Human Pulmonary surfactant-associated protein A,SP-A ELISA Kit

1. This study is suggestive that the PCR (polymerase chain reaction) for the detection of coa, mecA, and spa gene is a fast, accurate, and valuable diagnostic tool. PMID: 30074012
2. TGF beta markedly decreased expression of SP-A, SP-B, SP-C, fatty acid synthase, and the phospholipid transporter ABCA3. However, TGF beta increased protein levels of SP-D with little change in mRNA levels. PMID: 29621540
3. this study shows that concentrations of SP-A are associated with polarization of macrophages in pleural effusions of non-small cell lung cancer PMID: 29111316
4. the SPA and SPD levels in EBC were correlated with lung function, which contributed to COPD diagnosis. PMID: 28791362
5. Data (including data from studies using transgenic/knockout mice) suggest that surfactant protein A1 (SPA1) interferes with EGF binding to EGFR in pulmonary alveoli cell lines; SPA1 directly binds extracellular domain of EGFR; binding of SPA1 to EGFR appears to be different from binding of SPD to EGFR; binding of SPA1 to EGFR does not suppress EGF-induced phosphorylation of EGFR or cell proliferation. PMID: 28972165
6. This review intends to provide a current overview of the genetics, structure and extra-pulmonary functions of the surfactant collectin proteins. PMID: 28351530
7. The SFTPA1 haplotype comprising rs17881720-A and rs17879335-G was a resistance factor while the haplotype comprising rs1914663-T and rs1059225-G was found to be a susceptibility factor to tuberculosis in Han Chinese population. PMID: 27012150
8. SP-A transiently enhances the basal protein expression of CHC and alpha-adaptin. PMID: 26771574
9. the presence of SP-A1 allows pulmonary surfactant to adopt a particularly favorable structure with optimal biophysical properties PMID: 27508436
10. SP-A1 6A4 and SP-A2 1A5 genetic variants may influence the susceptibility to respiratory distress syndrome in late-preterm infants, independently of the effect of other perinatal factors. PMID: 27835691
11. Direct interaction between SP-A or SAP01 and human BD-3 seemed to be responsible for the inhibitory effects on chemotaxis of mast cells. PMID: 28188794
12. SP-A (+186A/G) and SP-B (1580C/T) polymorphisms are strongly associated with the risk of respiratory distress syndrome (RDS) in preterm infants. Notably, reduced serum SP-A levels were correlated with a high risk of RDS and may serve as novel biomarkers for RDS detection and monitoring. PMID: 28011976
13. Surfactant protein A levels differed among idiopathic pulmonary fibrosis, pulmonary sarcoidosis and chronic pulmonary obstructive disease. PMID: 27758987
14. Differences were found regarding SPA and pro-SPB expression in the vast majority of subjects: in some lungs, SPA was more expressed whereas in others pro-SPB showed an higher degree of immunoreactivity. The expression of both surfactant proteins was not strictly correlated with gestational age. PMID: 27734990
15. Study identifies SFTPA1 as a gene involved in familial idiopathic interstitial pneumonia and shows that altered SP-A1 expression is associated with a large spectrum of phenotypic pulmonary manifestations ranging from severe respiratory insufficiency occurring early in life to lung fibrosis and cancer in adult patients. PMID: 26792177
16. These results suggested that the measurement of SPA levels in the exhaled breath condensate may serve as a method for monitoring airway obstruction in patients with chronic obstructive pulmonary disease. PMID: 26707652
17. Human and murine data together indicate that SP-A, SP-D and MBL are synthesized in early gestational tissues, and may contribute to regulation of immune response at the feto-maternal interface during pregnancy. PMID: 26603976
18. SP-A in exhaled particles from small airways may represent a promising non-invasive biomarker of disease in chronic obstructive pulmonary disease patients. PMID: 26656890
19. In this study, the loci and haplotypes associated with pulmonary tuberculosis (PTB)were found mostly to be located in the SFTPA2 gene, suggesting that the effects of the SFTPA2 gene on PTB are stronger than those of SFTPA1. PMID: 24984162
20. Data suggest that that surfactant protein A(SP-A) levels may be important to maintain surfactant function in the presence of high cholesterol within surfactant. PMID: 25522687
21. SP-A modulates lung immune system in the area of non-infectious lung diseases such as acute and chronic pulmonary fibrosis and lung cancer. PMID: 24705741
22. 12 of which predicted to bind SP-A 3'UTRs. PMID: 25058539
23. This study shows that changes occur in the alveolar macrophage proteome in response to a single in vivo treatment with exogenous SP-A1 and/or SP-A2. PMID: 24954098
24. SP-A1 transcripts, which in turn negatively affect SP-A1 translation, possibly affecting SP-A1/SP-A2 ratio, with potential for clinical implication. PMID: 25326576
25. In this review, we highlight the associations of eosinophilic lung diseases with SP-A and SP-D levels and functions. PMID: 24960334
26. sequence variability at the 3'UTR of SFTPA1 and SFTPA2 gene variants differentially affects miRNA regulation of gene expression. PMID: 24793167
27. Results show that cloned surfactant-associated protein A (SPA) gene promoter had specific transcriptional activity in SPA high expression cells. PMID: 24939295
28. The result suggested that polymorphism of aa62 (CCA/CCG, rs1136451) of SP-A may be associated with the susceptibility to COPD in Xinjiang Uighurs. PMID: 22528218
29. The current meta-analysis indicates that common polymorphisms in the SP-A gene may contribute to increasing susceptibility to COPD, especially among Asian populations. PMID: 24093802
30. SP-A gene polymorphism is associated with kidney graft rejection. PMID: 24007361
31. SP-A inhibited lung cancer progression by recruiting and activating natural killer cells via controlling the polarization of tumor-associated macrophages. PMID: 23499372
32. The obtained results suggested that in vitro approach can be used to study pulmonary toxicity as long as the applied in vitro model mimics closely the complexity of in vivo situation. PMID: 22769972
33. Cat S may participate in the pathophysiology of cystic fibrosis by weakening the antibacterial activity of SP-A. PMID: 23707200
34. The aim of this report is to describe the genetic complexity of the SFTPA1 and SFTPA2 genes, as well as to review regulatory mechanisms that control SP-A expression in humans and other animal species.[review] PMID: 23069847
35. elevated expression in nasal mucosa in chronic rhinosinusitis with polyps PMID: 23406594
36. Surfactant Protein-A, like other host defense molecules in the reproductive tract, appears to be regulated by gonadal hormones. PMID: 22672628
37. Surfactant protein A associated with respiratory distress syndrome in Korean preterm infants: evidence of ethnic difference. PMID: 23038062
38. Lipoteichoic acid can increase SP-A synthesis in human alveolar type II epithelial cells through sequentially activating the MEK1-ERK1/2-NF-kappaB-dependent pathway PMID: 23031213
39. Gln238Lys missense variant of exon 6 in the SFTPA1 may have potential susceptibility in the development of IPF, which was shown in patients with sporadic IPF with a statistically higher frequency. PMID: 22884059
40. Surfactant protein-A suppresses eosinophil-mediated killing of Mycoplasma pneumoniae in allergic lungs PMID: 22384248
41. review focuses on published association studies of surfactant proteins A and D genetic polymorphisms with respiratory, and non-respiratory diseases in adults, children, and newborns [review] PMID: 22201752
42. SP-A protects lung epithelium from tissue injury caused by BD3 PMID: 22418431
43. Surfactant protein A is defective in abrogating inflammation in asthma. PMID: 21784968
44. genetic variants of the surfactant protein A1 confer a protective phenotype against severe acute respiratory syncytial infection PMID: 21601013
45. Both nasal polyps and nasal mucosa expressed SP-A mRNA and protein, but the expression was stronger in nasal polyps. PMID: 20873544
46. The expression of SP-A in allergic rhinitis and nasal polyps was dramatically higher than that in controls. PMID: 19894557
47. findings suggest that Suv39H1 and Suv39H2 are key hypoxia-induced methyltransferases; their decline in fetal lung during late gestation is critical for epigenetic changes resulting in the developmental induction of SP-A PMID: 21402781
48. Paucity of immunohistochemical SP-A expression in alveolar epithelial cells in diseased areas may predict a worse prognosis for patients with idiopathic interstitial pneumonias. PMID: 21435274
49. High SPA-1 is associated with invasion and metastasis of prostate cancer. PMID: 21251160
50. 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. PMID: 21270323

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HGNC: 10798

OMIM: 178500

KEGG: hsa:653509

STRING: 9606.ENSP00000397082

UniGene: Hs.535295