by alveolar type II cells.	Phosphatidylcholines	50-69	surfactant protein A1	Homo sapiens	0-30
8368329-1	1993	Pulmonary surfactant protein A (SP-A)-mediated uptake of phosphatidylcholine (PC) by alveolar type II cells was investigated.	Phosphatidylcholines	57-76	surfactant protein A1	Homo sapiens	0-30
8368329-1	1993	Pulmonary surfactant protein A (SP-A)-mediated uptake of phosphatidylcholine (PC) by alveolar type II cells was investigated.	Phosphatidylcholines	57-76	surfactant protein A1	Homo sapiens	32-36
8368329-1	1993	Pulmonary surfactant protein A (SP-A)-mediated uptake of phosphatidylcholine (PC) by alveolar type II cells was investigated.	Phosphatidylcholines	78-80	surfactant protein A1	Homo sapiens	0-30
8368329-1	1993	Pulmonary surfactant protein A (SP-A)-mediated uptake of phosphatidylcholine (PC) by alveolar type II cells was investigated.	Phosphatidylcholines	78-80	surfactant protein A1	Homo sapiens	32-36
8368329-2	1993	SP-A enhanced the uptake of liposomes containing dipalmitoylphosphatidylcholine (DPPC), 1-palmitoyl-2-linoleoyl phosphatidylcholine (PLPC), or 1,2-dihexadecyl-sn-glycero-3-phosphocholine (DPPC-ether), a diether analogue of DPPC, but about twice as much DPPC was taken up by type II cells as PLPC or DPPC-ether.	1,2-Dipalmitoylphosphatidylcholine	49-79	surfactant protein A1	Homo sapiens	0-4
8368329-2	1993	SP-A enhanced the uptake of liposomes containing dipalmitoylphosphatidylcholine (DPPC), 1-palmitoyl-2-linoleoyl phosphatidylcholine (PLPC), or 1,2-dihexadecyl-sn-glycero-3-phosphocholine (DPPC-ether), a diether analogue of DPPC, but about twice as much DPPC was taken up by type II cells as PLPC or DPPC-ether.	1,2-Dipalmitoylphosphatidylcholine	81-85	surfactant protein A1	Homo sapiens	0-4
8368329-2	1993	SP-A enhanced the uptake of liposomes containing dipalmitoylphosphatidylcholine (DPPC), 1-palmitoyl-2-linoleoyl phosphatidylcholine (PLPC), or 1,2-dihexadecyl-sn-glycero-3-phosphocholine (DPPC-ether), a diether analogue of DPPC, but about twice as much DPPC was taken up by type II cells as PLPC or DPPC-ether.	1-palmitoyl-2-linoleoylphosphatidylcholine	88-131	surfactant protein A1	Homo sapiens	0-4
8368329-2	1993	SP-A enhanced the uptake of liposomes containing dipalmitoylphosphatidylcholine (DPPC), 1-palmitoyl-2-linoleoyl phosphatidylcholine (PLPC), or 1,2-dihexadecyl-sn-glycero-3-phosphocholine (DPPC-ether), a diether analogue of DPPC, but about twice as much DPPC was taken up by type II cells as PLPC or DPPC-ether.	1-palmitoyl-2-linoleoylphosphatidylcholine	133-137	surfactant protein A1	Homo sapiens	0-4
8368329-2	1993	SP-A enhanced the uptake of liposomes containing dipalmitoylphosphatidylcholine (DPPC), 1-palmitoyl-2-linoleoyl phosphatidylcholine (PLPC), or 1,2-dihexadecyl-sn-glycero-3-phosphocholine (DPPC-ether), a diether analogue of DPPC, but about twice as much DPPC was taken up by type II cells as PLPC or DPPC-ether.	1,2-dihexadecyl-sn-glycero-3-phosphocholine	143-186	surfactant protein A1	Homo sapiens	0-4
8368329-2	1993	SP-A enhanced the uptake of liposomes containing dipalmitoylphosphatidylcholine (DPPC), 1-palmitoyl-2-linoleoyl phosphatidylcholine (PLPC), or 1,2-dihexadecyl-sn-glycero-3-phosphocholine (DPPC-ether), a diether analogue of DPPC, but about twice as much DPPC was taken up by type II cells as PLPC or DPPC-ether.	dppc-ether	188-198	surfactant protein A1	Homo sapiens	0-4
8368329-2	1993	SP-A enhanced the uptake of liposomes containing dipalmitoylphosphatidylcholine (DPPC), 1-palmitoyl-2-linoleoyl phosphatidylcholine (PLPC), or 1,2-dihexadecyl-sn-glycero-3-phosphocholine (DPPC-ether), a diether analogue of DPPC, but about twice as much DPPC was taken up by type II cells as PLPC or DPPC-ether.	1,2-Dipalmitoylphosphatidylcholine	188-192	surfactant protein A1	Homo sapiens	0-4
8368329-2	1993	SP-A enhanced the uptake of liposomes containing dipalmitoylphosphatidylcholine (DPPC), 1-palmitoyl-2-linoleoyl phosphatidylcholine (PLPC), or 1,2-dihexadecyl-sn-glycero-3-phosphocholine (DPPC-ether), a diether analogue of DPPC, but about twice as much DPPC was taken up by type II cells as PLPC or DPPC-ether.	1,2-Dipalmitoylphosphatidylcholine	188-192	surfactant protein A1	Homo sapiens	0-4
8368329-2	1993	SP-A enhanced the uptake of liposomes containing dipalmitoylphosphatidylcholine (DPPC), 1-palmitoyl-2-linoleoyl phosphatidylcholine (PLPC), or 1,2-dihexadecyl-sn-glycero-3-phosphocholine (DPPC-ether), a diether analogue of DPPC, but about twice as much DPPC was taken up by type II cells as PLPC or DPPC-ether.	dppc-ether	299-309	surfactant protein A1	Homo sapiens	0-4
8368329-3	1993	When subcellular distribution was analyzed, 51.3 +/- 2.9% (mean +/- SD, n = 3) of cell-associated radiolabeled DPPC was recovered in the lamellar body-rich fraction in the presence of SP-A, whereas only 19.3 +/- 1.9% (mean +/- SD, n = 3) was found to this fraction in the absence of SP-A.	1,2-Dipalmitoylphosphatidylcholine	111-115	surfactant protein A1	Homo sapiens	184-188
8368329-6	1993	Phosphatidylcholine that had been incorporated into lamellar bodies remained largely intact when SP-A was present.	Phosphatidylcholines	0-19	surfactant protein A1	Homo sapiens	97-101
8368329-7	1993	Subcellular fractionations of type II cells with radiolabeled SP-A and DPPC revealed that the sedimentation characteristics of cell-associated SP-A are different from those of DPPC, although a small broad peak of radiolabeled SP-A was found in the lamellar body fraction.	1,2-Dipalmitoylphosphatidylcholine	71-75	surfactant protein A1	Homo sapiens	143-147
8368329-7	1993	Subcellular fractionations of type II cells with radiolabeled SP-A and DPPC revealed that the sedimentation characteristics of cell-associated SP-A are different from those of DPPC, although a small broad peak of radiolabeled SP-A was found in the lamellar body fraction.	1,2-Dipalmitoylphosphatidylcholine	71-75	surfactant protein A1	Homo sapiens	143-147
8328957-1	1993	Collectin receptor (Clq receptor) has been shown to bind human Clq, mannose-binding protein (MBP), lung surfactant protein A (SP-A) and bovine conglutinin.	(R)-chloroquine	20-23	surfactant protein A1	Homo sapiens	104-124
8328957-1	1993	Collectin receptor (Clq receptor) has been shown to bind human Clq, mannose-binding protein (MBP), lung surfactant protein A (SP-A) and bovine conglutinin.	(R)-chloroquine	20-23	surfactant protein A1	Homo sapiens	126-130
8351444-4	1993	Methacholine (MCh) or isoproterenol (ISP), added to the medium at the beginning of period II, reduced the ratio of SP-A concentration in period II to that in period I, compared to samples without treatment.	Methacholine Chloride	14-17	surfactant protein A1	Homo sapiens	115-119
8351444-4	1993	Methacholine (MCh) or isoproterenol (ISP), added to the medium at the beginning of period II, reduced the ratio of SP-A concentration in period II to that in period I, compared to samples without treatment.	Isoproterenol	22-35	surfactant protein A1	Homo sapiens	115-119
8351444-4	1993	Methacholine (MCh) or isoproterenol (ISP), added to the medium at the beginning of period II, reduced the ratio of SP-A concentration in period II to that in period I, compared to samples without treatment.	Isoproterenol	37-40	surfactant protein A1	Homo sapiens	115-119
8351444-6	1993	The supernatant from explants stimulated by MCh was capable of reducing SP-A secretion from cultured epithelial cells.	Methacholine Chloride	44-47	surfactant protein A1	Homo sapiens	72-76
8471056-0	1993	Role of the C-terminal domain of pulmonary surfactant protein A in binding to alveolar type II cells and regulation of phospholipid secretion.	Phospholipids	119-131	surfactant protein A1	Homo sapiens	33-63
8388647-2	1993	Dibutyryl adenosine 3",5"-cyclic monophosphate (DBcAMP) treatment of human fetal lung in culture increases the rate of morphological differentiation and enhances expression of the surfactant protein A (SP-A) gene.	Bucladesine	0-46	surfactant protein A1	Homo sapiens	180-200
8388647-2	1993	Dibutyryl adenosine 3",5"-cyclic monophosphate (DBcAMP) treatment of human fetal lung in culture increases the rate of morphological differentiation and enhances expression of the surfactant protein A (SP-A) gene.	Bucladesine	0-46	surfactant protein A1	Homo sapiens	202-206
8388647-2	1993	Dibutyryl adenosine 3",5"-cyclic monophosphate (DBcAMP) treatment of human fetal lung in culture increases the rate of morphological differentiation and enhances expression of the surfactant protein A (SP-A) gene.	Bucladesine	48-54	surfactant protein A1	Homo sapiens	180-200
8388647-2	1993	Dibutyryl adenosine 3",5"-cyclic monophosphate (DBcAMP) treatment of human fetal lung in culture increases the rate of morphological differentiation and enhances expression of the surfactant protein A (SP-A) gene.	Bucladesine	48-54	surfactant protein A1	Homo sapiens	202-206
8388647-6	1993	When lung tissues that had been maintained for 5 days in 1% oxygen were transferred to an environment containing 20% oxygen, there was rapid morphological development and induction of SP-A gene expression.	Oxygen	60-66	surfactant protein A1	Homo sapiens	184-188
8388647-6	1993	When lung tissues that had been maintained for 5 days in 1% oxygen were transferred to an environment containing 20% oxygen, there was rapid morphological development and induction of SP-A gene expression.	Oxygen	117-123	surfactant protein A1	Homo sapiens	184-188
8388647-7	1993	The effects on morphological development were manifest within 24 h of transfer to the 20% oxygen environment; within 72 h, a marked stimulatory effect of DBcAMP on SP-A gene expression also was observed.	Bucladesine	154-160	surfactant protein A1	Homo sapiens	164-168
8388647-8	1993	Our findings further suggest that the effects of oxygen on the levels of SP-A and SP-A mRNA are concentration dependent.	Oxygen	49-55	surfactant protein A1	Homo sapiens	73-77
8388647-8	1993	Our findings further suggest that the effects of oxygen on the levels of SP-A and SP-A mRNA are concentration dependent.	Oxygen	49-55	surfactant protein A1	Homo sapiens	82-86
8388647-9	1993	Interestingly, the inductive effects of DBcAMP on SP-A gene expression were apparent only at oxygen concentrations &gt; or = 10%.	Bucladesine	40-46	surfactant protein A1	Homo sapiens	50-54
8388647-9	1993	Interestingly, the inductive effects of DBcAMP on SP-A gene expression were apparent only at oxygen concentrations &gt; or = 10%.	Oxygen	93-99	surfactant protein A1	Homo sapiens	50-54
8471056-3	1993	SP-A has been demonstrated to function as an inhibitor of phospholipid secretion by primary cultures of alveolar type II cells via a cell surface receptor for the protein.	Phospholipids	58-70	surfactant protein A1	Homo sapiens	0-4
8471056-5	1993	The purpose of the present study was to investigate the role of the C-terminal domain of SP-A in binding to type II cells and regulation of phospholipid secretion.	Phospholipids	140-152	surfactant protein A1	Homo sapiens	89-93
8471056-6	1993	A monoclonal antibody to human SP-A, whose epitope was localized at the C-terminal domain of the protein, abolished the inhibitory activity of human SP-A on lipid secretion by type II cells, and attenuated the ability of human SP-A to compete with 125I-(rat SP-A) for receptor binding.	Iodine-125	248-252	surfactant protein A1	Homo sapiens	31-35
8471056-6	1993	A monoclonal antibody to human SP-A, whose epitope was localized at the C-terminal domain of the protein, abolished the inhibitory activity of human SP-A on lipid secretion by type II cells, and attenuated the ability of human SP-A to compete with 125I-(rat SP-A) for receptor binding.	Iodine-125	248-252	surfactant protein A1	Homo sapiens	149-153
8471056-6	1993	A monoclonal antibody to human SP-A, whose epitope was localized at the C-terminal domain of the protein, abolished the inhibitory activity of human SP-A on lipid secretion by type II cells, and attenuated the ability of human SP-A to compete with 125I-(rat SP-A) for receptor binding.	Iodine-125	248-252	surfactant protein A1	Homo sapiens	149-153
8442601-12	1993	There was significantly less SP-A in the Gm+ PNEU group than in the Gm- PNEU group (p &lt; 0.02).	gm+ pneu	41-49	surfactant protein A1	Homo sapiens	29-33
8450241-8	1993	Residual contaminating levels of SpA in affinity purified MAbs were lowest with a low salt (NaCl, 150 mM) glycine (1 M) adsorption/washing buffer.	Salts	86-90	surfactant protein A1	Homo sapiens	33-36
8450241-8	1993	Residual contaminating levels of SpA in affinity purified MAbs were lowest with a low salt (NaCl, 150 mM) glycine (1 M) adsorption/washing buffer.	Sodium Chloride	92-96	surfactant protein A1	Homo sapiens	33-36
8450241-8	1993	Residual contaminating levels of SpA in affinity purified MAbs were lowest with a low salt (NaCl, 150 mM) glycine (1 M) adsorption/washing buffer.	Glycine	106-113	surfactant protein A1	Homo sapiens	33-36
8460712-4	1993	Decreased content of SP-A mRNA was the dominant response to dexamethasone added either early or later during culture.	Dexamethasone	60-73	surfactant protein A1	Homo sapiens	21-25
8460712-7	1993	The immediate inhibitory effect of 100 nM dexamethasone on SP-A mRNA content was completely blocked in the presence of cycloheximide.	Dexamethasone	42-55	surfactant protein A1	Homo sapiens	59-63
8460712-7	1993	The immediate inhibitory effect of 100 nM dexamethasone on SP-A mRNA content was completely blocked in the presence of cycloheximide.	Cycloheximide	119-132	surfactant protein A1	Homo sapiens	59-63
8460712-8	1993	SP-A gene transcription, measured by nuclear elongation assay, was decreased by 60% after 4- to 8-h exposure to 100 nM dexamethasone.	Dexamethasone	119-132	surfactant protein A1	Homo sapiens	0-4
8460712-9	1993	Stability of SP-A mRNA, determined both by addition of actinomycin D and by label-chase experiments, was transiently decreased immediately after adding dexamethasone (t1/2 approximately 3 h).	Dactinomycin	55-68	surfactant protein A1	Homo sapiens	13-17
8460712-9	1993	Stability of SP-A mRNA, determined both by addition of actinomycin D and by label-chase experiments, was transiently decreased immediately after adding dexamethasone (t1/2 approximately 3 h).	Dexamethasone	152-165	surfactant protein A1	Homo sapiens	13-17
8460712-10	1993	In tissue treated with dexamethasone for &gt; or = 8 h the stability of SP-A mRNA in control and treated explants was not different (t1/2 approximately 8 h).	Dexamethasone	23-36	surfactant protein A1	Homo sapiens	72-76
1334078-0	1992	Binding of surfactant protein A (SP-A) to herpes simplex virus type 1-infected cells is mediated by the carbohydrate moiety of SP-A.	Carbohydrates	104-116	surfactant protein A1	Homo sapiens	33-37
1334078-0	1992	Binding of surfactant protein A (SP-A) to herpes simplex virus type 1-infected cells is mediated by the carbohydrate moiety of SP-A.	Carbohydrates	104-116	surfactant protein A1	Homo sapiens	127-131
1334078-3	1992	SP-A was labeled with fluorescein isothiocyanate, and its binding to herpes simplex virus type 1-infected HEp-2 cells, as a model for virus-infected cells in general, was studied using flow cytometry.	Fluorescein-5-isothiocyanate	22-48	surfactant protein A1	Homo sapiens	0-4
1334078-7	1992	However, heparin inhibited binding of SP-A in a concentration-dependent manner.	Heparin	9-16	surfactant protein A1	Homo sapiens	38-42
1334078-8	1992	In addition, heparin could also dissociate cell-bound SP-A, indicating that polyanionic oligosaccharides are involved in the binding of SP-A to virus-infected cells.	Heparin	13-20	surfactant protein A1	Homo sapiens	54-58
1334078-8	1992	In addition, heparin could also dissociate cell-bound SP-A, indicating that polyanionic oligosaccharides are involved in the binding of SP-A to virus-infected cells.	Heparin	13-20	surfactant protein A1	Homo sapiens	136-140
1334078-8	1992	In addition, heparin could also dissociate cell-bound SP-A, indicating that polyanionic oligosaccharides are involved in the binding of SP-A to virus-infected cells.	polyanionic oligosaccharides	76-104	surfactant protein A1	Homo sapiens	54-58
1334078-8	1992	In addition, heparin could also dissociate cell-bound SP-A, indicating that polyanionic oligosaccharides are involved in the binding of SP-A to virus-infected cells.	polyanionic oligosaccharides	76-104	surfactant protein A1	Homo sapiens	136-140
1334078-11	1992	It is concluded that the carbohydrate moiety of SP-A is involved in the recognition of viruses by SP-A and may play a role in the antiviral defenses of the lung.	Carbohydrates	25-37	surfactant protein A1	Homo sapiens	48-52
1334078-11	1992	It is concluded that the carbohydrate moiety of SP-A is involved in the recognition of viruses by SP-A and may play a role in the antiviral defenses of the lung.	Carbohydrates	25-37	surfactant protein A1	Homo sapiens	98-102
1297913-0	1992	Analysis of pneumococcal PspA microheterogeneity in SDS polyacrylamide gels and the association of PspA with the cell membrane.	Sodium Dodecyl Sulfate	52-55	surfactant protein A1	Homo sapiens	25-29
1306239-6	1992	We revealed that SP-A binds specifically to dipalmitoylphosphatidylcholine and galactose-ceramide and asialo GM2, while SP-D binds specifically to phosphatidylinositol and glucose-ceramide.	1,2-Dipalmitoylphosphatidylcholine	44-74	surfactant protein A1	Homo sapiens	17-21
1306239-6	1992	We revealed that SP-A binds specifically to dipalmitoylphosphatidylcholine and galactose-ceramide and asialo GM2, while SP-D binds specifically to phosphatidylinositol and glucose-ceramide.	galactose-ceramide	79-97	surfactant protein A1	Homo sapiens	17-21
1306239-6	1992	We revealed that SP-A binds specifically to dipalmitoylphosphatidylcholine and galactose-ceramide and asialo GM2, while SP-D binds specifically to phosphatidylinositol and glucose-ceramide.	gm2	109-112	surfactant protein A1	Homo sapiens	17-21
1297913-0	1992	Analysis of pneumococcal PspA microheterogeneity in SDS polyacrylamide gels and the association of PspA with the cell membrane.	polyacrylamide	56-70	surfactant protein A1	Homo sapiens	25-29
1297913-3	1992	PspA was not released in significant amounts from pneumococcal membranes treated with sodium carbonate, but was solubilized with SDS.	sodium carbonate	86-102	surfactant protein A1	Homo sapiens	0-4
1297913-3	1992	PspA was not released in significant amounts from pneumococcal membranes treated with sodium carbonate, but was solubilized with SDS.	Sodium Dodecyl Sulfate	129-132	surfactant protein A1	Homo sapiens	0-4
1297913-5	1992	By SDS-PAGE and immunoblot analysis, we found two predominant molecular sizes of PspA in each strain examined.	Sodium Dodecyl Sulfate	3-6	surfactant protein A1	Homo sapiens	81-85
1415320-5	1992	The methanol:saline phase was separated and lyophilized to yield the SP-A product.	Methanol	4-12	surfactant protein A1	Homo sapiens	69-73
1415320-5	1992	The methanol:saline phase was separated and lyophilized to yield the SP-A product.	Sodium Chloride	13-19	surfactant protein A1	Homo sapiens	69-73
1415320-6	1992	SDS-PAGE and immunoblot analysis indicated that our preparation of SP-A had only minor contamination with human plasma proteins.	Sodium Dodecyl Sulfate	0-3	surfactant protein A1	Homo sapiens	67-71
1390920-0	1992	Calcium dependent conformational changes of surfactant protein A (SP-A) and its collagenase resistant fragment with or without dithiothreitol.	Calcium	0-7	surfactant protein A1	Homo sapiens	44-64
1431440-7	1992	In conclusion, this newly developed ELISA kit for the measurement of amniotic fluid SP-A is more effective than other methods currently available for the evaluation of fetal lung maturity, when it is considered that it requires only 0.2ml of amniotic fluid and provides results in only 2h without technical difficulties.	Deuterium	286-288	surfactant protein A1	Homo sapiens	84-88
1390920-4	1992	The magnitude of the fluorescence intensity change induced by Ca2+ was amplified by the addition of dithiothreitol (DTT) in both SP-A and CRF.	Dithiothreitol	100-114	surfactant protein A1	Homo sapiens	129-133
1390920-4	1992	The magnitude of the fluorescence intensity change induced by Ca2+ was amplified by the addition of dithiothreitol (DTT) in both SP-A and CRF.	Dithiothreitol	116-119	surfactant protein A1	Homo sapiens	129-133
1390920-0	1992	Calcium dependent conformational changes of surfactant protein A (SP-A) and its collagenase resistant fragment with or without dithiothreitol.	Calcium	0-7	surfactant protein A1	Homo sapiens	66-70
1390920-0	1992	Calcium dependent conformational changes of surfactant protein A (SP-A) and its collagenase resistant fragment with or without dithiothreitol.	Dithiothreitol	127-141	surfactant protein A1	Homo sapiens	44-64
1390920-0	1992	Calcium dependent conformational changes of surfactant protein A (SP-A) and its collagenase resistant fragment with or without dithiothreitol.	Dithiothreitol	127-141	surfactant protein A1	Homo sapiens	66-70
1390920-1	1992	Calcium-dependent conformational changes of surfactant protein A (SP-A) and the collagenase resistant fragment (CRF) of SP-A were studied by measuring fluorescence spectra.	Calcium	0-7	surfactant protein A1	Homo sapiens	44-64
1390920-1	1992	Calcium-dependent conformational changes of surfactant protein A (SP-A) and the collagenase resistant fragment (CRF) of SP-A were studied by measuring fluorescence spectra.	Calcium	0-7	surfactant protein A1	Homo sapiens	66-70
1390920-1	1992	Calcium-dependent conformational changes of surfactant protein A (SP-A) and the collagenase resistant fragment (CRF) of SP-A were studied by measuring fluorescence spectra.	Calcium	0-7	surfactant protein A1	Homo sapiens	120-124
1616052-1	1992	Tumor necrosis factor-alpha (TNF-alpha) and the phorbol ester, 12-O-tetradecanoyl-phorbol-13-acetate (TPA) decrease the synthesis of surfactant proteins association with decreased SP-A and SP-B mRNA.	Phorbol Esters	48-61	surfactant protein A1	Homo sapiens	180-184
1318335-5	1992	C1q coated to microtiter wells induced O2- release, which occurred microtiter wells induced O2- release, which occurred after a lag period of 10 to 20 min, and was then sustained over approximately 1 h. O2- production could be triggered by the purified pepsin-resistant, collagen-like fragment of C1q, but not by mannose-binding protein and pulmonary surfactant protein A, proteins that also contain collagen-like domains.	Oxygen	39-41	surfactant protein A1	Homo sapiens	341-371
1318335-5	1992	C1q coated to microtiter wells induced O2- release, which occurred microtiter wells induced O2- release, which occurred after a lag period of 10 to 20 min, and was then sustained over approximately 1 h. O2- production could be triggered by the purified pepsin-resistant, collagen-like fragment of C1q, but not by mannose-binding protein and pulmonary surfactant protein A, proteins that also contain collagen-like domains.	Oxygen	92-94	surfactant protein A1	Homo sapiens	341-371
1318335-5	1992	C1q coated to microtiter wells induced O2- release, which occurred microtiter wells induced O2- release, which occurred after a lag period of 10 to 20 min, and was then sustained over approximately 1 h. O2- production could be triggered by the purified pepsin-resistant, collagen-like fragment of C1q, but not by mannose-binding protein and pulmonary surfactant protein A, proteins that also contain collagen-like domains.	Oxygen	92-94	surfactant protein A1	Homo sapiens	341-371
1616052-4	1992	Inhibitory effects of both agents on SP-A gene transcription were readily detected within 6 h after exposure and persisted for 24 h. While TNF-alpha and TPA decreased cellular SP-B mRNA content, transcription of the SP-B gene was not influenced by these agents.	Tetradecanoylphorbol Acetate	153-156	surfactant protein A1	Homo sapiens	37-41
1616052-5	1992	In contrast to the inhibitory effects of TPA and TNF-alpha on SP-A and SP-B mRNAs, steady-state mRNA and rate of transcription of human manganese superoxide dismutase (MnSOD) were increased by both agents.	Tetradecanoylphorbol Acetate	41-44	surfactant protein A1	Homo sapiens	62-66
1616052-8	1992	The inhibitory effects of TPA and TNF-alpha on SP-A expression in pulmonary adenocarcinoma cells are associated with the inhibition of SP-A gene transcription.	Tetradecanoylphorbol Acetate	26-29	surfactant protein A1	Homo sapiens	47-51
1616052-1	1992	Tumor necrosis factor-alpha (TNF-alpha) and the phorbol ester, 12-O-tetradecanoyl-phorbol-13-acetate (TPA) decrease the synthesis of surfactant proteins association with decreased SP-A and SP-B mRNA.	Tetradecanoylphorbol Acetate	63-100	surfactant protein A1	Homo sapiens	180-184
1616052-8	1992	The inhibitory effects of TPA and TNF-alpha on SP-A expression in pulmonary adenocarcinoma cells are associated with the inhibition of SP-A gene transcription.	Tetradecanoylphorbol Acetate	26-29	surfactant protein A1	Homo sapiens	135-139
1616052-1	1992	Tumor necrosis factor-alpha (TNF-alpha) and the phorbol ester, 12-O-tetradecanoyl-phorbol-13-acetate (TPA) decrease the synthesis of surfactant proteins association with decreased SP-A and SP-B mRNA.	Tetradecanoylphorbol Acetate	102-105	surfactant protein A1	Homo sapiens	180-184
1616052-10	1992	Actinomycin D blocked the inhibitory effects of TNF-alpha and TPA on SP-A and SP-B mRNA, supporting a role for posttranscriptional events in the modulation of the expression of the surfactant proteins SP-A and SP-B.	Dactinomycin	0-13	surfactant protein A1	Homo sapiens	69-73
1616052-10	1992	Actinomycin D blocked the inhibitory effects of TNF-alpha and TPA on SP-A and SP-B mRNA, supporting a role for posttranscriptional events in the modulation of the expression of the surfactant proteins SP-A and SP-B.	Dactinomycin	0-13	surfactant protein A1	Homo sapiens	201-205
1616052-3	1992	SP-A gene transcription was inhibited by both TNF-alpha and TPA as assessed by nuclear run-on assays.	Tetradecanoylphorbol Acetate	60-63	surfactant protein A1	Homo sapiens	0-4
1616052-10	1992	Actinomycin D blocked the inhibitory effects of TNF-alpha and TPA on SP-A and SP-B mRNA, supporting a role for posttranscriptional events in the modulation of the expression of the surfactant proteins SP-A and SP-B.	Tetradecanoylphorbol Acetate	62-65	surfactant protein A1	Homo sapiens	69-73
1577827-0	1992	Specificity of lung surfactant protein SP-A for both the carbohydrate and the lipid moieties of certain neutral glycolipids.	Carbohydrates	57-69	surfactant protein A1	Homo sapiens	39-43
1616052-10	1992	Actinomycin D blocked the inhibitory effects of TNF-alpha and TPA on SP-A and SP-B mRNA, supporting a role for posttranscriptional events in the modulation of the expression of the surfactant proteins SP-A and SP-B.	Tetradecanoylphorbol Acetate	62-65	surfactant protein A1	Homo sapiens	201-205
1616057-9	1992	There was a marked synergy between SP-A and SP-B in the process of membrane fusion in the presence of calcium, which correlated with an early (10 min) and extensive rearrangement of the structures seen by electron microscopy followed by a delayed (24 h) appearance of small amounts of tubular myelin.	Calcium	102-109	surfactant protein A1	Homo sapiens	35-39
1577827-0	1992	Specificity of lung surfactant protein SP-A for both the carbohydrate and the lipid moieties of certain neutral glycolipids.	Glycolipids	112-123	surfactant protein A1	Homo sapiens	39-43
1577827-9	1992	Selected components among the neutral glycolipids are bound by radiolabeled human SP-A; these are identified by TLC-LSIMS as predominantly ceramide mono- and disaccharides (human surfactant) and ceramide tri- and tetrasaccharides (rat surfactant and type II cells).	Glycolipids	38-49	surfactant protein A1	Homo sapiens	82-86
1651668-2	1991	The phagocytosis of FITC-HSV-1 by alveolar macrophages, which was studied as a model for virus phagocytosis in general, was strongly enhanced in the presence of SP-A.	Fluorescein-5-isothiocyanate	20-24	surfactant protein A1	Homo sapiens	161-165
1577827-9	1992	Selected components among the neutral glycolipids are bound by radiolabeled human SP-A; these are identified by TLC-LSIMS as predominantly ceramide mono- and disaccharides (human surfactant) and ceramide tri- and tetrasaccharides (rat surfactant and type II cells).	Ceramides	139-147	surfactant protein A1	Homo sapiens	82-86
1577827-9	1992	Selected components among the neutral glycolipids are bound by radiolabeled human SP-A; these are identified by TLC-LSIMS as predominantly ceramide mono- and disaccharides (human surfactant) and ceramide tri- and tetrasaccharides (rat surfactant and type II cells).	Ceramides	195-203	surfactant protein A1	Homo sapiens	82-86
1577827-9	1992	Selected components among the neutral glycolipids are bound by radiolabeled human SP-A; these are identified by TLC-LSIMS as predominantly ceramide mono- and disaccharides (human surfactant) and ceramide tri- and tetrasaccharides (rat surfactant and type II cells).	tri- and tetrasaccharides	204-229	surfactant protein A1	Homo sapiens	82-86
1577827-10	1992	A recombinant carbohydrate recognition domain (CRD) of human SP-A inhibits the binding of human SP-A to galactosyl ceramide and to galactose- and mannose-bovine serum albumin, indicating that the CRD is directly involved in the binding of SP-A to these ligands.	Carbohydrates	14-26	surfactant protein A1	Homo sapiens	61-65
1577827-10	1992	A recombinant carbohydrate recognition domain (CRD) of human SP-A inhibits the binding of human SP-A to galactosyl ceramide and to galactose- and mannose-bovine serum albumin, indicating that the CRD is directly involved in the binding of SP-A to these ligands.	Carbohydrates	14-26	surfactant protein A1	Homo sapiens	96-100
1577827-10	1992	A recombinant carbohydrate recognition domain (CRD) of human SP-A inhibits the binding of human SP-A to galactosyl ceramide and to galactose- and mannose-bovine serum albumin, indicating that the CRD is directly involved in the binding of SP-A to these ligands.	Carbohydrates	14-26	surfactant protein A1	Homo sapiens	96-100
1577827-10	1992	A recombinant carbohydrate recognition domain (CRD) of human SP-A inhibits the binding of human SP-A to galactosyl ceramide and to galactose- and mannose-bovine serum albumin, indicating that the CRD is directly involved in the binding of SP-A to these ligands.	Galactosylceramides	104-123	surfactant protein A1	Homo sapiens	61-65
1577827-10	1992	A recombinant carbohydrate recognition domain (CRD) of human SP-A inhibits the binding of human SP-A to galactosyl ceramide and to galactose- and mannose-bovine serum albumin, indicating that the CRD is directly involved in the binding of SP-A to these ligands.	Galactosylceramides	104-123	surfactant protein A1	Homo sapiens	96-100
1577827-10	1992	A recombinant carbohydrate recognition domain (CRD) of human SP-A inhibits the binding of human SP-A to galactosyl ceramide and to galactose- and mannose-bovine serum albumin, indicating that the CRD is directly involved in the binding of SP-A to these ligands.	Galactosylceramides	104-123	surfactant protein A1	Homo sapiens	96-100
1577827-10	1992	A recombinant carbohydrate recognition domain (CRD) of human SP-A inhibits the binding of human SP-A to galactosyl ceramide and to galactose- and mannose-bovine serum albumin, indicating that the CRD is directly involved in the binding of SP-A to these ligands.	Galactose	131-140	surfactant protein A1	Homo sapiens	61-65
1577827-10	1992	A recombinant carbohydrate recognition domain (CRD) of human SP-A inhibits the binding of human SP-A to galactosyl ceramide and to galactose- and mannose-bovine serum albumin, indicating that the CRD is directly involved in the binding of SP-A to these ligands.	Galactose	131-140	surfactant protein A1	Homo sapiens	96-100
1577827-10	1992	A recombinant carbohydrate recognition domain (CRD) of human SP-A inhibits the binding of human SP-A to galactosyl ceramide and to galactose- and mannose-bovine serum albumin, indicating that the CRD is directly involved in the binding of SP-A to these ligands.	Galactose	131-140	surfactant protein A1	Homo sapiens	96-100
1577827-10	1992	A recombinant carbohydrate recognition domain (CRD) of human SP-A inhibits the binding of human SP-A to galactosyl ceramide and to galactose- and mannose-bovine serum albumin, indicating that the CRD is directly involved in the binding of SP-A to these ligands.	Mannose	146-153	surfactant protein A1	Homo sapiens	61-65
1577827-10	1992	A recombinant carbohydrate recognition domain (CRD) of human SP-A inhibits the binding of human SP-A to galactosyl ceramide and to galactose- and mannose-bovine serum albumin, indicating that the CRD is directly involved in the binding of SP-A to these ligands.	Mannose	146-153	surfactant protein A1	Homo sapiens	96-100
1577827-10	1992	A recombinant carbohydrate recognition domain (CRD) of human SP-A inhibits the binding of human SP-A to galactosyl ceramide and to galactose- and mannose-bovine serum albumin, indicating that the CRD is directly involved in the binding of SP-A to these ligands.	Mannose	146-153	surfactant protein A1	Homo sapiens	96-100
1577827-11	1992	These results provide evidence for a novel type of binding specificity for proteins that have Ca(2+)-dependent CRDs and raise the possibility that glycosphingolipids are endogenous ligands for SP-A.	Glycosphingolipids	147-165	surfactant protein A1	Homo sapiens	193-197
1327036-1	1992	We examined expression of the major surfactant-associated protein SP-A, a product characteristic of type II pneumocytes, in a panel of 126 non-small-cell lung carcinomas (NSCLC) by immunohistochemistry using routine paraffin-embedded material.	Paraffin	216-224	surfactant protein A1	Homo sapiens	66-70
1767859-10	1991	Defects in the ability of the SP-A gene to respond to extrauterine exposure and hyperoxia may be contributing to development of bronchopulmonary dysplasia, a common clinical complication of premature birth in humans.	extrauterine	54-66	surfactant protein A1	Homo sapiens	30-34
1805157-1	1991	Surfactant proteins A and B (SP-A and SP-B) were measured in human amniotic fluid by ELISA and correlated with lecithin to sphingomyelin ratio (L/S), phosphatidylglycerol (PG), and perinatal outcome.	Lecithins	111-119	surfactant protein A1	Homo sapiens	0-27
1805157-1	1991	Surfactant proteins A and B (SP-A and SP-B) were measured in human amniotic fluid by ELISA and correlated with lecithin to sphingomyelin ratio (L/S), phosphatidylglycerol (PG), and perinatal outcome.	Sphingomyelins	123-136	surfactant protein A1	Homo sapiens	0-27
1909733-5	1991	We found that 22% of the IgA and 15% of the IgG F(ab")2 bound to SPA-agarose.	Sepharose	69-76	surfactant protein A1	Homo sapiens	65-68
1373885-6	1992	MAb and polyclonal antibodies specific for B blood group antigen failed to react with SP-A from this patient or from patients who were in blood group B. Reactivity of anti-blood group MAb was lost after treatment of SP-A with endoglycosidase-F, demonstrating its reactivity with an epitope dependent on the asparagine-linked oligosaccharide at asparagine 187.	asparagine-linked oligosaccharide	307-340	surfactant protein A1	Homo sapiens	216-220
1373885-6	1992	MAb and polyclonal antibodies specific for B blood group antigen failed to react with SP-A from this patient or from patients who were in blood group B. Reactivity of anti-blood group MAb was lost after treatment of SP-A with endoglycosidase-F, demonstrating its reactivity with an epitope dependent on the asparagine-linked oligosaccharide at asparagine 187.	Asparagine	307-317	surfactant protein A1	Homo sapiens	216-220
1373885-7	1992	Reactivity of MAb-8 with SP-A persisted after endoglycosidase-F treatment, but was lost after digestion with collagenase as assessed by Western blot after SDS-PAGE.	Sodium Dodecyl Sulfate	155-158	surfactant protein A1	Homo sapiens	25-29
1373885-8	1992	Reactivity of MAb to SP-A was sensitive to beta-elimination, supporting the presence of another blood group antigenic site distinct from the epitope dependent on the asparagine-linked carbohydrate.	asparagine-linked carbohydrate	166-196	surfactant protein A1	Homo sapiens	21-25
1310226-0	1992	Exposure of surfactant protein A to ozone in vitro and in vivo impairs its interactions with alveolar cells.	Ozone	36-41	surfactant protein A1	Homo sapiens	12-32
1310226-2	1992	In vitro exposure of human or canine SP-A to ozone reduced the ability of this protein to inhibit phorbol-ester induced secretion of [3H]phosphatidylcholine by alveolar type II cells in culture.	Phorbol Esters	98-111	surfactant protein A1	Homo sapiens	37-41
1310226-2	1992	In vitro exposure of human or canine SP-A to ozone reduced the ability of this protein to inhibit phorbol-ester induced secretion of [3H]phosphatidylcholine by alveolar type II cells in culture.	[3h]phosphatidylcholine	133-156	surfactant protein A1	Homo sapiens	37-41
1310226-3	1992	Ozone-exposed human SP-A showed a decreased ability to enhance phagocytosis of herpes simplex virus and to stimulate superoxide anion production by alveolar macrophages.	Superoxides	117-133	surfactant protein A1	Homo sapiens	20-24
1310226-7	1992	The results of this study suggest that SP-A-alveolar cell interactions can be inhibited by ozone exposure, which may contribute to the toxicity of ozone in the lungs.	Ozone	91-96	surfactant protein A1	Homo sapiens	39-43
1310226-7	1992	The results of this study suggest that SP-A-alveolar cell interactions can be inhibited by ozone exposure, which may contribute to the toxicity of ozone in the lungs.	Ozone	147-152	surfactant protein A1	Homo sapiens	39-43
1958377-2	1991	Acute exposure to 100% O2 results in severe decreases in respiratory function and is accompanied by alterations in pulmonary surfactant metabolism, including the regulation of surfactant proteins A, B, and C (SP-A, SP-B, SP-C).	Oxygen	23-25	surfactant protein A1	Homo sapiens	176-207
1958377-2	1991	Acute exposure to 100% O2 results in severe decreases in respiratory function and is accompanied by alterations in pulmonary surfactant metabolism, including the regulation of surfactant proteins A, B, and C (SP-A, SP-B, SP-C).	Oxygen	23-25	surfactant protein A1	Homo sapiens	209-213
1872418-4	1991	In vitro exposure of human and canine SP-A to ozone led to decreases in 1) self-association of SP-A, 2) SP-A-mediated lipid aggregation, and 3) binding of SP-A to immobilized mannose.	Mannose	175-182	surfactant protein A1	Homo sapiens	38-42
1872418-8	1991	Oxidation of methionine and tryptophan residues in canine SP-A was detected following ozone exposure.	Methionine	13-23	surfactant protein A1	Homo sapiens	58-62
1872418-8	1991	Oxidation of methionine and tryptophan residues in canine SP-A was detected following ozone exposure.	Tryptophan	28-38	surfactant protein A1	Homo sapiens	58-62
1651668-5	1991	The addition of SP-A to the system was sufficient for the phagocytosis of FITC-HSV-1 by the alveolar macrophages, suggesting that SP-A acts as an opsonin.	Fluorescein-5-isothiocyanate	74-78	surfactant protein A1	Homo sapiens	16-20
1651668-5	1991	The addition of SP-A to the system was sufficient for the phagocytosis of FITC-HSV-1 by the alveolar macrophages, suggesting that SP-A acts as an opsonin.	Fluorescein-5-isothiocyanate	74-78	surfactant protein A1	Homo sapiens	130-134
1651668-6	1991	This hypothesis was further strengthened by the observation that F(ab")2 fragments of immunoglobulin G directed against SP-A could abolish FITC-HSV-1 phagocytosis by alveolar macrophages preincubated with SP-A.	ab")2	67-72	surfactant protein A1	Homo sapiens	120-124
1651668-6	1991	This hypothesis was further strengthened by the observation that F(ab")2 fragments of immunoglobulin G directed against SP-A could abolish FITC-HSV-1 phagocytosis by alveolar macrophages preincubated with SP-A.	ab")2	67-72	surfactant protein A1	Homo sapiens	205-209
1651668-6	1991	This hypothesis was further strengthened by the observation that F(ab")2 fragments of immunoglobulin G directed against SP-A could abolish FITC-HSV-1 phagocytosis by alveolar macrophages preincubated with SP-A.	Fluorescein-5-isothiocyanate	139-143	surfactant protein A1	Homo sapiens	120-124
1651668-7	1991	Comparing the opsonic capacity of serum and SP-A, SP-A proved to be twice as potent as serum in stimulating phagocytosis of FITC-HSV-1 by alveolar macrophages.	Fluorescein-5-isothiocyanate	124-128	surfactant protein A1	Homo sapiens	50-54
2018482-3	1991	We report here that vesicle aggregation is mediated by Ca2(+)-induced interactions between carbohydrate-binding domains and oligosaccharide moieties of SP-A.	Carbohydrates	91-103	surfactant protein A1	Homo sapiens	152-156
1709859-5	1991	Isobutylmethylxanthine accelerated and indomethacin inhibited the increases during culture in surfactant protein-A (SP-A), SP-A mRNA, SP-B mRNA, phosphatidylcholine content, and activity of fatty acid synthetase.	1-Methyl-3-isobutylxanthine	0-22	surfactant protein A1	Homo sapiens	94-114
1709859-5	1991	Isobutylmethylxanthine accelerated and indomethacin inhibited the increases during culture in surfactant protein-A (SP-A), SP-A mRNA, SP-B mRNA, phosphatidylcholine content, and activity of fatty acid synthetase.	1-Methyl-3-isobutylxanthine	0-22	surfactant protein A1	Homo sapiens	116-120
1709859-5	1991	Isobutylmethylxanthine accelerated and indomethacin inhibited the increases during culture in surfactant protein-A (SP-A), SP-A mRNA, SP-B mRNA, phosphatidylcholine content, and activity of fatty acid synthetase.	1-Methyl-3-isobutylxanthine	0-22	surfactant protein A1	Homo sapiens	123-127
1709859-5	1991	Isobutylmethylxanthine accelerated and indomethacin inhibited the increases during culture in surfactant protein-A (SP-A), SP-A mRNA, SP-B mRNA, phosphatidylcholine content, and activity of fatty acid synthetase.	Indomethacin	39-51	surfactant protein A1	Homo sapiens	94-114
1709859-5	1991	Isobutylmethylxanthine accelerated and indomethacin inhibited the increases during culture in surfactant protein-A (SP-A), SP-A mRNA, SP-B mRNA, phosphatidylcholine content, and activity of fatty acid synthetase.	Indomethacin	39-51	surfactant protein A1	Homo sapiens	123-127
1709859-7	1991	Increasing concentrations of prostaglandins E1 and E2 in the presence of indomethacin produced a parallel stimulation of cAMP content, SP-A, and fatty acid synthetase activity.	Alprostadil	29-46	surfactant protein A1	Homo sapiens	135-139
1709859-7	1991	Increasing concentrations of prostaglandins E1 and E2 in the presence of indomethacin produced a parallel stimulation of cAMP content, SP-A, and fatty acid synthetase activity.	Estradiol	51-53	surfactant protein A1	Homo sapiens	135-139
2064123-5	1991	SP-A has been reported to be essential for the formation of tubular myelin, to facilitate the adsorption of phospholipid to the air/liquid interface, and to stimulate uptake and inhibit secretion of surfactant in vitro.	Phospholipids	108-120	surfactant protein A1	Homo sapiens	0-4
1709859-7	1991	Increasing concentrations of prostaglandins E1 and E2 in the presence of indomethacin produced a parallel stimulation of cAMP content, SP-A, and fatty acid synthetase activity.	Indomethacin	73-85	surfactant protein A1	Homo sapiens	135-139
1656980-0	1991	Roles of collagenous domain and oligosaccharide moiety of pulmonary surfactant protein A in interactions with phospholipids.	Oligosaccharides	32-47	surfactant protein A1	Homo sapiens	58-88
1656980-0	1991	Roles of collagenous domain and oligosaccharide moiety of pulmonary surfactant protein A in interactions with phospholipids.	Phospholipids	110-123	surfactant protein A1	Homo sapiens	58-88
1656980-1	1991	Pulmonary surfactant protein A (SP-A), a main component of lung-specific lipid-protein complex (pulmonary surfactant), is characterized by a collagen-like sequence in its amino terminal half and by N-linked glycosylation.	Nitrogen	198-199	surfactant protein A1	Homo sapiens	0-30
1656980-1	1991	Pulmonary surfactant protein A (SP-A), a main component of lung-specific lipid-protein complex (pulmonary surfactant), is characterized by a collagen-like sequence in its amino terminal half and by N-linked glycosylation.	Nitrogen	198-199	surfactant protein A1	Homo sapiens	32-36
1656980-3	1991	In the present study we examined the roles of the oligosaccharide moiety of SP-A and its collagenous domain in causing the aggregation of phospholipid liposomes and enhancing the uptake of phospholipids by type II cells.	Oligosaccharides	50-65	surfactant protein A1	Homo sapiens	76-80
1656980-3	1991	In the present study we examined the roles of the oligosaccharide moiety of SP-A and its collagenous domain in causing the aggregation of phospholipid liposomes and enhancing the uptake of phospholipids by type II cells.	Phospholipids	138-150	surfactant protein A1	Homo sapiens	76-80
1656980-3	1991	In the present study we examined the roles of the oligosaccharide moiety of SP-A and its collagenous domain in causing the aggregation of phospholipid liposomes and enhancing the uptake of phospholipids by type II cells.	Phospholipids	189-202	surfactant protein A1	Homo sapiens	76-80
1656980-6	1991	Deglycosylated SP-A was able to enhance the uptake of phospholipids by type II cells, whereas removal of the collagenous domain of SP-A resulted in the loss of the ability to enhance phospholipid uptake.	Phospholipids	54-67	surfactant protein A1	Homo sapiens	15-19
1656980-6	1991	Deglycosylated SP-A was able to enhance the uptake of phospholipids by type II cells, whereas removal of the collagenous domain of SP-A resulted in the loss of the ability to enhance phospholipid uptake.	Phospholipids	54-66	surfactant protein A1	Homo sapiens	15-19
2018482-3	1991	We report here that vesicle aggregation is mediated by Ca2(+)-induced interactions between carbohydrate-binding domains and oligosaccharide moieties of SP-A.	Oligosaccharides	124-139	surfactant protein A1	Homo sapiens	152-156
1653895-2	1991	In previous studies we observed that dexamethasone has dose-dependent biphasic effects on the levels of SP-A and its mRNA in human fetal lung in vitro.	Dexamethasone	37-50	surfactant protein A1	Homo sapiens	104-108
1653895-3	1991	At concentrations of 10(-10)-10(-9) M, dexamethasone increased the levels of SP-A and its mRNA over those of control tissues, whereas at concentrations greater than or equal to 10(-8) M, the steroid was markedly inhibitory.	Dexamethasone	39-52	surfactant protein A1	Homo sapiens	77-81
1653895-4	1991	Our findings suggest that the inhibitory action of dexamethasone (greater than 10(-8) M) on SP-A mRNA levels was mediated by an effect to reduce SP-A mRNA stability, since the steroid caused a dose-dependent increase in the rate of transcription; however, an effect to increase transcription with premature termination leading to instability of mRNA transcripts could not be ruled out.	Dexamethasone	51-64	surfactant protein A1	Homo sapiens	92-96
1653895-4	1991	Our findings suggest that the inhibitory action of dexamethasone (greater than 10(-8) M) on SP-A mRNA levels was mediated by an effect to reduce SP-A mRNA stability, since the steroid caused a dose-dependent increase in the rate of transcription; however, an effect to increase transcription with premature termination leading to instability of mRNA transcripts could not be ruled out.	Dexamethasone	51-64	surfactant protein A1	Homo sapiens	145-149
1653895-4	1991	Our findings suggest that the inhibitory action of dexamethasone (greater than 10(-8) M) on SP-A mRNA levels was mediated by an effect to reduce SP-A mRNA stability, since the steroid caused a dose-dependent increase in the rate of transcription; however, an effect to increase transcription with premature termination leading to instability of mRNA transcripts could not be ruled out.	Steroids	176-183	surfactant protein A1	Homo sapiens	92-96
1653895-4	1991	Our findings suggest that the inhibitory action of dexamethasone (greater than 10(-8) M) on SP-A mRNA levels was mediated by an effect to reduce SP-A mRNA stability, since the steroid caused a dose-dependent increase in the rate of transcription; however, an effect to increase transcription with premature termination leading to instability of mRNA transcripts could not be ruled out.	Steroids	176-183	surfactant protein A1	Homo sapiens	145-149
1653895-9	1991	After 12 h of incubation in the presence of actinomycin-D and dexamethasone at 10(-9) and 10(-7) M, the levels of SP-A mRNA were reduced by 50% and 80%, respectively, compared to those in tissue incubated with actinomycin-D alone.	Dactinomycin	44-57	surfactant protein A1	Homo sapiens	114-118
1653895-9	1991	After 12 h of incubation in the presence of actinomycin-D and dexamethasone at 10(-9) and 10(-7) M, the levels of SP-A mRNA were reduced by 50% and 80%, respectively, compared to those in tissue incubated with actinomycin-D alone.	Dexamethasone	62-75	surfactant protein A1	Homo sapiens	114-118
1653895-9	1991	After 12 h of incubation in the presence of actinomycin-D and dexamethasone at 10(-9) and 10(-7) M, the levels of SP-A mRNA were reduced by 50% and 80%, respectively, compared to those in tissue incubated with actinomycin-D alone.	Dactinomycin	210-223	surfactant protein A1	Homo sapiens	114-118
1653895-10	1991	The inhibitory effects of glucocorticoids on SP-A mRNA levels were completely reversible and were blocked by the glucocorticoid antagonist RU486.	Mifepristone	139-144	surfactant protein A1	Homo sapiens	45-49
2042967-8	1991	Cyclic AMP and glucocorticoids have pronounced effects on the regulation of SP-A gene expression in human and rabbit fetal lung in culture.	Cyclic AMP	0-10	surfactant protein A1	Homo sapiens	76-80
2042967-11	1991	Furthermore, the combined effects of cAMP and glucocorticoids on SP-A gene transcription in human fetal lung in vitro are synergistic.	Cyclic AMP	37-41	surfactant protein A1	Homo sapiens	65-69
2249989-0	1990	Phorbol ester inhibits surfactant protein SP-A and SP-B expression.	Phorbol Esters	0-13	surfactant protein A1	Homo sapiens	42-46
1651967-3	1991	SP-A synthesis and gene expression are initiated in fetal lung tissue in concert with the developmental induction of surfactant glycerophospholipid synthesis.	Glycerophospholipids	128-147	surfactant protein A1	Homo sapiens	0-4
1651967-4	1991	In studies using midtrimester human fetal lung explants maintained in organ culture, we have observed that cyclic AMP and glucocorticoids have pronounced effects on morphologic development and on the levels of SP-A gene expression.	Cyclic AMP	107-117	surfactant protein A1	Homo sapiens	210-214
1651967-5	1991	Cyclic AMP analogues act primarily to induce SP-A gene transcription; whereas, glucocorticoids have complex effects at both the transcriptional and posttranscriptional levels.	Cyclic AMP	0-10	surfactant protein A1	Homo sapiens	45-49
1651967-7	1991	The prostaglandin synthesis inhibitor, indomethacin, markedly inhibits SP-A gene expression and cyclic AMP formation by human fetal lung in culture; the inhibitory effect of indomethacin on SP-A gene expression can be prevented by simultaneous incubation with either Bt2cAMP or PGE2.	Prostaglandins	4-17	surfactant protein A1	Homo sapiens	71-75
1651967-7	1991	The prostaglandin synthesis inhibitor, indomethacin, markedly inhibits SP-A gene expression and cyclic AMP formation by human fetal lung in culture; the inhibitory effect of indomethacin on SP-A gene expression can be prevented by simultaneous incubation with either Bt2cAMP or PGE2.	Indomethacin	39-51	surfactant protein A1	Homo sapiens	71-75
1651967-7	1991	The prostaglandin synthesis inhibitor, indomethacin, markedly inhibits SP-A gene expression and cyclic AMP formation by human fetal lung in culture; the inhibitory effect of indomethacin on SP-A gene expression can be prevented by simultaneous incubation with either Bt2cAMP or PGE2.	Indomethacin	174-186	surfactant protein A1	Homo sapiens	190-194
1651967-7	1991	The prostaglandin synthesis inhibitor, indomethacin, markedly inhibits SP-A gene expression and cyclic AMP formation by human fetal lung in culture; the inhibitory effect of indomethacin on SP-A gene expression can be prevented by simultaneous incubation with either Bt2cAMP or PGE2.	Bucladesine	267-274	surfactant protein A1	Homo sapiens	190-194
1651967-7	1991	The prostaglandin synthesis inhibitor, indomethacin, markedly inhibits SP-A gene expression and cyclic AMP formation by human fetal lung in culture; the inhibitory effect of indomethacin on SP-A gene expression can be prevented by simultaneous incubation with either Bt2cAMP or PGE2.	Dinoprostone	278-282	surfactant protein A1	Homo sapiens	190-194
1651967-8	1991	These findings are suggestive that prostaglandins acting through cyclic AMP also may serve an important role in the regulation of SP-A gene expression in human fetal lung tissue.	Prostaglandins	35-49	surfactant protein A1	Homo sapiens	130-134
1651967-8	1991	These findings are suggestive that prostaglandins acting through cyclic AMP also may serve an important role in the regulation of SP-A gene expression in human fetal lung tissue.	Cyclic AMP	65-75	surfactant protein A1	Homo sapiens	130-134
1667556-7	1991	Excessive accumulation of surfactant protein A and surfactant phospholipids in the alveoli could arise from their overproduction and hypersecretion by a subpopulation of Type II cells that are activated by silica, and possibly other agents.	Silicon Dioxide	206-212	surfactant protein A1	Homo sapiens	26-46
2249989-9	1990	Actinomycin D completely blocked the rapid decrease in SP-A and SP-B mRNAs caused by the phorbol ester, consistent with the concept that the inhibitory effect of TPA on the surfactant protein mRNAs required continued gene transcription and was not mediated solely by changes in SP-A or SP-B transcription.	Dactinomycin	0-13	surfactant protein A1	Homo sapiens	278-282
2249989-9	1990	Actinomycin D completely blocked the rapid decrease in SP-A and SP-B mRNAs caused by the phorbol ester, consistent with the concept that the inhibitory effect of TPA on the surfactant protein mRNAs required continued gene transcription and was not mediated solely by changes in SP-A or SP-B transcription.	Phorbol Esters	89-102	surfactant protein A1	Homo sapiens	55-59
2249989-9	1990	Actinomycin D completely blocked the rapid decrease in SP-A and SP-B mRNAs caused by the phorbol ester, consistent with the concept that the inhibitory effect of TPA on the surfactant protein mRNAs required continued gene transcription and was not mediated solely by changes in SP-A or SP-B transcription.	Phorbol Esters	89-102	surfactant protein A1	Homo sapiens	278-282
2249989-9	1990	Actinomycin D completely blocked the rapid decrease in SP-A and SP-B mRNAs caused by the phorbol ester, consistent with the concept that the inhibitory effect of TPA on the surfactant protein mRNAs required continued gene transcription and was not mediated solely by changes in SP-A or SP-B transcription.	Tetradecanoylphorbol Acetate	162-165	surfactant protein A1	Homo sapiens	55-59
2249989-9	1990	Actinomycin D completely blocked the rapid decrease in SP-A and SP-B mRNAs caused by the phorbol ester, consistent with the concept that the inhibitory effect of TPA on the surfactant protein mRNAs required continued gene transcription and was not mediated solely by changes in SP-A or SP-B transcription.	Tetradecanoylphorbol Acetate	162-165	surfactant protein A1	Homo sapiens	278-282
2249989-10	1990	Inhibitory effects of phorbol esters on SP-A and SP-B synthesis support the concept that protein kinase C modulates surfactant protein expression in this cell.	Phorbol Esters	22-36	surfactant protein A1	Homo sapiens	40-44
2249989-1	1990	Effects of the tumor promoter, 12-O-tetradecanoylphorbol-13-acetate (TPA), on expression of pulmonary surfactant proteins, SP-A and SP-B, were determined in a human pulmonary adenocarcinoma cell line (H441-4).	Tetradecanoylphorbol Acetate	69-72	surfactant protein A1	Homo sapiens	123-127
2249989-2	1990	TPA decreased cellular SP-A content in association with decreased de novo synthesis of SP-A as assessed by [35S]methionine incorporation.	Tetradecanoylphorbol Acetate	0-3	surfactant protein A1	Homo sapiens	23-27
2249989-2	1990	TPA decreased cellular SP-A content in association with decreased de novo synthesis of SP-A as assessed by [35S]methionine incorporation.	Tetradecanoylphorbol Acetate	0-3	surfactant protein A1	Homo sapiens	87-91
2249989-2	1990	TPA decreased cellular SP-A content in association with decreased de novo synthesis of SP-A as assessed by [35S]methionine incorporation.	Sulfur-35	108-111	surfactant protein A1	Homo sapiens	87-91
2249989-2	1990	TPA decreased cellular SP-A content in association with decreased de novo synthesis of SP-A as assessed by [35S]methionine incorporation.	Methionine	112-122	surfactant protein A1	Homo sapiens	87-91
2249989-4	1990	Phorbol 12,13-dibutyrate (PDBu), and adenosine 5"-O-(3-thiotriphosphate), and 1-oleoyl-2-acetyl-sn-glycerol also decreased SP-A content in these cells.	Phorbol 12,13-Dibutyrate	0-24	surfactant protein A1	Homo sapiens	123-127
2249989-4	1990	Phorbol 12,13-dibutyrate (PDBu), and adenosine 5"-O-(3-thiotriphosphate), and 1-oleoyl-2-acetyl-sn-glycerol also decreased SP-A content in these cells.	adenosine 5'-O-(3-thiotriphosphate)	37-71	surfactant protein A1	Homo sapiens	123-127
2175559-9	1990	Exposure of the explants to alpha-aminobutyric acid, a butyric acid analogue which is elevated in the blood of infants of diabetic mothers, resulted in a significant decrease in SP-A mRNA at a concentration 1/25 of that required for Na butyrate.	alpha-aminobutyric acid	28-51	surfactant protein A1	Homo sapiens	178-182
2175559-9	1990	Exposure of the explants to alpha-aminobutyric acid, a butyric acid analogue which is elevated in the blood of infants of diabetic mothers, resulted in a significant decrease in SP-A mRNA at a concentration 1/25 of that required for Na butyrate.	Butyric Acid	39-51	surfactant protein A1	Homo sapiens	178-182
2249989-4	1990	Phorbol 12,13-dibutyrate (PDBu), and adenosine 5"-O-(3-thiotriphosphate), and 1-oleoyl-2-acetyl-sn-glycerol also decreased SP-A content in these cells.	1-oleoyl-2-acetylglycerol	78-107	surfactant protein A1	Homo sapiens	123-127
2249989-6	1990	Inhibitory effects of TPA on SP-A synthesis were associated with concomitant decreases in SP-A mRNA.	Tetradecanoylphorbol Acetate	22-25	surfactant protein A1	Homo sapiens	29-33
2249989-6	1990	Inhibitory effects of TPA on SP-A synthesis were associated with concomitant decreases in SP-A mRNA.	Tetradecanoylphorbol Acetate	22-25	surfactant protein A1	Homo sapiens	90-94
2249989-8	1990	SP-A and SP-B mRNA contents decreased more rapidly after treatment with TPA than after actinomycin D.	Tetradecanoylphorbol Acetate	72-75	surfactant protein A1	Homo sapiens	0-4
2249989-8	1990	SP-A and SP-B mRNA contents decreased more rapidly after treatment with TPA than after actinomycin D.	Dactinomycin	87-100	surfactant protein A1	Homo sapiens	0-4
2249989-9	1990	Actinomycin D completely blocked the rapid decrease in SP-A and SP-B mRNAs caused by the phorbol ester, consistent with the concept that the inhibitory effect of TPA on the surfactant protein mRNAs required continued gene transcription and was not mediated solely by changes in SP-A or SP-B transcription.	Dactinomycin	0-13	surfactant protein A1	Homo sapiens	55-59
2261350-0	1990	Abnormal tryptic peptide from the spectrin alpha-chain resulting from alpha- or beta-chain mutations: two genetically distinct forms of the Sp alpha I/74 variant.	Peptides	17-24	surfactant protein A1	Homo sapiens	140-148
2271565-0	1990	Binding of calcium to SP-A, a surfactant-associated protein.	Calcium	11-18	surfactant protein A1	Homo sapiens	22-26
2271565-1	1990	SP-A is a lung-specific pulmonary surfactant-associated protein containing a calcium-dependent carbohydrate recognition domain and collagen-like sequence.	Calcium	77-84	surfactant protein A1	Homo sapiens	0-4
2271565-1	1990	SP-A is a lung-specific pulmonary surfactant-associated protein containing a calcium-dependent carbohydrate recognition domain and collagen-like sequence.	Carbohydrates	95-107	surfactant protein A1	Homo sapiens	0-4
2271565-4	1990	These properties of SP-A are dependent on the presence of calcium.	Calcium	58-65	surfactant protein A1	Homo sapiens	20-24
2271565-5	1990	We have estimated calcium binding parameters for SP-A from binding data obtained by equilibrium dialysis and gel permeation chromatography.	Calcium	18-25	surfactant protein A1	Homo sapiens	49-53
2271565-6	1990	Our results suggest that each SP-A monomer binds two to three calcium ions in conditions chosen as similar to those found in the alveolar lumen.	Calcium	62-69	surfactant protein A1	Homo sapiens	30-34
2271565-8	1990	Studies with a fragment of SP-A generated by limited proteolysis suggest the higher affinity site for calcium is located in the noncollagenous carboxy-terminal end of SP-A.	Calcium	102-109	surfactant protein A1	Homo sapiens	27-31
2271565-8	1990	Studies with a fragment of SP-A generated by limited proteolysis suggest the higher affinity site for calcium is located in the noncollagenous carboxy-terminal end of SP-A.	Calcium	102-109	surfactant protein A1	Homo sapiens	167-171
2271565-9	1990	This region of SP-A contains a carbohydrate recognition domain homologous to other C-type lectins.	Carbohydrates	31-43	surfactant protein A1	Homo sapiens	15-19
2271565-10	1990	The binding of calcium to this region of SP-A causes a conformational change as assessed by a small change in the intrinsic fluorescence spectrum and a marked change in the susceptibility to proteolysis.	Calcium	15-22	surfactant protein A1	Homo sapiens	41-45
2271565-11	1990	At physiological calcium concentrations, intact SP-A aggregates in a reversible fashion, a property that may be relevant to the formation of tubular myelin.	Calcium	17-24	surfactant protein A1	Homo sapiens	48-52
2322594-5	1990	Adsorption of lamellar bodies to an air/water interface was moderately rapid, but accelerated dramatically upon addition of exogenous SP-A in ratios of 1:2-16 (SP-A:phospholipid, w/w).	Phospholipids	165-177	surfactant protein A1	Homo sapiens	134-138
2167205-0	1990	Prostaglandins regulate surfactant protein A (SP-A) gene expression in human fetal lung in vitro.	Prostaglandins	0-14	surfactant protein A1	Homo sapiens	24-44
2167205-0	1990	Prostaglandins regulate surfactant protein A (SP-A) gene expression in human fetal lung in vitro.	Prostaglandins	0-14	surfactant protein A1	Homo sapiens	46-50
2167205-1	1990	We previously have observed that dexamethasone has a biphasic effect on surfactant protein A (SP-A) mRNA levels in human fetal lung in vitro.	Dexamethasone	33-46	surfactant protein A1	Homo sapiens	72-92
2167205-1	1990	We previously have observed that dexamethasone has a biphasic effect on surfactant protein A (SP-A) mRNA levels in human fetal lung in vitro.	Dexamethasone	33-46	surfactant protein A1	Homo sapiens	94-98
2167205-2	1990	At concentrations of 10(-10)-10(-9) M, dexamethasone increases the levels of SP-A mRNA, whereas, at concentrations greater than 10(-8) M, the steroid is markedly inhibitory.	Dexamethasone	39-52	surfactant protein A1	Homo sapiens	77-81
2167205-3	1990	In studies to define the molecular mechanisms for these effects, we observed that dexamethasone causes a dose-dependent stimulation of SP-A gene transcription, but paradoxically causes a dose-dependent inhibition of SP-A mRNA stability.	Dexamethasone	82-95	surfactant protein A1	Homo sapiens	135-139
2167205-3	1990	In studies to define the molecular mechanisms for these effects, we observed that dexamethasone causes a dose-dependent stimulation of SP-A gene transcription, but paradoxically causes a dose-dependent inhibition of SP-A mRNA stability.	Dexamethasone	82-95	surfactant protein A1	Homo sapiens	216-220
2167205-4	1990	In light of the well-characterized inhibitory effect of glucocorticoids on prostaglandin (PG) synthesis in a number of tissues, it was our objective in the present study to investigate the role of PGs on SP-A gene expression in human fetal lung in vitro and to determine whether the action of dexamethasone (greater than 10(-8) M) to reduce SP-A mRNA levels could be mediated by its effect to inhibit PG synthesis.	Phosphatidylglycerols	197-200	surfactant protein A1	Homo sapiens	204-208
2167205-4	1990	In light of the well-characterized inhibitory effect of glucocorticoids on prostaglandin (PG) synthesis in a number of tissues, it was our objective in the present study to investigate the role of PGs on SP-A gene expression in human fetal lung in vitro and to determine whether the action of dexamethasone (greater than 10(-8) M) to reduce SP-A mRNA levels could be mediated by its effect to inhibit PG synthesis.	Prostaglandins	197-199	surfactant protein A1	Homo sapiens	204-208
2167205-6	1990	Indomethacin, which also caused a pronounced reduction in the levels of these secreted prostanoids, had a marked effect to reduce SP-A mRNA levels in human fetal lung in vitro.	Indomethacin	0-12	surfactant protein A1	Homo sapiens	130-134
2167205-6	1990	Indomethacin, which also caused a pronounced reduction in the levels of these secreted prostanoids, had a marked effect to reduce SP-A mRNA levels in human fetal lung in vitro.	Prostaglandins	87-98	surfactant protein A1	Homo sapiens	130-134
2167205-11	1990	The finding that the inhibitory action of dexamethasone (10(-7) M) on SP-A mRNA levels could not be prevented by simultaneous incubation with either PGE2 or dibutyryl cAMP and that dexamethasone had no apparent effect on cAMP formation by the fetal lung in vitro is suggestive that the action of dexamethasone (greater than or equal to 10(-8) M) to reduce SP-A mRNA levels is mediated at least in part by actions alternative to its inhibitory effects on PG synthesis.	Dexamethasone	42-55	surfactant protein A1	Homo sapiens	70-74
2167205-11	1990	The finding that the inhibitory action of dexamethasone (10(-7) M) on SP-A mRNA levels could not be prevented by simultaneous incubation with either PGE2 or dibutyryl cAMP and that dexamethasone had no apparent effect on cAMP formation by the fetal lung in vitro is suggestive that the action of dexamethasone (greater than or equal to 10(-8) M) to reduce SP-A mRNA levels is mediated at least in part by actions alternative to its inhibitory effects on PG synthesis.	Dexamethasone	42-55	surfactant protein A1	Homo sapiens	356-360
2163206-5	1990	Limited studies suggest that secretion of surfactant protein A may be regulated by both cAMP-dependent and protein kinase C-dependent pathways.	Cyclic AMP	88-92	surfactant protein A1	Homo sapiens	42-62
2248600-14	1990	In addition, cyclic AMP and glucocorticoids act synergistically to increase SP-A gene transcription in human fetal lung in vitro.	Cyclic AMP	13-23	surfactant protein A1	Homo sapiens	76-80
2328319-6	1990	Reassociation studies using isolated Sp alpha and beta chains from an affected patient and an unaffected control subject showed that the Sp alpha I/74 Kd abnormal tryptic peptide resulted from a defect in the Sp alpha chain.	Peptides	171-178	surfactant protein A1	Homo sapiens	37-45
2328319-6	1990	Reassociation studies using isolated Sp alpha and beta chains from an affected patient and an unaffected control subject showed that the Sp alpha I/74 Kd abnormal tryptic peptide resulted from a defect in the Sp alpha chain.	Peptides	171-178	surfactant protein A1	Homo sapiens	137-145
2328319-6	1990	Reassociation studies using isolated Sp alpha and beta chains from an affected patient and an unaffected control subject showed that the Sp alpha I/74 Kd abnormal tryptic peptide resulted from a defect in the Sp alpha chain.	Peptides	171-178	surfactant protein A1	Homo sapiens	137-145
2328319-7	1990	Partial amino acid sequencing showed that the Sp alpha I/74 Kd peptide resulted from cleavage at lysine residue 42 of the Sp alpha I/80 Kd domain.	Lysine	97-103	surfactant protein A1	Homo sapiens	46-54
2328319-7	1990	Partial amino acid sequencing showed that the Sp alpha I/74 Kd peptide resulted from cleavage at lysine residue 42 of the Sp alpha I/80 Kd domain.	Lysine	97-103	surfactant protein A1	Homo sapiens	122-130
33823299-0	2021	Inflammatory response in human alveolar epithelial cells after TiO2 NPs or ZnO NPs exposure: inhibition of surfactant protein A expression as an indicator for loss of lung function.	titanium dioxide	63-67	surfactant protein A1	Homo sapiens	107-127
2324274-7	1990	There was a significant association between SpA antibody levels and either immunoglobulin G or immunoglobulin M teichoic acid antibody levels (r = 0.406, P less than 0.05; r = 0.571, P = 0.002, respectively).	Teichoic Acids	112-125	surfactant protein A1	Homo sapiens	44-47
2101805-9	1990	The percent of cells bound on SpA-Sepharose varied between 6% and 66%, representing the hairy cells with labile-bound smIgG.	Sepharose	34-43	surfactant protein A1	Homo sapiens	30-33
2277737-2	1990	Patients on HFOV had markedly lower BAL SP-A concentrations on days 1 and 2 compared to those on CMV, which may indicate influence of mode of ventilation on surfactant metabolism.	hfov	12-16	surfactant protein A1	Homo sapiens	40-44
2308037-5	1990	This increase in surfactant protein A content may reflect lung recovery from barotrauma and oxygen toxic effects or be a response to the primary pulmonary disease process.	Oxygen	92-98	surfactant protein A1	Homo sapiens	17-37
2106332-3	1990	Treatment for 3 days with IFN-gamma alone, dexamethasone alone, and IFN plus dexamethasone increased the content of surfactant protein A (SP-A, 28 to 36 kD) by approximately 3-, 2.5-, and 10-fold, respectively.	Dexamethasone	43-56	surfactant protein A1	Homo sapiens	116-136
2106332-3	1990	Treatment for 3 days with IFN-gamma alone, dexamethasone alone, and IFN plus dexamethasone increased the content of surfactant protein A (SP-A, 28 to 36 kD) by approximately 3-, 2.5-, and 10-fold, respectively.	Dexamethasone	43-56	surfactant protein A1	Homo sapiens	138-142
2106332-3	1990	Treatment for 3 days with IFN-gamma alone, dexamethasone alone, and IFN plus dexamethasone increased the content of surfactant protein A (SP-A, 28 to 36 kD) by approximately 3-, 2.5-, and 10-fold, respectively.	Dexamethasone	77-90	surfactant protein A1	Homo sapiens	116-136
2106332-3	1990	Treatment for 3 days with IFN-gamma alone, dexamethasone alone, and IFN plus dexamethasone increased the content of surfactant protein A (SP-A, 28 to 36 kD) by approximately 3-, 2.5-, and 10-fold, respectively.	Dexamethasone	77-90	surfactant protein A1	Homo sapiens	138-142
2106332-4	1990	The biphasic response pattern of SP-A to dexamethasone (stimulation initially and inhibition with continued culture) was not altered by the presence of IFN-gamma.	Dexamethasone	41-54	surfactant protein A1	Homo sapiens	33-37
2096666-8	1990	Since electron microscopic immuno-gold labelling demonstrated the presence of this protein in the LSSL, and electrochemically it proved to transport lipids from the surface layer to the subphase, it was suggested that Sp-A plays the role of an oxygen carrier.	Oxygen	244-250	surfactant protein A1	Homo sapiens	218-222
33823299-4	2021	A reduction in SP-A levels at 24 h of exposure to TiO2 NPs (concentration-dependent) or ZnO NPs (the higher concentration) was also observed, reversed by blocking the inflammatory response (by the inhibition of IL-6).	tio2 nps	50-58	surfactant protein A1	Homo sapiens	15-19
33823299-0	2021	Inflammatory response in human alveolar epithelial cells after TiO2 NPs or ZnO NPs exposure: inhibition of surfactant protein A expression as an indicator for loss of lung function.	Zinc Oxide	75-78	surfactant protein A1	Homo sapiens	107-127
33823299-4	2021	A reduction in SP-A levels at 24 h of exposure to TiO2 NPs (concentration-dependent) or ZnO NPs (the higher concentration) was also observed, reversed by blocking the inflammatory response (by the inhibition of IL-6).	zno nps	88-95	surfactant protein A1	Homo sapiens	15-19
33823299-5	2021	Loss of SP-A represents a relevant target of MONPs-induced inflammatory response that could contribute to cellular damage and loss of lung function.	monps	45-50	surfactant protein A1	Homo sapiens	8-12
33805734-3	2021	Two isolates carrying linezolid resistance genes were recovered from laryngological patients and characterized by determining their antimicrobial resistance patterns and using molecular methods such as spa typing, MLST, SCCmec typing, detection of virulence genes and ica operon expression, and analysis of antimicrobial resistance determinants.	Linezolid	22-31	surfactant protein A1	Homo sapiens	202-205
7828630-4	1994	Such binding effects the release of reactive oxygen species from resident alveolar macrophages if SP-A is properly presented to the target cell.	Reactive Oxygen Species	36-59	surfactant protein A1	Homo sapiens	98-102
34780278-6	2022	We found that SP-A post-transcriptionally restricts LPS-induced TLR4 protein expression in primary AMs from healthy humans, rats, wild-type and SP-A-/- mice by further decreasing cycloheximide-reduced TLR4 protein translation and enhances the co-localization of TLR4 with the late endosome/lysosome.	Cycloheximide	179-192	surfactant protein A1	Homo sapiens	14-18
34837569-6	2022	RESULTS: We identified 9766 patients with ax-SpA (924 AS and 8842 nr-SpA) and 691,862 without SpA who had COVID-19.	Amoxicillin	42-44	surfactant protein A1	Homo sapiens	45-48
34837569-7	2022	In the unmatched comparison, patients with ax-SpA had higher risk ratios (RR) for all outcomes.	Amoxicillin	43-45	surfactant protein A1	Homo sapiens	46-49
34837569-9	2022	Only the risk of VTE was higher in ax-SpA patients (RR: 1.219 (1.037-1.433), p = 0.016).	Amoxicillin	35-37	surfactant protein A1	Homo sapiens	38-41
34837569-10	2022	Amongst the ax-SpA group, males had worse outcomes in 9 out of the 11 domains except for VTE and cerebral infarction, while blacks had worse outcomes in all except for mortality and the need for renal replacement therapy.	Amoxicillin	12-14	surfactant protein A1	Homo sapiens	15-18
34837569-13	2022	Ax-SpA patients who had been prescribed non-steroidal anti-inflammatory drugs in the 3 months prior to COVID-19 had poorer outcomes.	Amoxicillin	0-2	surfactant protein A1	Homo sapiens	3-6
34837569-14	2022	CONCLUSION: In conclusion, COVID-19 outcomes were better in patients with ax-SpA as compared with PS matched controls except for increased risk for VTE.	Amoxicillin	74-76	surfactant protein A1	Homo sapiens	77-80
34917955-8	2021	Results indicate that, rotenone can bind with carbohydrate recognition domain (CRD) of SP-A, N-, and C- terminal peptide of SP-B, SP-C, and CRD of SP-D at multiples sites via several interaction mediators such as H bonds, C-H bonds, alkyl bonds, pi-pi stacked, Van der Waals interaction, and other.	Rotenone	23-31	surfactant protein A1	Homo sapiens	87-91
34917955-8	2021	Results indicate that, rotenone can bind with carbohydrate recognition domain (CRD) of SP-A, N-, and C- terminal peptide of SP-B, SP-C, and CRD of SP-D at multiples sites via several interaction mediators such as H bonds, C-H bonds, alkyl bonds, pi-pi stacked, Van der Waals interaction, and other.	Carbohydrates	46-58	surfactant protein A1	Homo sapiens	87-91
34633005-1	2021	An SPA-triazolium bromide-catalyzed transannular C-acylation of enol lactones is presented.	enol lactones	64-77	surfactant protein A1	Homo sapiens	3-6
34429648-13	2021	Conclusion: Our study shows significant perceived improvement from back pain after utilization of spa water.	Water	102-107	surfactant protein A1	Homo sapiens	98-101
34703757-3	2021	Further, after starting treatment with everolimus, serum levels of surfactant protein (SP)-A and SP-D, which reflect type II pneumocyte hyperplasia, decreased to the normal range.	Everolimus	39-49	surfactant protein A1	Homo sapiens	67-92
34171508-0	2021	A novel electrochemical immunosensor for the sensitive detection of tiamulin based on staphylococcal protein A and silver nanoparticle-graphene oxide nanocomposites.	tiamulin	68-76	surfactant protein A1	Homo sapiens	86-110
34429648-15	2021	Therefore, hot spring spa water had better therapeutic effect for back pain and emphasis should be given to integrate it with modern medicine and further experimental study to be conducted to recommend it for medical purposes.	Water	26-31	surfactant protein A1	Homo sapiens	22-25
34129043-1	2021	BACKGROUND: Staphylococcus aureus protein A (spa) typing can be used to expand characterization of the epidemiology of methicillin-susceptible S. aureus (MSSA) and methicillin-resistant S. aureus (MRSA) in neonatal intensive care units (NICU).	Methicillin	119-130	surfactant protein A1	Homo sapiens	45-48
34069828-1	2021	A quartz crystal microbalance with dissipation monitoring (QCM-D) was employed for in situ investigations of the effect of temperature and light on the conformational changes of a poly (triethylene glycol acrylate-co-spiropyran acrylate) (P (TEGA-co-SPA)) copolymer containing 12-14% of spiropyran at the silica-water interface.	poly (triethylene glycol acrylate-co-spiropyran acrylate)	180-237	surfactant protein A1	Homo sapiens	250-253
34129043-1	2021	BACKGROUND: Staphylococcus aureus protein A (spa) typing can be used to expand characterization of the epidemiology of methicillin-susceptible S. aureus (MSSA) and methicillin-resistant S. aureus (MRSA) in neonatal intensive care units (NICU).	Methicillin	164-175	surfactant protein A1	Homo sapiens	45-48
34129043-13	2021	The most common spa type, MSSA-t279, was not associated with increased morbidity or mortality but was mupirocin resistant and associated with clustered NICU beds.	Mupirocin	102-111	surfactant protein A1	Homo sapiens	16-19
34245611-3	2021	Surfactant protein, SP-A, an immune modulator, is developmentally upregulated in fetal lung with surfactant phospholipid synthesis.	Phospholipids	108-120	surfactant protein A1	Homo sapiens	20-24
34144387-4	2021	The ASAS-perSpA is a cross-sectional study that recruited consecutive patients with SpA (as diagnosed by their rheumatologist) from 68 centers worldwide and collected patient and disease data.	Aspirin	4-8	surfactant protein A1	Homo sapiens	84-87
34194664-8	2021	These distinctly different mechanisms were observed to be highly correlated to the protein secondary and tertiary structures of spA and spG ligands, as explicated from the perspective of hydrogen bonding.	Hydrogen	187-195	surfactant protein A1	Homo sapiens	128-131
34390784-1	2021	BACKGROUND: Ammonium persulfate (APS), an oxidizing agent used in hair products, manufacturing, and pool/spa water, can cause skin reactions including allergic contact dermatitis.	ammonium peroxydisulfate	12-31	surfactant protein A1	Homo sapiens	105-108
34390784-1	2021	BACKGROUND: Ammonium persulfate (APS), an oxidizing agent used in hair products, manufacturing, and pool/spa water, can cause skin reactions including allergic contact dermatitis.	ammonium peroxydisulfate	33-36	surfactant protein A1	Homo sapiens	105-108
34390784-1	2021	BACKGROUND: Ammonium persulfate (APS), an oxidizing agent used in hair products, manufacturing, and pool/spa water, can cause skin reactions including allergic contact dermatitis.	Water	109-114	surfactant protein A1	Homo sapiens	105-108
34390784-11	2021	Swimming pool/spa chemicals are important sources of APS exposure.	ammonium peroxydisulfate	53-56	surfactant protein A1	Homo sapiens	14-17
34088508-6	2021	SpA crosslinking of VH3-IgG and VH3-IgE bound to cognate receptors of mast cells and basophils promotes histamine release and anaphylaxis.	Histamine	104-113	surfactant protein A1	Homo sapiens	0-3
34297513-2	2021	METHODS: A retrospective analysis of 172 patients with ax-SpA was performed to assess the presence of active inflammatory and structural changes of the symphysis pubis on MRI scans, and their association with clinical factors and the SPARCC (Spondyloarthritis Research Consortium of Canada) scoring of the sacroiliac joint were evaluated.	Amoxicillin	55-57	surfactant protein A1	Homo sapiens	58-61
34297513-7	2021	CONCLUSIONS: The MRI changes of the symphysis pubis were seen in 55.2% of the patients with ax-SpA and were associated with C-reactive protein, erythrocyte sedimentation rate, and symptom duration.	Amoxicillin	92-94	surfactant protein A1	Homo sapiens	95-98
35091782-13	2022	The use of ASAS axial SpA criteria may provide early detection of axial involvement.	asas	11-15	surfactant protein A1	Homo sapiens	22-25
35034269-1	2022	The thermal mineral water of Penon de los Banos spa (Mexico City) has been used for over 500 years starting in pre-Hispanic times and is famous for the treatment of various pathologies.	Water	20-25	surfactant protein A1	Homo sapiens	48-51
35576315-4	2022	We present a patient with a stable history of liquid injectable silicone (LIS) given 20 years prior who developed chronic periocular and facial hypersensitivity after undergoing microneedling at a medi-spa.	Silicones	64-72	surfactant protein A1	Homo sapiens	202-205
35411515-4	2022	Second, the structural path analysis for environmental input-output analysis (EIOA-SPA) model is used to quantify the transfer of carbon emissions between sectors in various regions.	Carbon	130-136	surfactant protein A1	Homo sapiens	83-86
35486525-2	2022	The RO experiments with NaCl aqueous solution (2000 ppm) indicated that the introduction of hydroxyethylurea groups markedly improved the permeability of water (1.86 x 10-12 m3/m2sPa) to approximately 19 times higher than that of a membrane prepared via the BTESPA homopolymerization, with NaCl rejection remaining nearly unchanged (96%).	ro	4-6	surfactant protein A1	Homo sapiens	179-182
35486525-2	2022	The RO experiments with NaCl aqueous solution (2000 ppm) indicated that the introduction of hydroxyethylurea groups markedly improved the permeability of water (1.86 x 10-12 m3/m2sPa) to approximately 19 times higher than that of a membrane prepared via the BTESPA homopolymerization, with NaCl rejection remaining nearly unchanged (96%).	Sodium Chloride	24-28	surfactant protein A1	Homo sapiens	179-182
35486525-2	2022	The RO experiments with NaCl aqueous solution (2000 ppm) indicated that the introduction of hydroxyethylurea groups markedly improved the permeability of water (1.86 x 10-12 m3/m2sPa) to approximately 19 times higher than that of a membrane prepared via the BTESPA homopolymerization, with NaCl rejection remaining nearly unchanged (96%).	2-Hydroxyethylurea	92-108	surfactant protein A1	Homo sapiens	179-182
35486525-2	2022	The RO experiments with NaCl aqueous solution (2000 ppm) indicated that the introduction of hydroxyethylurea groups markedly improved the permeability of water (1.86 x 10-12 m3/m2sPa) to approximately 19 times higher than that of a membrane prepared via the BTESPA homopolymerization, with NaCl rejection remaining nearly unchanged (96%).	Water	154-159	surfactant protein A1	Homo sapiens	179-182
35486525-2	2022	The RO experiments with NaCl aqueous solution (2000 ppm) indicated that the introduction of hydroxyethylurea groups markedly improved the permeability of water (1.86 x 10-12 m3/m2sPa) to approximately 19 times higher than that of a membrane prepared via the BTESPA homopolymerization, with NaCl rejection remaining nearly unchanged (96%).	btespa	258-264	surfactant protein A1	Homo sapiens	179-182
35486525-2	2022	The RO experiments with NaCl aqueous solution (2000 ppm) indicated that the introduction of hydroxyethylurea groups markedly improved the permeability of water (1.86 x 10-12 m3/m2sPa) to approximately 19 times higher than that of a membrane prepared via the BTESPA homopolymerization, with NaCl rejection remaining nearly unchanged (96%).	Sodium Chloride	290-294	surfactant protein A1	Homo sapiens	179-182
35307994-7	2022	International SpA, Rome, Italy) water in UVB-irradiated immortalized human keratinocytes.	Water	32-37	surfactant protein A1	Homo sapiens	14-17
35041940-0	2022	Genotyping of methicillin-resistant Staphylococcus aureus isolates causing invasive infections using spa typing and their correlation with antibiotic susceptibility.	Methicillin	14-25	surfactant protein A1	Homo sapiens	101-104
35215145-0	2022	Phosphomimetic Tyrosine Mutations in Spa47 Inhibit Type Three Secretion ATPase Activity and Shigella Virulence Phenotype.	Tyrosine	15-23	surfactant protein A1	Homo sapiens	37-40
35215145-6	2022	Results presented here demonstrate a direct correlation between Spa47 tyrosine phosphorylation state, Spa47 ATPase activity, T3SS function, and Shigella virulence.	Tyrosine	70-78	surfactant protein A1	Homo sapiens	64-67
34980610-4	2022	This protocol describes an original innovative multicentre international study aimed to assess safety and efficacy of aDBS vs cDBS using a new generation of DBS IPG in PD (AlphaDBS system by Newronika SpA, Milan, Italy).	dibromsalan	157-160	surfactant protein A1	Homo sapiens	201-204
34980610-4	2022	This protocol describes an original innovative multicentre international study aimed to assess safety and efficacy of aDBS vs cDBS using a new generation of DBS IPG in PD (AlphaDBS system by Newronika SpA, Milan, Italy).	2-Isopropoxyethanol	161-164	surfactant protein A1	Homo sapiens	201-204
34988956-5	2022	RESULTS: We found that 13 (29.5%) of 42 patients with ax-SpA had coccydynia.	Amoxicillin	54-56	surfactant protein A1	Homo sapiens	57-60
34988956-9	2022	CONCLUSION: Our study supports the increased prevalence of coccydynia in patients with ax-SpA.	Amoxicillin	87-89	surfactant protein A1	Homo sapiens	90-93
34857709-4	2022	METHODS: The SPA Project is a multicenter, observational, cross-sectional, cohort study investigating healthy children, aged 5-8 years as to sodium and fluid intake by means of urinary sodium and creatinine from multiple samples taken in different days in order to characterize them in lower/higher sodium and lower/higher fluid intake.	Sodium	141-147	surfactant protein A1	Homo sapiens	13-16
34857709-4	2022	METHODS: The SPA Project is a multicenter, observational, cross-sectional, cohort study investigating healthy children, aged 5-8 years as to sodium and fluid intake by means of urinary sodium and creatinine from multiple samples taken in different days in order to characterize them in lower/higher sodium and lower/higher fluid intake.	Sodium	185-191	surfactant protein A1	Homo sapiens	13-16
34857709-4	2022	METHODS: The SPA Project is a multicenter, observational, cross-sectional, cohort study investigating healthy children, aged 5-8 years as to sodium and fluid intake by means of urinary sodium and creatinine from multiple samples taken in different days in order to characterize them in lower/higher sodium and lower/higher fluid intake.	Creatinine	196-206	surfactant protein A1	Homo sapiens	13-16
34857709-4	2022	METHODS: The SPA Project is a multicenter, observational, cross-sectional, cohort study investigating healthy children, aged 5-8 years as to sodium and fluid intake by means of urinary sodium and creatinine from multiple samples taken in different days in order to characterize them in lower/higher sodium and lower/higher fluid intake.	Sodium	299-305	surfactant protein A1	Homo sapiens	13-16
35259478-2	2022	We aimed to assess the prevalence of left ventricular (LV) systolic and diastolic dysfunction and valvular heart disease (VHD) by transthoracic echocardiography (TTE) in ax-SpA patients without history of CVD.	Amoxicillin	170-172	surfactant protein A1	Homo sapiens	173-176
35259478-12	2022	LV diastolic TTE parameters are altered in ax-SpA.	Amoxicillin	43-45	surfactant protein A1	Homo sapiens	46-49
34870817-4	2022	Group B SRCR domains, found in WC1, CD163, CD5, CD6, Spalpha and DMBT1, are approximately 100-110 amino acids long and contain 6-8 cysteines predicted to form 3-4 disulfide bonds.	Cysteine	131-140	surfactant protein A1	Homo sapiens	53-60