Evidence map›Paper›PMID 7651409›Full record

ArticleMolecular and cellular biology1995

A subset of SR proteins activates splicing of the cardiac troponin T alternative exon by direct interactions with an exonic enhancer.

J Ramchatesingh, A M Zahler, K M Neugebauer, M B Roth, T A Cooper

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers.

0numbers the graph read from it
0cells of the map it votes in
102citing papers in PubMed
8.0field-weighted citation impact, top 2% 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

102 citing papers in PubMed, 179 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. POWERDRESS and HDA9 interact and promote histone H3 deacetylation at specific genomic sites in Arabidopsis.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Global impact of RNA splicing on transcriptome remodeling in the heart.Journal of Zhejiang University. Science. B · 2012
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

42 more citing papers are in PubMed but not listed here.

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

5 authors at 2 institutions in 1 country.

J RamchatesinghDepartment of Pathology, Baylor College of Medicine, Houston, Texas 77030, USA.
A M Zahler
K M Neugebauer
M B Roth
T A Cooper
Fred Hutch Cancer Center · USBaylor College of Medicine · US

Funding

STRUCTURE AND FUNCTION IN THE NUCLEUSR01GM048435 · NIGMS · FRED HUTCHINSON CANCER RESEARCH CENTER · PI ROTH, MARK B · 1994 to 2006
$3.0M
NIGMS NIH HHS GM48435-01
6 · The paper itself

Abstract

The cardiac troponin T pre-mRNA contains an exonic splicing enhancer that is required for inclusion of the alternative exon 5. Here we show that enhancer activity is exquisitely sensitive to changes in the sequence of a 9-nucleotide motif (GAGGAAGAA) even when its purine content is preserved. A series of mutations that increased or decreased the level of exon inclusion in vivo were used to correlate enhancer strength with RNA-protein interactions in vitro. Analyses involving UV cross-linking and immunoprecipitation indicated that only four (SRp30a, SRp40, SRp55, and SRp75) of six essential splicing factors known as SR proteins bind to the active enhancer RNA. Moreover, purified SRp40 and SRp55 activate splicing of exon 5 when added to a splicing-deficient S100 extract. Purified SRp30b did not stimulate splicing in S100 extracts, which is consistent with its failure to bind the enhancer RNA. In vitro competition of SR protein splicing activity and UV cross-linking demonstrated that the sequence determinants for SR protein binding were precisely coincident with the sequence determinants of enhancer strength. Thus, a subset of SR proteins interacts directly with the exonic enhancer to promote inclusion of a poorly defined alternative exon. Independent regulation of the levels of SR proteins may, therefore, contribute to the developmental regulation of exon inclusion.

Indexed as

Alternative SplicingBase SequenceCross-Linking ReagentsExonsHeLa CellsHumansMolecular Sequence DataMyocardiumPoint MutationPrecipitin TestsProtein BindingRNA-Binding ProteinsStructure-Activity RelationshipSubcellular FractionsTroponinTroponin TCross-Linking ReagentsRNA-Binding ProteinsTroponinTroponin T

Identifiers

PMID7651409
PMCPMC230736
OpenAlexW2156449254

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.