Evidence map›Paper›PMID 9384594›Full record

ArticleThe EMBO journal1997

Functional crosstalk between exon enhancers, polypyrimidine tracts and branchpoint sequences.

M Buvoli, S A Mayer, J G Patton

Abstract read
In one paragraph

Article in The EMBO journal, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
–field-weighted citation impact
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

17 citing papers in PubMed.

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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

3 authors.

M BuvoliDepartment of Molecular Biology, Vanderbilt University, Box 1820 Station B, Nashville, TN 37235, USA.
S A Mayer
J G Patton

Funding

REGULATION OF ALPHA TROPOMYOSIN SPLICINGR01GM050418 · NIGMS · VANDERBILT UNIVERSITY · PI PATTON, JAMES G. · 1994 to 1997
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NIGMS NIH HHS GM50418
6 · The paper itself

Abstract

We recently identified enhancer elements that activate the weak 3' splice site of alpha-tropomyosin exon 2 as well as a variety of heterologous weak 3' splice sites. To understand their mechanism of action, we devised an iterative selection strategy to identify functional pyrimidine tracts and branchpoint sequences in the presence or absence of enhancer elements. Surprisingly, we found that strong pyrimidine tracts were selected regardless of the presence of enhancer elements. However, the presence of enhancer elements resulted in the selection of multiple, non-consensus branchpoint sequences. Thus, enhancer elements apparently activate weak 3' splice sites primarily by increasing the efficiency of splicing of introns containing branchpoint sequences with less than optimal U2-branchpoint pairing arrangements. Comparison of consensus sequences from both our selection strategy and compilations of published intron sequences suggests that exon enhancer elements could be widespread and play an important role in the selection of 3' splice sites.

Indexed as

ExonsPyrimidinesRNA SplicingAnimalsModels, GeneticNucleic Acid ConformationRatsRNA, Small NuclearSelection, GeneticTropomyosinPyrimidinesRNA, Small NuclearTropomyosin

Identifiers

PMID9384594
PMCPMC1170318

What OpenQuestion holds

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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.