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Gene Review

SFTPA2B  -  surfactant protein A2B

Homo sapiens

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Disease relevance of SFTPA2


Psychiatry related information on SFTPA2

  • We speculate that this SP-A2 protein, like other serous secretions from airway submucosal glands, functions in local antimicrobial host defense mechanisms in the conducting airways [5].

High impact information on SFTPA2

  • We show that certain SP-A1 alleles (6A2 and 6A3) and an SP-A1/SP-A2 haplotype (6A2/1A0) were associated with RDS [6].
  • According to the results of conditional logistic-regression analysis, diseases associated with premature birth did not explain the association between the odds of a particular homozygous SP-A1 genotype (6A2/6A2 and 6A3/6A3) and RDS [6].
  • Maximal induction of SP-A occurred with 3-10 nM dexamethasone and approximately 300 nM cortisol for 72 hr, and stimulation diminished at higher concentrations [7].
  • We propose that glucocorticoids have both stimulatory and inhibitory effects on SP-A gene expression [7].
  • When explants were exposed to cortisol for only 24 hr, SP-A content was transiently increased above the level in continuously treated tissue and subsequently was similar to control [7].

Chemical compound and disease context of SFTPA2


Biological context of SFTPA2

  • Characterization of two overlapping genomic clones revealed that the SP-A pseudogene lies in a reverse orientation 15 kb away from the 5' side of SP-A1 [10].
  • The SP-A and SP-D loci were also oriented relative to the centromere, with the overall order being: centromere-SP-D-SP-A2-pseudogene-SP-A1- telomere [10].
  • The relative location of SP-A2 and SP-D was then ascertained by testing a number of sequence tagged sites against the Stanford TNG3 and G3 radiation hybrid panels [10].
  • The human surfactant protein (SP) A locus has been assigned to chromosome 10q22-q23 and consists of two very similar genes, SP-A1 and SP-A2, as well as a truncated pseudogene [10].
  • Organization of the human SP-A and SP-D loci at 10q22-q23. Physical and radiation hybrid mapping reveal gene order and orientation [10].

Anatomical context of SFTPA2

  • Only SP-A2 mRNA was detected in RNA isolated from human fetal trachea and bronchi [11].
  • Our results suggest that SP-A2, and not SP-A1, is produced in the human fetal tracheal and bronchial epithelium and in submucosal glands [11].
  • Immunohistochemical analysis revealed positive reactivity for SP-A in a subgroup of epithelial cells in the intestine [12].
  • We demonstrate that both SP-A genes are expressed in human small and large intestine [12].
  • Somatic cell hybrid mapping places the human SP-A and SP-D genes at 10q22-q23 while MBL is localised at 10q21 [13].

Associations of SFTPA2 with chemical compounds

  • SP-A2 binds with a higher affinity to a wider variety of sugars than SP-A1 at either 1 or 5 mM Ca(2+) [14].
  • All of the SP-A proteins bind to fucose with the greatest affinity [14].
  • To explore whether a tryptophan (present in 6A(4)) or an arginine (present in other SP-A1 alleles and in all SP-A2 alleles) at amino acid 219 alters protein behavior, two truncated proteins that varied only at amino acid 219 were oxidized by exposure to ozone [15].
  • CONCLUSIONS: Gene polymorphism resulting in the substitution of glutamine with lysine at residue 223 in the carbohydrate recognition domain of SP-A2 increases susceptibility to meningococcal disease, as well as the risk of death [16].
  • The region -32/+63 relative to the start of SP-A1 transcription mediated both basal promoter activity and dexamethasone repression of transcription [8].

Other interactions of SFTPA2

  • The human SP-A gene locus includes two functional genes, SFTPA1 and SFTPA2 which are expressed independently, and a pseudo gene [17].
  • MEASUREMENTS: The SNPs in four exons and intermediate introns of the SP-A1 and SP-A2 were screened by polymerase chain reaction and sequencing [18].
  • DNA samples from 441 premature singleton infants and 480 twin or multiple infants were genotyped for surfactant-specific protein (SP)-A1, SP-A2, and SP-B exon 4 polymorphisms and intron 4 size variants in a homogeneous white population [19].
  • Competition and supershift EMSA indicate that the ubiquitously expressed transcription factor Sp1, a GC box-binding protein of approximately 100 kDa, is a component of the complex of proteins that bind the GT box of SP-A2 [20].
  • A significantly higher frequency of the AGA allele (A1660G) of SP-A2 was observed in patients with ABPA in comparison with control subjects (P =.0156, odds ratio [OR] = 4.78, 95% CI = 1.23 < OR < 18.52) [21].

Analytical, diagnostic and therapeutic context of SFTPA2

  • Low-stringency PCR using the SFTP1 primer pair suggested the presence of at least two additional SP-A-related genes in the same region [22].
  • SP-A protein was localized by immunocytochemistry to scattered epithelial cells in the airway surface epithelium and in submucosal glands of the fetal trachea and bronchi [11].
  • SP-A mRNA (2.2 kb) was detected by Northern blot analysis in human fetal trachea, as well as in primary and more distal bronchi [11].
  • SP-A mRNA was localized by in situ hybridization in the fetal trachea and bronchi in scattered cells in the surface epithelium and, most prominently, in submucosal glands [11].
  • By UV cross-linking and SDS-PAGE/EMSA analysis, we have identified a approximately 55-kDa GT box-binding factor in type II cell nuclear proteins that preferentially binds the GT box of SP-A2 over the consensus Sp1 GC box sequence [20].


  1. Genetics of the hydrophilic surfactant proteins A and D. Floros, J., Hoover, R.R. Biochim. Biophys. Acta (1998) [Pubmed]
  2. SP-A1 and SP-A2 variants differentially enhance association of Pseudomonas aeruginosa with rat alveolar macrophages. Mikerov, A.N., Umstead, T.M., Huang, W., Liu, W., Phelps, D.S., Floros, J. Am. J. Physiol. Lung Cell Mol. Physiol. (2005) [Pubmed]
  3. Association of polymorphisms in the collagen region of human SP-A1 and SP-A2 genes with pulmonary tuberculosis in Indian population. Madan, T., Saxena, S., Murthy, K.J., Muralidhar, K., Sarma, P.U. Clin. Chem. Lab. Med. (2002) [Pubmed]
  4. Role of collectins in innate immunity against aspergillosis. Madan, T., Kaur, S., Saxena, S., Singh, M., Kishore, U., Thiel, S., Reid, K.B., Sarma, P.U. Med. Mycol. (2005) [Pubmed]
  5. In situ hybridization of SP-A mRNA in adult human conducting airways. Khubchandani, K.R., Goss, K.L., Engelhardt, J.F., Snyder, J.M. Pediatric pathology & molecular medicine. (2001) [Pubmed]
  6. Association between the surfactant protein A (SP-A) gene locus and respiratory-distress syndrome in the Finnish population. Rämet, M., Haataja, R., Marttila, R., Floros, J., Hallman, M. Am. J. Hum. Genet. (2000) [Pubmed]
  7. Glucocorticoids both stimulate and inhibit production of pulmonary surfactant protein A in fetal human lung. Liley, H.G., White, R.T., Benson, B.J., Ballard, P.L. Proc. Natl. Acad. Sci. U.S.A. (1988) [Pubmed]
  8. Glucocorticoid inhibition of human SP-A1 promoter activity in NCI-H441 cells. Hoover, R.R., Thomas, K.H., Floros, J. Biochem. J. (1999) [Pubmed]
  9. Pulmonary surfactant-associated protein A as a marker of respiratory distress in forensic pathology: assessment of the immunohistochemical and biochemical findings. Maeda, H., Fujita, M.Q., Zhu, B.L., Ishida, K., Quan, L., Oritani, S., Taniguchi, M. Legal medicine (Tokyo, Japan) (2003) [Pubmed]
  10. Organization of the human SP-A and SP-D loci at 10q22-q23. Physical and radiation hybrid mapping reveal gene order and orientation. Hoover, R.R., Floros, J. Am. J. Respir. Cell Mol. Biol. (1998) [Pubmed]
  11. SP-A2 gene expression in human fetal lung airways. Goss, K.L., Kumar, A.R., Snyder, J.M. Am. J. Respir. Cell Mol. Biol. (1998) [Pubmed]
  12. Both human SP-A1 and Sp-A2 genes are expressed in small and large intestine. Lin, Z., deMello, D., Phelps, D.S., Koltun, W.A., Page, M., Floros, J. Pediatric pathology & molecular medicine. (2001) [Pubmed]
  13. The genomics of soluble proteins with collagenous domains: C1q, MBL, SP-A, SP-D, conglutinin, and CL-43. Kölble, K., Reid, K.B. Behring Inst. Mitt. (1993) [Pubmed]
  14. Recombinant human SP-A1 and SP-A2 proteins have different carbohydrate-binding characteristics. Oberley, R.E., Snyder, J.M. Am. J. Physiol. Lung Cell Mol. Physiol. (2003) [Pubmed]
  15. Surfactant protein A and B genetic variants predispose to idiopathic pulmonary fibrosis. Selman, M., Lin, H.M., Montaño, M., Jenkins, A.L., Estrada, A., Lin, Z., Wang, G., DiAngelo, S.L., Guo, X., Umstead, T.M., Lang, C.M., Pardo, A., Phelps, D.S., Floros, J. Hum. Genet. (2003) [Pubmed]
  16. Genetic polymorphism of the binding domain of surfactant protein-A2 increases susceptibility to meningococcal disease. Jack, D.L., Cole, J., Naylor, S.C., Borrow, R., Kaczmarski, E.B., Klein, N.J., Read, R.C. Clin. Infect. Dis. (2006) [Pubmed]
  17. Surfactant protein a - from genes to human lung diseases. Heinrich, S., Hartl, D., Griese, M. Current medicinal chemistry (2006) [Pubmed]
  18. Association of polymorphisms in pulmonary surfactant protein A1 and A2 genes with high-altitude pulmonary edema. Saxena, S., Kumar, R., Madan, T., Gupta, V., Muralidhar, K., Sarma, P.U. Chest (2005) [Pubmed]
  19. Surfactant protein A and B genetic variants in respiratory distress syndrome in singletons and twins. Marttila, R., Haataja, R., Guttentag, S., Hallman, M. Am. J. Respir. Crit. Care Med. (2003) [Pubmed]
  20. A GT box element is essential for basal and cyclic adenosine 3',5'-monophosphate regulation of the human surfactant protein A2 gene in alveolar type II cells: evidence for the binding of lung nuclear factors distinct from Sp1. Young, P.P., Mendelson, C.R. Mol. Endocrinol. (1997) [Pubmed]
  21. 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. Saxena, S., Madan, T., Shah, A., Muralidhar, K., Sarma, P.U. J. Allergy Clin. Immunol. (2003) [Pubmed]
  22. Assignment of the human pulmonary surfactant protein D gene (SFTP4) to 10q22-q23 close to the surfactant protein A gene cluster. Kölble, K., Lu, J., Mole, S.E., Kaluz, S., Reid, K.B. Genomics (1993) [Pubmed]
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