Affinage

SFTPA2

Pulmonary surfactant-associated protein A2 · UniProt Q8IWL1

Length
248 aa
Mass
26.2 kDa
Annotated
2026-06-10
47 papers in source corpus 23 papers cited in narrative 23 extracted findings
Cross-family judge vs UniProt: tie faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

SFTPA2 encodes SP-A2, a calcium-dependent carbohydrate-binding collectin of pulmonary surfactant that contributes to innate host defense and surfactant structural organization in the lung (PMID:12505869, PMID:17542781). SP-A2 assembles into higher-order supratrimeric oligomers, and this degree of oligomeric assembly correlates with tighter binding to bacterial Re-LPS, calcium-dependent self-association, and the capacity to aggregate LPS and phospholipids (PMID:17542781); through its lectin/carbohydrate-recognition domain SP-A2 binds a wide range of sugars with higher affinity than the SP-A1 gene product (PMID:12505869). Functionally, SP-A2 variants enhance the association and internalization of bacteria such as Pseudomonas aeruginosa by alveolar macrophages more potently than SP-A1, an activity dependent on mammalian post-translational modification (PMID:15377498, PMID:17220308), and modulate surfactant phospholipid handling by inhibiting type II cell phosphatidylcholine secretion and organizing SP-B-containing lipid monolayers (PMID:15065867, PMID:17678872). SP-A1 and SP-A2 gene products are functionally non-redundant: both are required together for tubular myelin formation in vivo (PMID:20048345). SP-A2 shapes host responses to infection and injury in an allele-specific manner, with the Gln223Lys polymorphism governing binding to Mycoplasma pneumoniae membrane fractions, EGFR-dependent limitation of mucin production and neutrophil influx, NF-κB-dependent TNF-α induction, and IL-13/MUC5AC-driven airway responses, where the 223Q allele and 223Q-spanning peptides are protective (PMID:25957169, PMID:32513852, PMID:35874703). SFTPA2 expression is controlled transcriptionally through a CRE-like element (CRESP-A2) bound by fetal lung nuclear proteins for basal and cAMP-inducible activity (PMID:8770068), TTF-1 binding elements (PMID:9843844), and an intronic AP-1/Jun element mediating phorbol ester repression (PMID:10914330), with additional regulation by 5'-UTR splice variants affecting mRNA stability and translation (PMID:15894557). Pathogenic SFTPA2 mutations (including G231V and F198S) preserve protein production but abolish secretion, causing intracellular aggregation that is alleviated by the chaperone GRP78/BiP and the chemical chaperone 4-PBA (PMID:30293573, PMID:32855221).

Mechanistic history

Synthesis pass · year-by-year structured walk · 14 steps
  1. 1994 High

    Establishing the SFTPA2 gene/transcript architecture and its distinct developmental and hormonal regulation defined SP-A2 as a separately controlled gene rather than a redundant duplicate of SP-A1.

    Evidence Primer extension, RACE and sequencing of fetal lung cDNAs plus organ culture with cAMP/dexamethasone

    PMID:8179012 PMID:8179013

    Open questions at the time
    • Did not address functional consequences of the SP-A1/SP-A2 sequence differences
    • Promoter elements responsible for differential regulation not yet mapped
  2. 1996 High

    Identifying the CRESP-A2 CRE-like element answered how SP-A2 achieves basal and cAMP-inducible transcription in type II cells, distinguishing its regulation from a canonical CRE.

    Evidence Reporter transfection, competitive EMSA, UV cross-linking and mutagenesis in primary human type II cells

    PMID:8770068

    Open questions at the time
    • Identities of the ~50/36/30 kDa CRESP-A2-binding proteins not determined
    • Relationship between the ~30 kDa protein loss and differentiation not mechanistically resolved
  3. 1998 Medium

    Mapping TTF-1 binding elements in the proximal promoter identified a lineage-specific transcription factor input governing SP-A2 expression in alveolar epithelium.

    Evidence DNase I footprinting, EMSA with recombinant TTF-1, and reporter transfection (baboon ortholog)

    PMID:9843844

    Open questions at the time
    • Performed on baboon genes; human element positioning not directly tested here
    • Combinatorial logic with CRESP-A2 not resolved
  4. 2000 Medium

    An intronic AP-1/Jun element explained phorbol-ester repression of SP-A2, linking PKC signaling to negative transcriptional control.

    Evidence Deletional reporter analysis, EMSA, antibody supershift and mutagenesis in NCI-H441 cells

    PMID:10914330

    Open questions at the time
    • Physiological stimulus driving Jun recruitment in vivo not identified
    • Specific Jun family member not pinpointed
  5. 2002 Medium

    Direct carbohydrate-binding comparison established that SP-A2 binds sugars with higher affinity and broader specificity than SP-A1, providing a biochemical basis for differential lectin function.

    Evidence Carbohydrate-binding assays with recombinant SP-A1 and SP-A2 at defined calcium concentrations

    PMID:12505869

    Open questions at the time
    • Structural basis of the affinity difference not defined
    • In vivo relevance of submucosal-gland-restricted SP-A2 expression not tested
  6. 2004 Medium

    Functional assays showed SP-A2 variants are more active than SP-A1 in promoting bacterial phagocytosis and in suppressing type II cell PC secretion, beginning the case for SP-A2 as the more biologically active gene product.

    Evidence Phagocytic index assay and PC secretion assay using insect-cell-expressed variants plus ozone-oxidation analysis

    PMID:15065867 PMID:15377498

    Open questions at the time
    • Insect-cell proteins lack mammalian PTMs
    • Mechanism linking oxidation of specific residues to activity loss not resolved
  7. 2005 Medium

    5'-UTR splice variants were shown to tune SP-A output post-transcriptionally via mRNA stability and translational efficiency, adding a layer of expression control beyond promoter activity.

    Evidence Luciferase reporter constructs with qPCR and mRNA decay assays

    PMID:15894557

    Open questions at the time
    • Trans-acting factors recognizing the 5'-UTRs not identified
    • Reporter context may not reflect native SP-A mRNA
  8. 2007 High

    Biophysical and improved expression studies linked SP-A2 supratrimeric oligomerization to LPS binding/aggregation and confirmed PTM-dependent phagocytic potency, connecting quaternary structure to innate-immune function.

    Evidence Analytical ultracentrifugation, DSC, fluorescence spectroscopy and binding assays; CHO-expressed variants in macrophage assays; lipid monolayer microscopy; hemagglutination inhibition

    PMID:17220308 PMID:17520282 PMID:17542781 PMID:17678872

    Open questions at the time
    • No atomic structure of the oligomer
    • SP-A1 vs SP-A2 equivalence against avian-like IAV indicates the activity difference is pathogen-specific, mechanism unresolved
  9. 2010 High

    Humanized transgenic and rescue experiments demonstrated that tubular myelin formation requires both SP-A1 and SP-A2, defining a non-redundant structural cooperation between the two gene products in vivo.

    Evidence Electron microscopy in humanized transgenic mice on SP-A-null background, human BAL analysis, and exogenous SP-A rescue

    PMID:20048345

    Open questions at the time
    • Molecular interface mediating SP-A1/SP-A2 cooperation unknown
    • Functional consequence of tubular myelin loss for surfactant function not quantified here
  10. 2015 High

    The Gln223Lys polymorphism was shown to control SP-A2 binding to M. pneumoniae and allele-specific limitation of mucin production through EGFR signaling, defining a genotype-dependent host-defense mechanism.

    Evidence Humanized SP-A2 transgenic mice with MMF challenge, pharmacologic EGFR inhibition, and EGFR phosphorylation Westerns

    PMID:25957169

    Open questions at the time
    • Direct biochemical interaction of SP-A2 with EGFR not demonstrated
    • How allelic binding difference translates to EGFR modulation not resolved
  11. 2018 Medium

    In vivo infection, lung-function and stress studies extended the allele- and gene-specific functional hierarchy of SP-A2 to survival, airway resistance, miRNA-mediated stress responses, and revealed pathogenic mutations as secretion-deficient.

    Evidence Humanized transgenic mouse K. pneumoniae survival and methacholine challenge, ozone-stress miRNA profiling, and CHO-cell secretion/aggregation assays of mutant SP-A2

    PMID:29202868 PMID:29394894 PMID:30293573 PMID:30459763

    Open questions at the time
    • Molecular basis of sex-specific SP-A2 effects not fully defined
    • Cell-surface receptors mediating differential phagocytic-cell binding not identified
  12. 2020 Medium

    Studies on disease mutations and 223Q-derived peptides clarified that pathogenic SFTPA2 mutations cause GRP78-regulated intracellular aggregation, and that the 223Q lectin-domain region dampens NF-κB-driven inflammation.

    Evidence GRP78 overexpression/knockdown and 4-PBA in CHO cells with ex vivo carrier tissue; SP-A KO mouse and RAW 264.7 cells with 20-mer peptides and NF-κB/p38 Westerns

    PMID:30293573 PMID:32513852 PMID:32855221

    Open questions at the time
    • Structural nature of the aggregates and the exact GRP78 interaction interface unknown
    • Whether peptide effects translate beyond rodent/cell models untested
  13. 2022 Medium

    Allele-specific protection in asthma models established SP-A2 223Q (full-length and peptides) as a suppressor of IL-13/MUC5AC-driven mucin and airway hyperresponsiveness, generalizing the 223 polymorphism's role to allergic airway disease.

    Evidence Recombinant protein treatment of asthmatic primary bronchial epithelial cells and humanized SP-A2 mice in house dust mite and IL-13 challenge models

    PMID:35874703

    Open questions at the time
    • Receptor/target through which 223Q peptides act on epithelium not defined
    • Durability and human applicability of peptide protection not established
  14. 2024 Medium

    A SARS-CoV-2 model probed SP-A2 variant effects on viral lung injury, indicating SP-A reduces viral titers while the 1A0 variant associates with severe injury and altered innate signaling.

    Evidence Humanized hACE2 + SP-A variant double-transgenic mice with SARS-CoV-2 challenge, transcriptomics and cytokine multiplex (preprint)

    PMID:bio_10.1101_2024.09.11.612497

    Open questions at the time
    • Preprint not peer-reviewed
    • Mechanistic link between variant and the implicated signaling pathways not established

Open questions

Synthesis pass · forward-looking unresolved questions
  • How SP-A2 oligomers engage specific alveolar macrophage and epithelial receptors to drive phagocytosis, EGFR/NF-κB modulation, and surfactant organization remains structurally and mechanistically undefined.
  • No atomic structure of SP-A2 oligomers or its receptor complexes
  • Direct SP-A2 receptor(s) on phagocytic cells not molecularly identified
  • Mechanism connecting carbohydrate binding to downstream EGFR and NF-κB signaling unresolved

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Localization
GO:0005576 extracellular region 2 GO:0005783 endoplasmic reticulum 1
Pathway
R-HSA-168256 Immune System 4
Partners
EGFRGRP78/HSPA5SFTPA1SFTPB
Complex memberships
tubular myelin (SP-A1/SP-A2)

Evidence

Reading pass · 23 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2004 SP-A2 variants (1A0, 1A) enhance association of Pseudomonas aeruginosa with rat alveolar macrophages significantly more than SP-A1 variants (6A2, 6A4), with SP-A1 phagocytic index approximately 52-95% of SP-A2 activity; coexpressed SP-A1/SP-A2 at certain concentrations were more active than single gene products. Light microscopy-based phagocytic index assay using insect cell-expressed human SP-A variants with rat alveolar macrophages American journal of physiology. Lung cellular and molecular physiology Medium 15377498
2007 CHO cell-expressed SP-A2 variants stimulate phagocytosis (cell association and internalization) of P. aeruginosa by rat and human alveolar macrophages more than SP-A1 variants, with activity order 1A1>1A0>6A2>6A4; CHO-expressed SP-A was considerably more active than insect cell-expressed variants, implicating mammalian post-translational modifications in SP-A phagocytic activity. Light microscopy (cell association) and FACS (internalization) using CHO cell-expressed SP-A variants with rat and human alveolar macrophages Infection and immunity High 17220308
2004 SP-A2 variant (1A0) and coexpressed SP-A1/SP-A2 (1A0/6A2) inhibit ATP-stimulated phosphatidylcholine secretion from alveolar type II cells to a greater extent than SP-A1 (6A2); this biological activity is susceptible to ozone-induced oxidation. SP-A1 forms higher-order multimers than SP-A2 under various conditions, and ozone oxidation involves cysteine, methionine, and tryptophan residues. In vitro PC secretion assay with alveolar type II cells; oligomerization analysis; ozone exposure with amino acid oxidation characterization Biochemistry Medium 15065867
2002 Recombinant SP-A2 binds carbohydrates with higher affinity and to a wider variety of sugars than SP-A1 at 1 or 5 mM Ca2+; all SP-A proteins bind fucose with greatest affinity; SP-A2 is only expressed in submucosal glands of conducting airways whereas both SP-A1 and SP-A2 are in alveoli. Carbohydrate-binding assays with recombinant human SP-A1 and SP-A2 proteins under defined calcium concentrations American journal of physiology. Lung cellular and molecular physiology Medium 12505869
2007 SP-A2 (1A0) forms higher-order supratrimeric oligomers than SP-A1; greater supratrimeric assembly correlates with lower Kd for binding to bacterial Re-LPS, greater self-association in the presence of calcium, and greater capability to aggregate Re-LPS and phospholipids; SP-A1 is more resistant to trypsin degradation than SP-A2; coexpressed SP-A1/SP-A2 has greater thermal stability and combines properties of each. Analytical ultracentrifugation, differential scanning calorimetry, fluorescence spectroscopy, LPS binding and aggregation assays, proteolysis resistance assay using recombinant baculovirus-derived proteins The Biochemical journal High 17542781
2010 Formation of tubular myelin in vivo requires both SP-A1 and SP-A2 gene products; humanized transgenic mice expressing only SP-A1(6A4) or only SP-A2(1A3) lacked tubular myelin, while mice carrying both had tubular myelin; tubular myelin was observed in human bronchoalveolar lavage only when both SP-A1 and SP-A2 were present; in vivo rescue confirmed tubular myelin restored only by exogenous SP-A containing both SP-A1 and SP-A2. Electron microscopy in humanized transgenic mice on SP-A knockout background; human BAL analysis; in vivo rescue with exogenous SP-A administration The Journal of biological chemistry High 20048345
2007 SP-A1 (6A2) and SP-A2 (1A0) variants have differential effects on the organization of phospholipid monolayers containing SP-B; lipid films with SP-B and SP-A2 (1A0) showed surface features similar to those with native human SP-A, including fluorescent probe-excluding clusters coexisting with liquid-expanded and liquid-condensed phases, whereas SP-A1 (6A2) showed different protein distribution. Fluorescence microscopy of phospholipid monolayers at the air-water interface containing SP-B and SP-A variants Biochimica et biophysica acta Medium 17678872
1994 SP-A2 gene is more highly regulated by cAMP and during fetal development than SP-A1; in adult lung, 65% of SP-A mRNA is from SP-A2, while in 28-week neonate only SP-A1 transcripts were detected; cAMP and glucocorticoids (dexamethasone) differentially regulate SP-A1 and SP-A2 transcription. Primer extension analysis of human adult and fetal lung tissues; organ culture of fetal lung with DBcAMP and dexamethasone; Northern analysis The American journal of physiology Medium 8179013
1994 SP-A2 mRNA transcripts are always comprised of sequences within six exons (with an extra exon II encoding additional 5'-UTR sequences absent in SP-A1); most SP-A1 transcripts use five exons; both genes produce alternatively spliced transcripts from alternate exons; SP-A1 majority transcripts initiate 5 bp downstream of the SP-A2 transcription initiation site. Primer extension, RACE (rapid amplification of cDNA ends), sequencing of 47 full-length primer-extended cDNAs from human fetal lung explants The American journal of physiology High 8179012
1996 A CRE-like element (CRESP-A2: TGACCTTA) at -242 bp in the SP-A2 promoter is essential for basal and cAMP-inducible expression in alveolar type II cells; nuclear proteins from fetal lung bind specifically to CRESP-A2, with proteins of ~50, 36, and 30 kDa identified by UV cross-linking; upon DBcAMP-induced differentiation, the ~30 kDa protein binding is lost; mutation of CRESP-A2 markedly reduces both basal and cAMP-stimulated expression; CRESP-A2 binds different proteins than the canonical CRE. Transfection of SP-A2 5'-flanking DNA-hGH fusion genes into primary human type II cells; competitive EMSA; UV cross-linking with nuclear extracts; site-directed mutagenesis of CRESP-A2 The American journal of physiology High 8770068
1998 In baboon SP-A2 and SP-A1 genes, three TTF-1 (thyroid transcription factor-1) binding elements are present within 255 bp of 5'-flanking sequence of each gene but differ in position and spacing; 255 bp of 5'-flanking DNA from either bSP-A1 or bSP-A2 is sufficient to mediate high basal and cAMP-inducible expression in type II cells. DNase I footprinting, EMSA with bacterially expressed TTF-1 and type II cell nuclear extracts, transfection of 5'-flanking DNA-hGH fusion genes into primary type II cells The American journal of physiology Medium 9843844
2000 Phorbol ester (TPA) represses SP-A2 promoter activity (~55-65% reduction); a region in SP-A2 intron 1 (+309/+329) forms TPA-induced sequence-specific DNA-protein complexes; the consensus AP-1-like sequence (TCACTGA in SP-A2) is required for complex formation; TPA-induced complex contains Jun family proteins (not Fos); mutation of this AP-1-like site prevents TPA-induced complex formation. Deletional analysis of SP-A promoter by transfection in NCI-H441 cells; EMSA with NCI-H441 nuclear proteins; antibody supershift for Jun/Fos family proteins; site-directed mutagenesis of AP-1-like site Experimental lung research Medium 10914330
2005 SP-A 5'-UTR splice variants differentially regulate SP-A production through mRNA stability and translational efficiency; the ABD variant has the lowest rate of mRNA decay; ABD and AB'D' 5'-UTR variants have higher translational efficiency than control; A'D' and A'CD' have lower translational efficiency than control; all four variants studied increased luciferase mRNA stability. In vitro transient expression of hSP-A 5'-UTR constructs with luciferase reporter; quantitative real-time PCR for mRNA levels; mRNA decay assays American journal of physiology. Lung cellular and molecular physiology Medium 15894557
2015 Allelic differences in SP-A2 at position Gln223Lys affect binding to Mycoplasma pneumoniae membrane fractions (MMF); humanized SP-A2 transgenic mice with 223K allele exhibit reduced neutrophil influx and mucin production when challenged with MMF compared to SP-A-/- mice; mice expressing 223Q have increased neutrophil influx and mucin production similar to SP-A-/- mice; SP-A interaction with EGFR signaling pathway limits MMF-stimulated mucin production in an allele-specific manner; EGFR phosphorylation is increased in MMF-challenged SP-A-/- lungs and pharmacologic EGFR inhibition reduces mucin production. Humanized SP-A2 transgenic mouse model with MMF challenge; measurement of neutrophil recruitment and mucin production; pharmacologic EGFR inhibition; Western blot for EGFR phosphorylation; tracheal epithelial cell cultures Journal of immunology High 25957169
2020 A 20-mer peptide derived from the lectin/carbohydrate recognition domain of SP-A2 containing the 223Q variant significantly decreases TNF-α mRNA and protein levels during M. pneumoniae infection; the 223Q-20mer peptide reduces NF-κB p65 phosphorylation in both SP-A KO mice and RAW 264.7 cells; neither 20-mer (223Q or 223K) affected p38 phosphorylation. SP-A knockout mouse model challenged with live M. pneumoniae; RAW 264.7 macrophage cell line; qPCR for TNF-α mRNA; ELISA for TNF-α protein; Western blot for NF-κB p65 and p38 phosphorylation Infection and immunity Medium 32513852
2018 Pathogenic mutations in SFTPA2 (including G231V and F198S) cause preserved protein production but abolished secretion; mutant SP-A2 forms aggregates intracellularly; chemical chaperone 4-PBA enhances secretion and decreases aggregation of mutant SP-A2; GRP78 (BiP) overexpression reduces mutant SP-A2 aggregation while GRP78 knockdown enhances it; 4-PBA upregulates GRP78 expression, partially accounting for its aggregate-alleviating effect. In vitro expression of mutant SP-A2 in CHO-K1 cells; secretion and aggregation assays; MG-132 proteasome inhibition; chymotrypsin degradation assay; GRP78 overexpression and shRNA knockdown; Western blot Biochimica et biophysica acta. Molecular basis of disease Medium 30293573
2020 Pathogenic SFTPA2 mutations preserve protein production but abolish SP-A secretion in cell models; ex vivo lung tissue from mutation carriers showed altered SP-A expression patterns; secretion defect confirmed in 11 different SFTPA1/SFTPA2 mutations. In vitro expression of mutant proteins with secretion/production assays; ex vivo immunostaining of lung tissue from mutation carriers The European respiratory journal Medium 32855221
2007 SP-A1 and SP-A2 CHO-expressed variants both display α(2,3)-linked sialic acids and have similar activity against influenza A virus PR-8 strain (which preferentially binds α(2,3)-linked sialic acids), suggesting no difference between SP-A1 and SP-A2 in inhibiting hemagglutination of avian-like IAV strains. Hemagglutination inhibition assay with CHO-expressed SP-A variants; sialic acid linkage analysis Medical microbiology and immunology Medium 17520282
2022 Full-length recombinant SP-A2 223Q is more effective than SP-A2 223K at reducing IL-13-induced MUC5AC gene expression in primary bronchial epithelial cells from asthmatic participants; 10- and 20-mer peptides spanning position 223Q of SP-A2 reduce eosinophilic inflammation, mucin production and airway hyperresponsiveness in a house dust mite mouse model and protect from lung function decline during IL-13 challenge. Recombinant protein treatment of primary human bronchial epithelial cells; humanized SP-A2 transgenic mouse models; house dust mite and IL-13 challenge models; measurement of mucin (MUC5AC), eosinophils, and airway hyperresponsiveness Frontiers in immunology Medium 35874703
2018 SP-A2 (1A3) transgenic male mice show increased total and central airway resistance after methacholine challenge following K. pneumoniae infection; allele-specific differences exist with SP-A2 (1A3) exhibiting significantly higher lung resistance than SP-A2 (1A0); sex-specific differences in airway responses are observed with SP-A2 variants. Humanized transgenic mouse model; flexiVent forced oscillation technique measurements after K. pneumoniae infection and methacholine challenge Respiratory research Medium 29394894
2018 SP-A1 and SP-A2 variants differentially affect survival after K. pneumoniae infection in a gene-, variant-, and sex-specific manner with order co-ex = SP-A2 > SP-A1 > KO; SP-A1 and SP-A2 differentially bind to phagocytic (but not non-phagocytic) cells; alveolar macrophages from SP-A1 and SP-A2 transgenic mice exhibit differential expression of cell surface proteins; treatment of KO mice with exogenous SP-A1 or SP-A2 significantly improves survival. Humanized transgenic mouse survival study with intratracheal K. pneumoniae infection; flow cytometry for cell surface protein expression on AMs; SP-A binding assays with phagocytic and non-phagocytic cells; exogenous SP-A rescue treatment Frontiers in immunology Medium 30459763
2017 SP-A2 in male transgenic mice influences miRNA-mediated sex-specific differences in response to ozone-induced oxidative stress; 11 miRNAs were differentially expressed under oxidative stress with targets including BCL2, CAT, FOXO1, IL-6, NF-κB, SOD2, and STAT3; SP-A2 promotes anti-apoptotic BCL2 mRNA increase and pro-inflammatory IL-6 elevation after oxidative stress; SOD2 protein increased while CAT was unchanged; sex hormones contribute to miRNome changes (confirmed by gonadectomy). Humanized SP-A2 transgenic and KO mice with ozone exposure; miRNA microarray; qPCR for target mRNAs; ELISA for cytokines and proteins; gonadectomy experiment Biology of sex differences Medium 29202868
2024 Human SP-A2 variant 1A0 transgenic mice infected with SARS-CoV-2 show more severe acute lung injury and higher mortality, similar to SP-A KO mice; SP-A-expressing mice have reduced viral titers relative to KO; 1A0 mice show upregulation of MyD88, Stat3, IL-18, and Jak2; Mapk1 is significantly downregulated in 6A2 versus 1A0 mice; NOD1/2 and Trem1 signaling pathways are involved; IL-6, G-CSF, and IL-1β levels are higher in KO and 1A0 mice. Humanized double-transgenic mice (hACE2 + individual SP-A variants) with intranasal SARS-CoV-2 challenge; survival monitoring; lung histology; viral titer measurement; transcriptomic analysis; cytokine/chemokine multiplex assay bioRxivpreprint Medium bio_10.1101_2024.09.11.612497

Source papers

Stage 0 corpus · 47 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2003 Association of polymorphisms in the collagen region of SP-A2 with increased levels of total IgE antibodies and eosinophilia in patients with allergic bronchopulmonary aspergillosis. The Journal of allergy and clinical immunology 97 12743564
2004 Differences in biochemical properties and in biological function between human SP-A1 and SP-A2 variants, and the impact of ozone-induced oxidation. Biochemistry 86 15065867
2005 Differences in the translation efficiency and mRNA stability mediated by 5'-UTR splice variants of human SP-A1 and SP-A2 genes. American journal of physiology. Lung cellular and molecular physiology 85 15894557
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
1997 Effect of genotype on the levels of surfactant protein A mRNA and on the SP-A2 splice variants in adult humans. The Biochemical journal 73 9003399
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
2007 Surfactant protein A2 (SP-A2) variants expressed in CHO cells stimulate phagocytosis of Pseudomonas aeruginosa more than do SP-A1 variants. Infection and immunity 66 17220308
1994 Characterization of mRNA transcripts and organization of human SP-A1 and SP-A2 genes. The American journal of physiology 65 8179012
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
1998 Differential regulation of SP-A1 and SP-A2 genes by cAMP, glucocorticoids, and insulin. The American journal of physiology 50 9486201
1998 Regulation of expression of human SP-A1 and SP-A2 genes in fetal lung explant culture. Biochimica et biophysica acta 47 9689918
2007 Structural and functional differences among human surfactant proteins SP-A1, SP-A2 and co-expressed SP-A1/SP-A2: role of supratrimeric oligomerization. The Biochemical journal 44 17542781
2018 Genetic Association of Pulmonary Surfactant Protein Genes, SFTPA1, SFTPA2, SFTPB, SFTPC, and SFTPD With Cystic Fibrosis. Frontiers in immunology 42 30333828
2005 Variants of the SFTPA1 and SFTPA2 genes and susceptibility to tuberculosis in Ethiopia. Human genetics 40 16292672
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
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
2001 Both human SP-A1 and Sp-A2 genes are expressed in small and large intestine. Pediatric pathology & molecular medicine 34 11552738
2007 Differential effects of human SP-A1 and SP-A2 variants on phospholipid monolayers containing surfactant protein B. Biochimica et biophysica acta 33 17678872
2012 Genetic complexity of the human surfactant-associated proteins SP-A1 and SP-A2. Gene 32 23069847
2002 Association of polymorphisms in the collagen region of human SP-A1 and SP-A2 genes with pulmonary tuberculosis in Indian population. Clinical chemistry and laboratory medicine 32 12476938
1996 A CRE-like element plays an essential role in cAMP regulation of human SP-A2 gene in alveolar type II cells. The American journal of physiology 30 8770068
2018 Survival of Surfactant Protein-A1 and SP-A2 Transgenic Mice After Klebsiella pneumoniae Infection, Exhibits Sex-, Gene-, and Variant Specific Differences; Treatment With Surfactant Protein Improves Survival. Frontiers in immunology 29 30459763
2017 SP-A2 contributes to miRNA-mediated sex differences in response to oxidative stress: pro-inflammatory, anti-apoptotic, and anti-oxidant pathways are involved. Biology of sex differences 29 29202868
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
2007 Inhibition of hemagglutination activity of influenza A viruses by SP-A1 and SP-A2 variants expressed in CHO cells. Medical microbiology and immunology 26 17520282
2015 Genetic variation in SP-A2 leads to differential binding to Mycoplasma pneumoniae membranes and regulation of host responses. Journal of immunology (Baltimore, Md. : 1950) 24 25957169
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
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
1998 Differential regulation of baboon SP-A1 and SP-A2 genes: structural and functional analysis of 5'-flanking DNA. The American journal of physiology 21 9843844
2019 Differential Effects of Human SP-A1 and SP-A2 on the BAL Proteome and Signaling Pathways in Response to Klebsiella pneumoniae and Ozone Exposure. Frontiers in immunology 18 30972061
2019 Differential Impact of Co-expressed SP-A1/SP-A2 Protein on AM miRNome; Sex Differences. Frontiers in immunology 17 31475015
2020 Sex and SP-A2 Dependent NAD(H) Redox Alterations in Mouse Alveolar Macrophages in Response to Ozone Exposure: Potential Implications for COVID-19. Antioxidants (Basel, Switzerland) 16 32992843
2003 A single round PCR method for genotyping human surfactant protein (SP)-A1, SP-A2 and SP-D gene alleles. Tissue antigens 16 12753670
2021 Differential Regulation of Human Surfactant Protein A Genes, SFTPA1 and SFTPA2, and Their Corresponding Variants. Frontiers in immunology 14 34917085
2020 The Importance of Redox Status in the Frame of Lifestyle Approaches and the Genetics of the Lung Innate Immune Molecules, SP-A1 and SP-A2, on Differential Outcomes of COVID-19 Infection. Antioxidants (Basel, Switzerland) 13 32854247
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. Experimental lung research 13 10914330
2018 Chemical chaperone 4-phenylbutyric acid alleviates the aggregation of human familial pulmonary fibrosis-related mutant SP-A2 protein in part through effects on GRP78. Biochimica et biophysica acta. Molecular basis of disease 11 30293573
2020 A 20-Mer Peptide Derived from the Lectin Domain of SP-A2 Decreases Tumor Necrosis Factor Alpha Production during Mycoplasma pneumoniae Infection. Infection and immunity 8 32513852
2020 Differential Sex-Dependent Regulation of the Alveolar Macrophage miRNome of SP-A2 and co-ex (SP-A1/SP-A2) and Sex Differences Attenuation after 18 h of Ozone Exposure. Antioxidants (Basel, Switzerland) 7 33260937
2022 Small Peptide Derivatives Within the Carbohydrate Recognition Domain of SP-A2 Modulate Asthma Outcomes in Mouse Models and Human Cells. Frontiers in immunology 6 35874703
2020 Differences in the alveolar macrophage toponome in humanized SP-A1 and SP-A2 transgenic mice. JCI insight 6 33141765
2013 Long-range PCR based sequencing of the highly homologous genes, SFTPA1 and SFTPA2. Molecular and cellular probes 4 23354021
2022 Avian surfactant protein (SP)-A2 first arose in an early tetrapod before the divergence of amphibians and gradually lost the collagen domain. Developmental and comparative immunology 3 36306971
2015 Human Surfactant Proteins A2 (SP-A2) and B (SP-B) Genes as Determinants of Respiratory Distress Syndrome. Indian pediatrics 3 26061924

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