Affinage

SFTPA1

Pulmonary surfactant-associated protein A1 · UniProt Q8IWL2

Length
248 aa
Mass
26.2 kDa
Annotated
2026-06-10
100 papers in source corpus 44 papers cited in narrative 44 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

SFTPA1 encodes SP-A1, a calcium-dependent C-type lectin (collectin) that operates at the interface of pulmonary surfactant homeostasis and innate immune defense (PMID:1993679, PMID:9813377). The protein assembles into large disulfide-bonded oligomers built on a collagen-like triple helix, and both oligomerization and downstream carbohydrate processing depend on an intact collagenous domain (PMID:2610270); its C-terminal carbohydrate recognition domain (CRD) carries the higher-affinity calcium-binding site whose occupancy drives the conformational change and reversible aggregation underlying surfactant organization (PMID:2271565). SP-A1 specifically binds DPPC and surfactant phospholipids through a mechanism requiring both the diacylglycerol moiety and the phosphocholine head group (PMID:1993679), enhances phospholipid adsorption and lowers surface tension at the air-liquid interface (PMID:2713385, PMID:27508436), and is genetically required — together with SP-A2 — for tubular myelin formation in vivo (PMID:8790375, PMID:20048345). Secretion requires hydroxylation of the collagenous domain, without which high-mannose precursors accumulate intracellularly (PMID:3355864), and the protein traffics through an EEA1-positive early endosome before being recycled to the cell surface via Rab4 vesicles while surfactant lipid is diverted to Rab7/CD63 lamellar-body compartments (PMID:11435209), with P63/CKAP4 (and the SP-A-binding protein BP55) acting as the type II cell receptor for this clearance pathway (PMID:8843792, PMID:20054143). In innate immunity SP-A1 functions as a calcium- and mannose-dependent opsonin, binding bacterial capsular polysaccharides, a 60-kDa mycobacterial cell-wall protein, and influenza neuraminidase, and bridging pathogens to macrophage receptors including the 210-kDa SPR210 to enhance phagocytosis and clearance (PMID:9124386, PMID:9271309, PMID:9176265, PMID:7998980); it can also directly permeabilize LPS membranes by extracting LPS into calcium-dependent protein-lipid aggregates (PMID:18599636), and it restrains TLR-driven inflammation through a TLR2-dependent mechanism (PMID:23700442). SP-A function is abolished by peroxynitrite-mediated nitration of CRD tyrosines and by neutrophil serine protease degradation (PMID:8806782, PMID:15047952). Disease-causing missense mutations in the CRD abolish secretion while preserving protein production, and this secretory block triggers necroptosis of alveolar type II cells via an IRE1α→JNK→RIPK3 pathway, causing idiopathic pulmonary fibrosis (PMID:26792177, PMID:31601679, PMID:32855221).

Mechanistic history

Synthesis pass · year-by-year structured walk · 22 steps
  1. 1989 High

    Established the structural basis of SP-A assembly, defining it as a collagenous oligomeric protein whose higher-order organization and calcium-dependent aggregation depend on an intact collagen-like domain.

    Evidence Collagenase digestion, circular dichroism, thermal denaturation, and disulfide mapping of purified SP-A

    PMID:2610270

    Open questions at the time
    • No atomic-resolution structure of the oligomer
    • Stoichiometry of physiological oligomers not defined
  2. 1990 High

    Localized calcium binding to the CRD and linked calcium-induced conformational change to the reversible aggregation underlying surfactant organization, connecting a metal-binding event to function.

    Evidence Equilibrium dialysis, limited proteolysis fragments, and intrinsic fluorescence of SP-A

    PMID:2271565

    Open questions at the time
    • Structural detail of the calcium-induced conformational change unresolved
  3. 1991 High

    Defined the lipid-binding specificity of SP-A, showing it recognizes DPPC via both acyl and head-group features and that the collagenous (not glycan) domain is required, mechanistically distinguishing lipid binding from lectin activity.

    Evidence 125I-SP-A thin-layer chromatogram overlay binding assays with domain-deletion and chemical variants

    PMID:1993679

    Open questions at the time
    • Did not resolve how lipid and carbohydrate binding are coordinated in vivo
  4. 1988 High

    Showed that collagenous-domain hydroxylation gates intracellular transport and secretion, establishing a post-translational checkpoint for SP-A maturation.

    Evidence Metabolic labeling and subcellular fractionation of primary type II cells with prolyl-hydroxylation inhibitors

    PMID:3355864

    Open questions at the time
    • Did not identify the trafficking receptor or quality-control machinery
  5. 1993 Medium

    Demonstrated receptor-mediated endocytic recycling of SP-A into lamellar bodies by type II cells, framing SP-A as a recycled component of surfactant homeostasis.

    Evidence Electron microscopy of SP-A-colloidal gold conjugates with competitive inhibition in rat type II cells

    PMID:8417113

    Open questions at the time
    • Receptor identity not established at this stage
    • Single-lab EM-based readout
  6. 1996 Medium

    Identified BP55 as a functional type II-cell receptor mediating SP-A-dependent, ATP-dependent lipid uptake to a non-degrading compartment, providing the first molecular handle on the recycling receptor.

    Evidence Liposome uptake assay in rat type II cells with anti-BP55 antibody inhibition and ATP/temperature dependence

    PMID:8843792

    Open questions at the time
    • Molecular identity of BP55 not cloned here
    • Single antibody-based inhibition
  7. 2001 High

    Resolved that SP-A and surfactant lipid share an early endosome but then diverge — SP-A recycles via Rab4 vesicles while lipid routes to lamellar bodies — clarifying that SP-A is recycled rather than co-trafficked with its cargo.

    Evidence Immunofluorescence with endosomal markers plus bafilomycin and calmodulin inhibitors in rat type II cells

    PMID:11435209

    Open questions at the time
    • Did not name the receptor driving the divergence
  8. 2009 Medium

    Named P63/CKAP4 as the SP-A receptor on type II cells mediating surfactant clearance, connecting recycling to a defined protein and rescuable phenotype.

    Evidence Receptor identification and SP-A rescue in SP-A-null mice (review citing original work)

    PMID:20054143

    Open questions at the time
    • Accessed via review
    • Relationship between P63/CKAP4 and BP55 not reconciled in timeline
  9. 1996 High

    A null mouse demonstrated that SP-A is specifically required for tubular myelin assembly while being dispensable for bulk surfactant pool size and lung mechanics, isolating its in vivo structural role.

    Evidence Homologous-recombination SP-A knockout with EM, lipid analysis, and lung function measurements

    PMID:8790375

    Open questions at the time
    • Molecular mechanism of tubular myelin assembly not defined
  10. 2010 High

    Showed that tubular myelin formation requires both SP-A1 and SP-A2 gene products together, establishing functional non-redundancy between the two paralogs in vivo.

    Evidence Humanized SP-A1-only and SP-A2-only transgenic mice with EM and exogenous SP-A rescue, corroborated in human BAL

    PMID:20048345

    Open questions at the time
    • Stoichiometric/structural basis for the SP-A1/SP-A2 requirement not resolved
  11. 1994 High

    Established SP-A as a mannose-dependent calcium-dependent opsonin recognizing diverse microbial ligands, defining its lectin-based innate-immune mechanism.

    Evidence Influenza saturation binding, hemagglutination inhibition, and ligand-blot identification of viral neuraminidase

    PMID:7998980

    Open questions at the time
    • Did not test in vivo consequence at this stage
  12. 1997 High

    Extended opsonic recognition to bacterial and mycobacterial ligands and identified the 210-kDa macrophage SP-A receptor (SPR210) bridging pathogens to phagocytes.

    Evidence Binding and phagocytosis/killing assays for Klebsiella polysaccharide, M. tuberculosis 60-kDa protein, and BCG with anti-SPR210 blocking

    PMID:9124386 PMID:9176265 PMID:9271309

    Open questions at the time
    • SPR210 molecular identity and signaling not fully defined
  13. 1998 High

    Genetic knockout confirmed in vivo that SP-A is required for efficient bacterial clearance, validating its opsonic role at the organismal level.

    Evidence Intratracheal bacterial challenge of SP-A-/- mice with clearance and tubular myelin readouts

    PMID:9813377

    Open questions at the time
    • Did not dissect macrophage signaling downstream of opsonization
  14. 2002 High

    Demonstrated, with knockout and rescue, that SP-A both promotes viral clearance and restrains lung inflammation, showing a dual antimicrobial and immunomodulatory function in vivo.

    Evidence IAV and adenovirus infection of SP-A-/- mice with SP-A rescue and cytokine/clearance readouts

    PMID:10484466 PMID:11839553

    Open questions at the time
    • Did not identify the receptor mediating the anti-inflammatory effect
  15. 2013 High

    Defined a TLR2-dependent anti-inflammatory mechanism, showing SP-A suppresses TLR-ligand-induced cytokines and preterm delivery through a specific receptor pathway.

    Evidence Cytokine assays in TLR2/TLR4 knockout macrophages and an in vivo preterm-delivery model

    PMID:23700442

    Open questions at the time
    • Direct SP-A/TLR2 physical interaction not shown
    • Mechanism for non-TLR2 ligands unresolved
  16. 2008 High

    Revealed a direct, non-opsonic bactericidal mechanism whereby SP-A permeabilizes LPS membranes by extracting lipid into calcium-dependent protein-lipid aggregates.

    Evidence Epifluorescence microscopy, monolayer relaxation, and DSC on Re-LPS films with SP-A

    PMID:18599636

    Open questions at the time
    • In vivo relevance of direct permeabilization vs opsonization not quantified
  17. 1996 High

    Showed SP-A function is inactivated by peroxynitrite nitration of CRD tyrosines, linking oxidative/nitrosative stress to loss of surfactant and immune activity.

    Evidence Peroxynitrite exposure with nitrotyrosine quantification and lipid-aggregation/mannose-binding assays with scavenger controls

    PMID:8806782

    Open questions at the time
    • In vivo extent of nitration during disease not established here
  18. 2004 High

    Identified neutrophil serine proteases as efficient inactivators of SP-A in inflamed (cystic fibrosis) airways, providing a disease-relevant degradation mechanism.

    Evidence In vitro protease degradation of purified and native BAL SP-A with inhibitor controls

    PMID:15047952

    Open questions at the time
    • Functional consequence of degradation in patients not directly measured
  19. 1994 High

    Established hormonal and gene-specific transcriptional control of SP-A, with cAMP stimulatory and glucocorticoids/phorbol esters inhibitory, defining regulatory inputs.

    Evidence Primer extension, nuclear run-on transcription, and mRNA stability assays in fetal lung explants and H441 cells with RU486/cycloheximide controls

    PMID:2249989 PMID:8179013 PMID:8460712 PMID:9294011

    Open questions at the time
    • Specific transcription factors and labile mediators not identified
  20. 2016 Medium

    Linked SFTPA1 CRD missense mutations to impaired secretion and familial pulmonary fibrosis, establishing SFTPA1 as a Mendelian disease gene.

    Evidence Germline mutation identification, in vitro secretion assay, and patient lung immunohistochemistry

    PMID:26792177

    Open questions at the time
    • Cellular death mechanism not yet defined at this stage
    • Single-family/single-lab functional assay
  21. 2019 High

    Defined the cellular pathomechanism of mutant SP-A1, showing that secretion failure triggers type II-cell necroptosis through IRE1α→JNK→RIPK3, with genetic and pharmacological rescue establishing causality.

    Evidence Sftpa1 knock-in mice with IRE1α/JNK/RIPK3 dissection, JNK inhibitor rescue, and RIPK3 overexpression reversal

    PMID:31601679

    Open questions at the time
    • Mechanism connecting retained protein to IRE1α activation not fully resolved
  22. 2020 High

    Generalized the disease mechanism by showing that 11 distinct SFTPA1/SFTPA2 mutations share a common abolition of secretion with preserved production, defining a unified molecular signature of pathogenicity.

    Evidence Systematic in vitro expression/secretion assays for 11 mutations with ex vivo patient tissue immunostaining

    PMID:32855221

    Open questions at the time
    • Whether all mutations converge on the same necroptotic pathway not tested

Open questions

Synthesis pass · forward-looking unresolved questions
  • How SP-A1 oligomers physically template tubular myelin in cooperation with SP-A2, and how the retained mutant protein activates the IRE1α ER-stress sensor, remain unresolved.
  • No structure of the tubular-myelin lattice
  • Molecular link between secretion block and IRE1α activation undefined
  • Reconciliation of BP55, P63/CKAP4, and SPR210 receptor identities incomplete

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0038024 cargo receptor activity 4 GO:0008289 lipid binding 3 GO:0098772 molecular function regulator activity 2
Localization
GO:0005576 extracellular region 3 GO:0005768 endosome 2 GO:0031410 cytoplasmic vesicle 2
Pathway
R-HSA-168256 Immune System 4 R-HSA-5653656 Vesicle-mediated transport 3 R-HSA-5357801 Programmed Cell Death 1
Partners
CKAP4SFTPA2TLR2

Evidence

Reading pass · 44 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1991 SP-A specifically and strongly binds dipalmitoylphosphatidylcholine (DPPC) in a calcium-dependent manner; binding requires the intact collagenous domain but not the oligosaccharide moiety; the nonpolar diacylglycerol group and the specific polar head group (phosphocholine) are both required; deglycosylated SP-A retains binding but the collagenase-resistant collagenous fragment does not. 125I-SP-A thin-layer chromatogram overlay binding assay, EGTA inhibition, phospholipase C/A2 treatments, competitive inhibition with deglycosylated and collagenase-resistant SP-A fragments The Journal of biological chemistry High 1993679
1989 SP-A forms large oligomers dependent on an intact collagen-like domain; the cysteines in the non-collagen domain form intrachain disulfide bonds (between residues 135–226 and 204–218); the protein has a collagen-like triple helix and exhibits calcium-dependent aggregation at physiological calcium concentrations. Collagenase digestion, circular dichroism spectroscopy, thermal denaturation, disulfide bond mapping The American journal of physiology High 2610270
1990 Each SP-A monomer binds two to three calcium ions; the higher-affinity calcium-binding site is located in the C-terminal carbohydrate recognition domain (CRD); calcium binding to this domain causes a conformational change and promotes reversible protein aggregation relevant to tubular myelin formation. Equilibrium dialysis, gel permeation chromatography, limited proteolysis fragment studies, intrinsic fluorescence spectroscopy Biochemistry High 2271565
1988 The hydroxylation of the collagenous domain of SP-A is required for its intracellular transport to the lamellar body fraction and secretion; disruption of triple-helix formation (by alpha,alpha'-dipyridyl or cis-4-hydroxy-L-proline) causes accumulation of high-mannose precursors intracellularly without secretion; carbohydrate processing (sialylation) is also dependent on an intact collagenous domain. Metabolic labeling of type II cells, inhibitor treatment, subcellular fractionation, endoglycosidase H resistance assay Biochimica et biophysica acta High 3355864
1989 After intratracheal instillation, both SP-A protein and surfactant lipids are taken up by lung cells and incorporated into lamellar body-enriched secretory granules in a time-dependent manner, consistent with receptor-mediated recycling. Intratracheal instillation of radiolabeled lipid-SP-A complex, subcellular fractionation on discontinuous sucrose density gradients Journal of applied physiology Medium 2708254
1989 SP-A enhances the surface activity of lipid extract surfactant by improving the rate of phospholipid adsorption and spreading at the air-liquid interface, resulting in stable lipid monolayer formation at lower phospholipid and calcium concentrations. Pulsating bubble surfactometer assay of lipid extract surfactant reconstituted with purified SP-A Biochimica et biophysica acta Medium 2713385
1991 SP-A interacts with alveolar macrophages via a specific, mannose-dependent receptor distinct from the classical mannose receptor; binding and uptake occur via coated pits/vesicles and material is transported to secondary lysosomes; excess SP-A competitively inhibits uptake. Electron microscopy of SP-A-coated gold particles incubated with rat alveolar macrophages, competitive inhibition with mannan-BSA/galactosyl-BSA, mannose receptor down-regulation experiments Experimental cell research Medium 1846339
1989 SP-A uptake by macrophages and monocytes is mannose-dependent; the interaction is mediated at least in part by SP-A binding to mannose residues on the macrophage surface (not solely via the mannose receptor), as monocytes lacking mannose receptor activity still internalize SP-A gold particles in a mannose-dependent manner. Electron microscopy of SP-A-coated gold particles with human macrophages/monocytes, competitive inhibition with mannosyl-BSA vs galactosyl-BSA, ConA labeling of cell surface European journal of cell biology Medium 2627938
1992 SP-A enhances serum-independent phagocytosis of several bacterial species (E. coli, P. aeruginosa, S. aureus) by alveolar macrophages in a concentration-dependent manner; the effect is species- and growth-phase-dependent; more complex oligomeric SP-A is most effective. Phagocytosis assay of non-opsonized bacteria with purified SP-A variants (recombinant human SP-A1, SP-A2, and proteinosis-derived SP-A) and isolated alveolar macrophages European journal of cell biology Medium 1639094
1993 SP-A is internalized by alveolar type II cells via the endosomal system (including multivesicular bodies) into lamellar bodies; internalization is receptor-mediated (inhibited by excess unlabeled SP-A and by alkylation); cell shape/cytoskeletal organization regulates SP-A recycling efficiency. Electron microscopy of SP-A-colloidal gold conjugates in primary rat type II cells, competitive inhibition, fluid-phase marker co-internalization The journal of histochemistry and cytochemistry Medium 8417113
1996 A null mutation of the murine SP-A gene eliminates tubular myelin formation in the lung without altering postnatal survival, lung morphology, surfactant phospholipid pool sizes, SP-B/C/D levels, or lung compliance; SP-A is specifically required for tubular myelin assembly. Homologous recombination gene targeting in mice (SP-A -/- knockout), electron microscopy, lung function measurements, lipid analysis, Northern/Western blot Proceedings of the National Academy of Sciences of the United States of America High 8790375
1997 SP-A binds to Klebsiella pneumoniae K21a capsular polysaccharides containing Man-alpha1-Man sequences in a mannose-dependent manner (inhibited by mannan), opsonizes bacteria for alveolar macrophages via SP-A receptors, and activates macrophage mannose receptor-mediated phagocytosis; SP-A-mediated killing of K21a was demonstrated. SP-A agglutination assay, SP-A-coated particle binding to bacterial surface, binding to immobilized capsular polysaccharide, phagocytosis and killing assays with alveolar macrophages, mannan inhibition The American journal of physiology High 9124386
1997 SP-A binds to Mycobacterium tuberculosis in a calcium- and concentration-dependent manner (Kd ~1.9 nM) via sugar moieties (deglycosylated SP-A has minimal binding); SP-A specifically binds a 60-kDa M. tuberculosis cell-wall protein; SP-A mediates M. tuberculosis attachment to murine alveolar macrophages, and this is blocked by anti-SP-A antibodies, mannosyl-BSA, and type V collagen. 125I-SP-A binding assay, Kd determination, deglycosylation, ligand blot for 60-kDa cell-wall protein, 51Cr-labeled bacterial attachment assay, inhibition by antibodies and competing ligands American journal of respiratory cell and molecular biology High 9271309
1997 SP-A binds BCG in a calcium-, carbohydrate-, and dose-dependent manner and enhances uptake of BCG-SP-A complexes by rat bone marrow macrophages, rat alveolar macrophages, and human monocytes; enhanced uptake is mediated in part by the 210-kDa SP-A receptor (SPR210) on macrophages, as anti-SPR210 antibodies block association. 125I-SP-A binding to BCG, fluorescent microscopy cell-association assay, electron microscopy, SPR210 antibody blocking, receptor modulation experiments The American journal of physiology High 9176265
1994 SP-A binds to influenza virus (A/X31) through its lectin domain in a calcium-dependent, saturable, concentration-dependent manner and inhibits virus-mediated hemagglutination; both SP-A and MBP bind a common 68-kDa viral neuraminidase; purified neuraminidase inhibits SP-A binding to intact virus. Saturation binding assay, hemagglutination inhibition assay, ligand blot analysis, neuraminidase isolation and competitive inhibition The Biochemical journal High 7998980
1996 Nitration of SP-A tyrosine residues in the carbohydrate recognition domain (CRD) by peroxynitrite (formed by NO + superoxide) decreases the ability of SP-A to aggregate lipids and bind mannose; the degree of functional inhibition correlates monotonically with nitrotyrosine content. SP-A exposure to peroxynitrite-generating systems (SIN-1, spermine NONOate + xanthine oxidase), nitrotyrosine quantification, mannose-binding assay, lipid aggregation assay, SOD and urate scavenger controls Archives of biochemistry and biophysics High 8806782
1995 SP-A receptor activity on macrophages is inversely regulated with respect to mannose receptor expression; agents that increase macrophage activation (PMA, LPS, IFN-γ) increase SP-A binding while decreasing mannose receptor activity; dexamethasone has the opposite effect. SP-A binding assay and mannose receptor activity assay on rat bone marrow macrophages and human monocytes treated with pharmacological agents and in vivo dexamethasone/LPS injection The American journal of physiology Medium 8572233
1999 Glycoprotein-340 (gp-340) co-purifies with SP-A from alveolar proteinosis lavage and binds SP-A in a calcium-dependent manner independent of SP-A lectin activity; however, gp-340 does not affect SP-A binding to alveolar macrophages or SP-A-stimulated macrophage chemotaxis, indicating gp-340 is not the SP-A receptor mediating chemotaxis. Co-purification and protein sequencing, SP-A binding inhibition assay, macrophage chemotaxis assay American journal of respiratory cell and molecular biology Medium 10101009
1996 SP-A-binding protein BP55 on type II pneumocyte cell membranes mediates SP-A-dependent lipid (DPPC liposome) uptake; this process is temperature-dependent, ATP-dependent, and blocked by an auto-anti-idiotypic antibody against BP55; SP-A-mediated uptake directs lipid to a non-degrading compartment. Liposome uptake assay in freshly isolated rat type II cells, ATP depletion, temperature dependence, anti-BP55 antibody inhibition The American journal of physiology Medium 8843792
2001 After endocytosis in type II cells, SP-A and surfactant lipids first enter a common EEA1-positive early endosomal compartment; subsequently SP-A is rapidly recycled to the cell surface via Rab4-associated recycling vesicles and does not enter classic lamellar bodies, whereas lipid is directed to Rab7/CD63/lamellar body compartments; calmodulin inhibition blocks both components at the early endosome. Immunofluorescence with endosomal markers (EEA1, Rab4, Rab7, CD63, lamellar body marker 3C9), bafilomycin A1 and calmodulin inhibitor experiments in isolated rat type II cells American journal of physiology. Lung cellular and molecular physiology High 11435209
2004 Neutrophil serine proteases (cathepsin G, elastase, proteinase-3) rapidly degrade SP-A at very low concentrations; cathepsin G is the most potent; these proteases are present in CF BAL fluid and cause time-dependent degradation of endogenous SP-A in CF BAL; degradation is blocked by serine protease inhibitors. In vitro protease degradation assay of purified SP-A and native BAL SP-A, dose-response and time-course with inhibitor (DFP, MNEI) controls Thorax High 15047952
2001 Type II cells and alveolar macrophages contribute approximately equally to SP-A catabolism in vivo; macrophages are the primary catabolic cell (with ~80% of macrophage-associated label in lung-digest macrophages not recoverable by lavage). Intratracheal instillation of residualizing 125I-dilactitol-tyramine-SP-A in mice, time-course measurement of radioactivity in isolated type II cells, lavage macrophages, and lung-digest macrophages American journal of physiology. Lung cellular and molecular physiology Medium 11350807
2001 Amiodarone inhibits SP-A degradation by alveolar macrophages both in vitro and in vivo without affecting DPPC degradation; amiodarone perturbs lysosomal enzyme distribution and blocks the endocytic pathway after early endosomes; SP-A but not DPPC catabolism is thereby inhibited. Rabbit alveolar macrophage exposure to amiodarone in vitro, tracheal instillation with amiodarone in newborn rabbits, lysosomal enzyme distribution, endocytic tracer studies American journal of physiology. Lung cellular and molecular physiology Medium 11597911
2003 SP-A is required for increased DPPC uptake in response to hyperventilation or secretagogues in vivo; SP-A-/- mice fail to upregulate DPPC uptake under these stimuli; SP-A also modulates lysosomal-type phospholipase A2-mediated degradation of internalized DPPC. Intratracheal instillation of 3H-DPPC in SP-A +/+ and -/- mice, CO2-induced hyperventilation, secretagogue (8-Br-cAMP) treatment, PLA2 activity assay in isolated lungs American journal of physiology. Lung cellular and molecular physiology High 12676766
1998 SP-A(-/-) mice have markedly decreased tubular myelin, clear Group B Streptococci and Pseudomonas aeruginosa less efficiently than wild-type, and have normal phospholipid composition and surfactant clearance, demonstrating an in vivo role for SP-A in innate pulmonary defense. Gene-targeted SP-A knockout mice, bacterial clearance assay (intratracheal challenge), electron microscopy for tubular myelin, phospholipid analysis Biochimica et biophysica acta High 9813377
2002 In the absence of SP-A, influenza A virus clearance is decreased and lung inflammation is increased; exogenous SP-A restores viral clearance and reduces inflammation in SP-A-/- mice; SP-A deficiency is associated with decreased neutrophil myeloperoxidase activity and altered Th1/Th2 immune balance. Intranasal IAV infection of SP-A -/- vs +/+ mice, viral clearance measurement, BAL cytokine/lymphocyte analysis, myeloperoxidase activity assay, SP-A rescue experiment American journal of physiology. Lung cellular and molecular physiology High 11839553
1999 SP-A enhances viral clearance of adenovirus from the lung and inhibits adenovirus-induced lung inflammation; SP-A-/- mice show increased PMN in BAL, elevated TNF-α, IL-6, IL-1β, and chemokine expression, and decreased alveolar macrophage uptake of adenovirus; co-administration of human SP-A to SP-A-/- mice ameliorates these defects. Intratracheal adenoviral infection of SP-A -/- vs +/+ mice, BAL analysis, cytokine mRNA and protein measurement, fluorescent adenovirus uptake by macrophages, SP-A rescue The American journal of physiology High 10484466
2010 Formation of tubular myelin (TM) in vivo requires both SP-A1 and SP-A2 gene products; humanized transgenic mice expressing only SP-A1 or only SP-A2 lack TM; TM is restored only when both gene products are present together; TM is absent in human BAL containing primarily one gene product and restored by exogenous SP-A containing both. Humanized transgenic mice (SP-A1 or SP-A2 cDNA-driven by SP-C promoter on SP-A KO background), electron microscopy for TM, Southern blot, immunohistochemistry, in vivo rescue with exogenous SP-A, human BAL analysis The Journal of biological chemistry High 20048345
2004 Human SP-A2 variants enhance association of P. aeruginosa with rat alveolar macrophages more effectively than SP-A1 variants; SP-A2 phagocytic index is approximately 52–95% higher than SP-A1; co-expressed SP-A1/SP-A2 variants at certain concentrations are more active than single gene products. Light microscopy phagocytosis index assay with insect-cell-expressed human SP-A1 and SP-A2 variant proteins and rat alveolar macrophages American journal of physiology. Lung cellular and molecular physiology Medium 15377498
2002 SP-A1 and SP-A2 have different carbohydrate-binding specificities; SP-A2 binds with higher affinity to a wider variety of sugars than SP-A1 at both 1 and 5 mM Ca2+; all SP-A proteins bind fucose with highest affinity. Carbohydrate-binding assay with immobilized sugars using recombinant human SP-A1, SP-A2 proteins and native human alveolar SP-A at different calcium concentrations American journal of physiology. Lung cellular and molecular physiology Medium 12505869
2013 SP-A suppresses TLR ligand-induced preterm delivery and inflammatory responses via a TLR2-dependent mechanism; SP-A inhibits LPS-, peptidoglycan-, and poly(I:C)-induced IL-1β, TNF-α, and CCL5 production, with the effect on PGN (TLR2 ligand) being TLR2-dependent as demonstrated in TLR2 knockout macrophages. Mouse macrophage cell line (RAW264.7), primary amniotic fluid and peritoneal macrophages from TLR4 and TLR2 knockout mice, cytokine ELISA, mouse preterm delivery model with intrauterine SP-A administration PloS one High 23700442
2008 SP-A permeabilizes rough LPS (Re-LPS) membranes by forming calcium-dependent protein-lipid aggregates on the membrane surface that extract LPS molecules from the membrane, decreasing van der Waals interactions between acyl chains and rendering the membrane leaky; coexistence of gel and fluid lipid phases in the LPS membrane is required for susceptibility to SP-A permeabilization. Epifluorescence microscopy of TR-SP-A on Re-LPS films, monolayer relaxation experiments, differential scanning calorimetry, membrane permeability assay Biophysical journal High 18599636
2009 P63/CKAP4 functions as a receptor for SP-A on alveolar type II cells and mediates SP-A-dependent surfactant clearance; SP-A null mice deficient in clathrin-dependent uptake use an actin-mediated pathway; administration of SP-A to SP-A-null mice rescues the phenotype. SP-A receptor identification, SP-A gene-targeted mice, SP-A rescue experiment, pharmacological pathway analysis (clathrin vs. actin pathways) — review citing original experimental work Cellular physiology and biochemistry Medium 20054143
1990 Phorbol ester (TPA) inhibits SP-A synthesis by decreasing de novo SP-A synthesis and SP-A mRNA levels in a time- and dose-dependent manner; the effect requires continued gene transcription and is not mediated solely by changes in SP-A transcription; actinomycin D blocks the rapid TPA-induced mRNA decrease, suggesting involvement of a labile destabilizing RNA species. 35S-methionine incorporation in H441-4 adenocarcinoma cells, SP-A mRNA Northern blot, actinomycin D RNA stability assay, dose-response and kinetics of inhibition The Journal of biological chemistry Medium 2249989
1993 Glucocorticoid inhibition of SP-A is receptor-mediated (blocked by RU 486), involves induction of a labile protein that decreases SP-A gene transcription (~60% reduction) and transiently reduces SP-A mRNA stability (t1/2 ~3 h initially vs ~8 h at steady state); the dominant response to glucocorticoid in fetal human lung is inhibition of SP-A mRNA. Human fetal lung explant culture with dexamethasone, nuclear elongation transcription assay, mRNA stability by actinomycin D and label-chase, cycloheximide, RU 486 blocking The American journal of physiology High 8460712
1997 Phorbol ester (TPA) acts primarily at the level of gene transcription to down-regulate SP-A in both H441 cells and human fetal lung explants, reducing SP-A gene transcription rate to ~28% of control. Nuclear elongation assay (run-on transcription), mRNA quantification, dose-response in H441 cells and human fetal lung explants Biochimica et biophysica acta Medium 9294011
1994 SP-A1 and SP-A2 genes are differentially regulated: cAMP preferentially increases SP-A2 mRNA (~5-fold) over SP-A1 mRNA (~2-fold) in human fetal lung, while dexamethasone inhibits SP-A1 and SP-A2 equally (~70%); in H441 cells, dexamethasone inhibits SP-A1 but not SP-A2 mRNA, and cAMP increases both equally. Primer extension analysis of SP-A1 and SP-A2 mRNA in human fetal lung explants and H441 cells treated with DBcAMP, dexamethasone, and insulin The American journal of physiology Medium 8179013
2016 A germline heterozygous missense mutation in SFTPA1 (p.Trp211Arg) located in the carbohydrate recognition domain impairs SP-A1 secretion, as demonstrated by functional studies; immunohistochemistry shows altered SP-A expression pattern in patient alveolar epithelium; this mutation segregates with IIP/IPF and lung adenocarcinoma. Germline mutation identification, in vitro functional secretion assay (cell transfection), immunohistochemistry on patient lung tissue Human molecular genetics Medium 26792177
2019 A homozygous missense mutation in SFTPA1 disturbs SP-A1 protein secretion and causes IPF via necroptosis of alveolar epithelial type II cells; the cellular mechanism involves phosphorylation of IRE1α leading to JNK-mediated upregulation of RIPK3; JNK inhibition ameliorates pulmonary fibrosis in knock-in mice, and RIPK3 overexpression reverses this protection. Sftpa1 knock-in (KI) mice carrying patient mutation, secretion assay, IRE1α phosphorylation, JNK inhibitor treatment, RIPK3 overexpression, lung histology, influenza challenge The Journal of experimental medicine High 31601679
2020 Pathogenic SFTPA1 (and SFTPA2) mutations preserve protein production but abolish secretion; this secretion defect is the shared functional consequence of 11 distinct mutations tested in vitro; SP-A expression pattern is altered in lung tissue of patients carrying these mutations. In vitro expression and secretion assay for 11 SFTPA1/SFTPA2 mutations in cell models, ex vivo immunostaining of patient lung tissue The European respiratory journal High 32855221
2016 Human SP-A1 allows pulmonary surfactant to achieve lower surface tension after adsorption and during compression-expansion cycling than surfactant with SP-A2 alone or no SP-A; SP-A1 also confers greater resistance to serum inhibition of surfactant function than equivalent amounts of SP-A2. Captive bubble surfactometer assay of humanized transgenic mouse surfactant (expressing SP-A1, SP-A2, or both), reconstituted porcine hydrophobic surfactant with recombinant SP-A1 or SP-A2 added Biophysical journal Medium 27508436
2011 SP-A is produced by human endometrium/decidua and selectively inhibits prostaglandin F2α (PGF2α) production by term decidual stromal cells at a post-transcriptional level without affecting other inflammatory mediators; decidual SP-A expression decreases with labor onset. Immunohistochemistry and RT-PCR for SP-A localization, isolated decidual stromal cell culture with SP-A treatment, ELISA for PGF2α and other mediators, RT-PCR for eicosanoid gene expression The Journal of clinical endocrinology and metabolism Medium 21270323
1996 SP-A does not stimulate endocytosis of lipid vesicles by type II cells or MLE-12 cells but does cause surface aggregation of lipid; SP-B and SP-C stimulate lipid endocytosis, with SP-C being most potent; SP-A's role in surfactant recycling is thus distinct from SP-B and SP-C. Fluorescently labeled lipid vesicle binding and endocytosis assay at 4°C and 37°C in rat type II cells and MLE-12 cells with purified SP-A, SP-B, SP-C The American journal of physiology Medium 8772529
2009 SP-A has a bacteriostatic effect on Mycoplasma pneumoniae by binding surface disaturated phosphatidylglycerols and the Mp membrane protein MPN372; SP-A deficiency leads to exaggerated inflammatory responses (TNF-α-driven) and more severe physiological consequences after Mp infection in mice. SP-A -/- vs. wild-type mouse infection with M. pneumoniae, airway hyperresponsiveness measurement, BAL cytokine analysis, pharmacological TNF-α inhibition Journal of immunology Medium 19494306

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2005 Surfactant proteins SP-A and SP-D: structure, function and receptors. Molecular immunology 413 16213021
1996 Altered surfactant function and structure in SP-A gene targeted mice. Proceedings of the National Academy of Sciences of the United States of America 350 8790375
2005 The lung collectins, SP-A and SP-D, modulate pulmonary innate immunity. Molecular immunology 157 15589315
2000 Polymorphisms of human SP-A, SP-B, and SP-D genes: association of SP-B Thr131Ile with ARDS. Clinical genetics 154 11076040
1991 Pulmonary surfactant protein A (SP-A) specifically binds dipalmitoylphosphatidylcholine. The Journal of biological chemistry 149 1993679
1992 Characterization of a second human pulmonary surfactant-associated protein SP-A gene. American journal of respiratory cell and molecular biology 122 1372511
2021 SP-A and SP-D: Dual Functioning Immune Molecules With Antiviral and Immunomodulatory Properties. Frontiers in immunology 121 33542724
2013 Blood biomarkers MMP-7 and SP-A: predictors of outcome in idiopathic pulmonary fibrosis. Chest 114 23715088
2002 Absence of SP-A modulates innate and adaptive defense responses to pulmonary influenza infection. American journal of physiology. Lung cellular and molecular physiology 114 11839553
2016 Germline SFTPA1 mutation in familial idiopathic interstitial pneumonia and lung cancer. Human molecular genetics 109 26792177
1997 SP-A enhances phagocytosis of Klebsiella by interaction with capsular polysaccharides and alveolar macrophages. The American journal of physiology 105 9124386
1992 Lung surfactant protein A (SP-A) enhances serum-independent phagocytosis of bacteria by alveolar macrophages. European journal of cell biology 103 1639094
1990 Binding of calcium to SP-A, a surfactant-associated protein. Biochemistry 101 2271565
1997 SP-A enhances uptake of bacillus Calmette-Guérin by macrophages through a specific SP-A receptor. The American journal of physiology 100 9176265
1999 Glycoprotein-340 binds surfactant protein-A (SP-A) and stimulates alveolar macrophage migration in an SP-A-independent manner. American journal of respiratory cell and molecular biology 94 10101009
2002 Serum levels of CC16, SP-A and SP-B reflect tobacco-smoke exposure in asymptomatic subjects. The European respiratory journal 93 12449168
2001 Surfactant protein A (SP-A): the alveolus and beyond. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 92 11149893
1998 Surfactant protein A (SP-A) gene targeted mice. Biochimica et biophysica acta 89 9813377
1992 Murine pulmonary surfactant SP-A gene: cloning, sequence, and transcriptional activity. The American journal of physiology 85 1443158
2004 Effects of ageing and smoking on SP-A and SP-D levels in bronchoalveolar lavage fluid. The European respiratory journal 81 15572540
1998 KGF increases SP-A and SP-D mRNA levels and secretion in cultured rat alveolar type II cells. American journal of respiratory cell and molecular biology 81 9476903
1989 Studies of the structure of lung surfactant protein SP-A. The American journal of physiology 81 2610270
2004 SP-A1 and SP-A2 variants differentially enhance association of Pseudomonas aeruginosa with rat alveolar macrophages. American journal of physiology. Lung cellular and molecular physiology 76 15377498
1998 Characteristics of surfactant from SP-A-deficient mice. The American journal of physiology 76 9700084
1997 Surfactant protein A (SP-A) mediates attachment of Mycobacterium tuberculosis to murine alveolar macrophages. American journal of respiratory cell and molecular biology 76 9271309
1994 Binding of human collectins (SP-A and MBP) to influenza virus. The Biochemical journal 73 7998980
1989 Cellular uptake and processing of surfactant lipids and apoprotein SP-A by rat lung. Journal of applied physiology (Bethesda, Md. : 1985) 73 2708254
2004 Linkage of neutrophil serine proteases and decreased surfactant protein-A (SP-A) levels in inflammatory lung disease. Thorax 71 15047952
1994 Human SP-A1 and SP-A2 genes are differentially regulated during development and by cAMP and glucocorticoids. The American journal of physiology 71 8179013
2009 Genetic complexity of the human innate host defense molecules, surfactant protein A1 (SP-A1) and SP-A2--impact on function. Critical reviews in eukaryotic gene expression 70 19392648
2019 A homozygous SFTPA1 mutation drives necroptosis of type II alveolar epithelial cells in patients with idiopathic pulmonary fibrosis. The Journal of experimental medicine 64 31601679
2010 Humanized SFTPA1 and SFTPA2 transgenic mice reveal functional divergence of SP-A1 and SP-A2: formation of tubular myelin in vivo requires both gene products. The Journal of biological chemistry 64 20048345
2002 FDC-SP, a novel secreted protein expressed by follicular dendritic cells. Journal of immunology (Baltimore, Md. : 1950) 62 12193705
2010 Role of surfactant protein A and D (SP-A and SP-D) in human antiviral host defense. Frontiers in bioscience (Scholar edition) 60 20036966
2005 Surfactant proteins SP-A and SP-D in human health and disease. Archivum immunologiae et therapiae experimentalis 59 16314824
1999 SP-A enhances viral clearance and inhibits inflammation after pulmonary adenoviral infection. The American journal of physiology 59 10484466
1995 Differential regulation of the mannose and SP-A receptors on macrophages. The American journal of physiology 58 8572233
1989 Effect of surfactant-associated protein-A (SP-A) on the activity of lipid extract surfactant. Biochimica et biophysica acta 58 2713385
1990 Phorbol ester inhibits surfactant protein SP-A and SP-B expression. The Journal of biological chemistry 57 2249989
1993 Biphasic glucocorticoid regulation of pulmonary SP-A: characterization of inhibitory process. The American journal of physiology 56 8460712
1991 Specific interaction of lung surfactant protein A (SP-A) with rat alveolar macrophages. Experimental cell research 55 1846339
1994 SP-A, SP-B, and SP-C in surfactant subtypes around birth: reexamination of alveolar life cycle of surfactant. The American journal of physiology 54 8179020
1996 Nitration of surfactant protein A (SP-A) tyrosine residues results in decreased mannose binding ability. Archives of biochemistry and biophysics 53 8806782
2010 Susceptibility of mice genetically deficient in SP-A or SP-D gene to invasive pulmonary aspergillosis. Molecular immunology 52 20413160
1989 The interaction of a lung surfactant protein (SP-A) with macrophages is mannose dependent. European journal of cell biology 52 2627938
2013 Surfactant protein (SP)-A suppresses preterm delivery and inflammation via TLR2. PloS one 51 23700442
1995 SP-A deficiency in primate model of bronchopulmonary dysplasia with infection. In situ mRNA and immunostains. American journal of respiratory and critical care medicine 51 7881683
1998 Differential regulation of SP-A1 and SP-A2 genes by cAMP, glucocorticoids, and insulin. The American journal of physiology 50 9486201
1988 Requirement of the collagenous domain for carbohydrate processing and secretion of a surfactant protein, SP-A. Biochimica et biophysica acta 50 3355864
2016 Surfactant proteins, SP-A and SP-D, in respiratory fungal infections: their role in the inflammatory response. Respiratory research 49 27250970
1996 Overexpression of surfactant protein SP-A, SP-B, and SP-C mRNA in rat lungs with lipopolysaccharide-induced injury. Laboratory investigation; a journal of technical methods and pathology 48 8569184
1998 Regulation of expression of human SP-A1 and SP-A2 genes in fetal lung explant culture. Biochimica et biophysica acta 47 9689918
2001 Macrophage and type II cell catabolism of SP-A and saturated phosphatidylcholine in mouse lungs. American journal of physiology. Lung cellular and molecular physiology 45 11350807
2016 Human Pulmonary Surfactant Protein SP-A1 Provides Maximal Efficiency of Lung Interfacial Films. Biophysical journal 44 27508436
2001 Localization and functions of SP-A and SP-D at mucosal surfaces. Pediatric pathology & molecular medicine 44 11486736
2018 Genetic Association of Pulmonary Surfactant Protein Genes, SFTPA1, SFTPA2, SFTPB, SFTPC, and SFTPD With Cystic Fibrosis. Frontiers in immunology 42 30333828
1996 Roles of SP-A, SP-B, and SP-C in modulation of lipid uptake by pulmonary epithelial cells in vitro. The American journal of physiology 42 8772529
1992 Surfactant protein A (SP-A) is decreased in acute parenchymal lung injury associated with polytrauma. European journal of clinical investigation 41 1478239
2005 Variants of the SFTPA1 and SFTPA2 genes and susceptibility to tuberculosis in Ethiopia. Human genetics 40 16292672
2002 Surfactant proteins SP-A and SP-D as modulators of the allergic inflammation in asthma. Pathobiology : journal of immunopathology, molecular and cellular biology 40 12771511
2020 Functional assessment and phenotypic heterogeneity of SFTPA1 and SFTPA2 mutations in interstitial lung diseases and lung cancer. The European respiratory journal 39 32855221
2002 Recombinant human SP-A1 and SP-A2 proteins have different carbohydrate-binding characteristics. American journal of physiology. Lung cellular and molecular physiology 39 12505869
2001 Role of surfactant protein A (SP-A)/lipid interactions for SP-A functions in the lung. Pediatric pathology & molecular medicine 39 11486733
1996 Clara cell protein (CC-16) and surfactant-associated protein A (SP-A) in asbestos-exposed workers. Chest 38 8620724
2013 Ligands and receptors of lung surfactant proteins SP-A and SP-D. Frontiers in bioscience (Landmark edition) 37 23747872
2021 Human Surfactant Protein SP-A1 and SP-A2 Variants Differentially Affect the Alveolar Microenvironment, Surfactant Structure, Regulation and Function of the Alveolar Macrophage, and Animal and Human Survival Under Various Conditions. Frontiers in immunology 35 34484180
2018 Differential effects of innate immune variants of surfactant protein-A1 (SFTPA1) and SP-A2 (SFTPA2) in airway function after Klebsiella pneumoniae infection and sex differences. Respiratory research 35 29394894
2000 Effect of surfactant protein A (SP-A) on the production of cytokines by human pulmonary macrophages. Shock (Augusta, Ga.) 35 11028547
2001 Both human SP-A1 and Sp-A2 genes are expressed in small and large intestine. Pediatric pathology & molecular medicine 34 11552738
2012 Genetic complexity of the human surfactant-associated proteins SP-A1 and SP-A2. Gene 32 23069847
2009 P63 (CKAP4) as an SP-A receptor: implications for surfactant turnover. Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology 32 20054143
2001 Amiodarone inhibits lung degradation of SP-A and perturbs the distribution of lysosomal enzymes. American journal of physiology. Lung cellular and molecular physiology 32 11597911
2016 Surfactant Proteins SP-A and SP-D Ameliorate Pneumonia Severity and Intestinal Injury in a Murine Model of Staphylococcus Aureus Pneumonia. Shock (Augusta, Ga.) 30 26849628
2000 Comparison of SP-A and LPS effects on the THP-1 monocytic cell line. American journal of physiology. Lung cellular and molecular physiology 30 10893209
2000 Tolerance of SP-A-deficient mice to hyperoxia or exercise. Journal of applied physiology (Bethesda, Md. : 1985) 30 10926649
1998 Suppressive effects of SP-A on ionomycin-induced IL-8 production and release by eosinophils. International archives of allergy and immunology 30 9758900
1996 SP-A-binding protein BP55 is involved in surfactant endocytosis by type II pneumocytes. The American journal of physiology 30 8843792
2013 Differences in the alveolar macrophage proteome in transgenic mice expressing human SP-A1 and SP-A2. Journal of proteomics and genomics research 29 24729982
2019 Resistance towards metronidazole in Blastocystis sp.: A pathogenic consequence. PloS one 28 30794628
2012 Air pollution and epigenetics: effects on SP-A and innate host defence in the lung. Swiss medical weekly 28 22553125
2008 SP-A permeabilizes lipopolysaccharide membranes by forming protein aggregates that extract lipids from the membrane. Biophysical journal 28 18599636
2011 Surfactant protein-A (SP-A) selectively inhibits prostaglandin F2alpha (PGF2alpha) production in term decidua: implications for the onset of labor. The Journal of clinical endocrinology and metabolism 27 21270323
2003 SP-A is necessary for increased clearance of alveolar DPPC with hyperventilation or secretagogues. American journal of physiology. Lung cellular and molecular physiology 27 12676766
2001 Endocytosed SP-A and surfactant lipids are sorted to different organelles in rat type II pneumocytes. American journal of physiology. Lung cellular and molecular physiology 27 11435209
2009 SP-A preserves airway homeostasis during Mycoplasma pneumoniae infection in mice. Journal of immunology (Baltimore, Md. : 1950) 26 19494306
1990 Identification and Plant Interaction of a Phyllobacterium sp., a Predominant Rhizobacterium of Young Sugar Beet Plants. Applied and environmental microbiology 26 16348158
2016 Novel expression of a functional trimeric fragment of human SP-A with efficacy in neutralisation of RSV. Immunobiology 25 27793398
2015 Surfactant protein A (SP-A) inhibits agglomeration and macrophage uptake of toxic amine modified nanoparticles. Nanotoxicology 25 25676620
2006 TGF-beta1 in SP-A preparations influence immune suppressive properties of SP-A on human CD4+ T lymphocytes. American journal of physiology. Lung cellular and molecular physiology 25 16648238
2011 SP-A1, SP-A2 and SP-D gene polymorphisms in severe acute respiratory syncytial infection in Chilean infants. Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases 24 21601013
2005 Rare SP-A alleles and the SP-A1-6A(4) allele associate with risk for lung carcinoma. Clinical genetics 24 15996209
2020 Serum SP-A and KL-6 levels can predict the improvement and deterioration of patients with interstitial pneumonia with autoimmune features. BMC pulmonary medicine 23 33267857
2002 Surfactant protein A and D (SP-A, AP-D) levels in patients with septic ARDS. Research communications in molecular pathology and pharmacology 23 15244040
2008 Circulating surfactant protein A (SP-A), a marker of lung injury, is associated with insulin resistance. Diabetes care 22 18285549
2006 Association of common haplotypes of surfactant protein A1 and A2 (SFTPA1 and SFTPA2) genes with severity of lung disease in cystic fibrosis. Pediatric pulmonology 22 16429424
1997 Transcriptional regulation of surfactant proteins SP-A and SP-B by phorbol ester. Biochimica et biophysica acta 22 9294011
2010 Surfactant protein (SP)-A and SP-D as antimicrobial and immunotherapeutic agents. Recent patents on anti-infective drug discovery 21 20230362
2006 Neither SP-A nor NH2-terminal domains of SP-A can substitute for SP-D in regulation of alveolar homeostasis. American journal of physiology. Lung cellular and molecular physiology 21 16500946
1995 Human SP-A: then and now. The American journal of physiology 21 7864137
1993 Internalization of surfactant protein A (SP-A) into lamellar bodies of rat alveolar type II cells in vitro. The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society 21 8417113

Missed literature

Know a paper Affinage missed for SFTPA1? Flag it for the maintainers and the community.

No submissions yet.