Evidence map›Paper›PMID 16574722›Full record

ArticleJournal of clinical pathology2006

Alternative splicing factor ASF/SF2 is down regulated in inflamed muscle.

Z Xiong, A Shaibani, Y-P Li, Y Yan, S Zhang, Y Yang, F Yang, H Wang, X-F Yang

Open access · bronzeAbstract read
In one paragraph

Article in Journal of clinical pathology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

19 citing papers in PubMed, 33 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. 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

9 authors at 3 institutions in 1 country.

Z XiongLaboratory of Immunopathology, Department of Pharmacology, Temple University School of Medicine, Philadelphia, Pennsylvania 19140, USA.
A Shaibani
Y-P Li
Y Yan
S Zhang
Y Yang
F Yang
H Wang
X-F Yang
Temple University · USBaylor College of Medicine · USSt. Luke's Episcopal Hospital · US

Funding

Mechanisms of Muscle WastingR01AR052511 · NIAMS · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI LI, YI-PING · 2007 to 2011
$1.3M
Survival of CD4+CD25+ Regulatory T CellsK08AI054514 · NIAID · TEMPLE UNIV OF THE COMMONWEALTH · PI YANG, XIAO-FENG · 2003 to 2007
$589k
NIAID NIH HHS AI054514NIAMS NIH HHS R01 AR052511
6 · The paper itself

Abstract

backgroundIn our recent studies, alternative splicing has been shown to have a major role in inflammation and autoimmune muscle diseases.

aimTo examine the novel hypothesis that the expression of an essential alternative splicing factor, alternative splicing factor 2 (ASF/SF2), is modulated in muscle inflammation.

methodsASF/SF2 expression in muscle biopsy samples from eight patients with inflammatory myopathy and six non-myositic controls was determined by using western blot with anti-ASF/SF2 antibodies. To further elucidate the mechanism of reduced ASF/SF2 expression in inflamed muscle, differentiated C2C12 myotubes were stimulated with proinflammatory cytokine tumour necrosis factor alpha (TNFalpha), followed by western blot analysis of ASF/SF2 expression.

resultsASF/SF2 expression in the muscle biopsy samples from patients with inflammatory myopathy was found to be lower (mean of relative densitometric units 41.1 (2SD 20.7)) than that of the non-myositic controls (mean of relative densitometric units 76.7 (39.6); p<0.05). In addition to this, ASF/SF2 expression was seen to be significantly down regulated (sevenfold) in C2C12 myotubes compared with expression variations in the beta-actin control (0.62-fold; mean 1.22 (0.40); p<0.05).

conclusionCollectively, it is shown, for the first time, that alternative splicing factor ASF/SF2 is down regulated in autoimmune inflammatory myositis-potentially via a TNFalpha-mediated pathway. The development of (1) novel autoantigen isoform microarrays for disease diagnosis and prognosis; (2) novel autoantigen-tolerising treatments for autoimmune diseases; and (3) novel splicing-redirection treatments can be facilitated by the ongoing study of alternative splicing of autoantigen transcripts.

Indexed as

Down-RegulationAgedAged, 80 and overAlternative SplicingAnimalsAutoimmune DiseasesBiopsyCells, CulturedFemaleHumansMaleMiceMiddle AgedMuscle Fibers, SkeletalMuscle, SkeletalMyositisNuclear ProteinsRNA-Binding ProteinsSerine-Arginine Splicing FactorsTumor Necrosis Factor-alpha

Identifiers

PMID16574722
PMCPMC1860460
OpenAlexW2158491818

What OpenQuestion holds

Textmetadata
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.