Evidence map›Paper›PMID 23069847›Full record

ReviewGene2013

Genetic complexity of the human surfactant-associated proteins SP-A1 and SP-A2.

Patricia Silveyra, Joanna Floros

Abstract readReview
In one paragraph

Review in Gene, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.2field-weighted citation impact, top 18% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

25 citing papers in PubMed, 41 citations in OpenAlex.

  1. Regulation of translation by upstream translation initiation codons of surfactant protein A1 splice variants.American journal of physiology. Lung cellular and molecular physiology · 2015
    Trial
  2. Review
  3. Article
  4. Article
  5. Article
  6. Surfactant protein levels and genetic variants as biomarkers for COVID-19 severity in children.American journal of physiology. Lung cellular and molecular physiology · 2025
    Article
  7. Article
  8. The Immune Modulatory Role of Surfactants inJournal of inflammation research · 2025
    Review
  9. Review
  10. Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Patricia SilveyraCenter for Host Defense, Inflammation, and Lung Disease (CHILD) Research, Department of Pediatrics, Pennsylvania State University College of Medicine, Hershey, PA, 17033, USA.
Joanna Floros
Pennsylvania State University · US

Funding

SURFACTANT PROTEINS AND RESPIRATORY DISTRESS SYNDROMER37HL034788 · NHLBI · PENNSYLVANIA STATE UNIV HERSHEY MED CTR · PI FLOROS, JOANNA · 1996 to 2005
$3.2M
SURFACTANT PROTEINS AND RESPIRATORY DISTRESS SYNDROMER01HL034788 · NHLBI · PENNSYLVANIA STATE UNIV HERSHEY MED CTR · PI FLOROS, JOANNA · 1985 to 2011
$3.0M
NHLBI NIH HHS HL34788NHLBI NIH HHS R01 HL034788NHLBI NIH HHS R37 HL034788
6 · The paper itself

Abstract

Pulmonary surfactant protein A (SP-A) plays a key role in innate lung host defense, in surfactant-related functions, and in parturition. In the course of evolution, the genetic complexity of SP-A has increased, particularly in the regulatory regions (i.e. promoter, untranslated regions). Although most species have a single SP-A gene, two genes encode SP-A in humans and primates (SFTPA1 and SFTPA2). This may account for the multiple functions attributed to human SP-A, as well as the regulatory complexity of its expression by a relatively diverse set of protein and non-protein cellular factors. The interplay between enhancer cis-acting DNA sequences and trans-acting proteins that recognize these DNA elements is essential for gene regulation, primarily at the transcription initiation level. Furthermore, regulation at the mRNA level is essential to ensure proper physiological levels of SP-A under different conditions. To date, numerous studies have shown significant complexity of the regulation of SP-A expression at different levels, including transcription, splicing, mRNA decay, and translation. A number of trans-acting factors have also been described to play a role in the control of SP-A expression. 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.

Indexed as

AnimalsBase SequenceGene Expression RegulationGenetic VariationHumansPromoter Regions, GeneticPulmonary Surfactant-Associated Protein ARNA, MessengerTranscription, GeneticUntranslated RegionsPulmonary Surfactant-Associated Protein ARNA, MessengerSFTPA1 protein, humanSFTPA2 protein, humanUntranslated Regionscarbohydrate recognition domainCRDEvolutionGenetic variantsInnate immunitySFTPA1SFTPA2SFTPA3Psingle nucleotide polymorphismSNPSP-ASP-CSP-Dsurfactant protein Asurfactant protein A1 genesurfactant protein A2 genesurfactant protein A3, pseudogenesurfactant protein Csurfactant protein DSurfactant proteinsTranscriptional regulationuntranslated regionUTR

Identifiers

PMID23069847
PMCPMC3570704
OpenAlexW2094486967

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.