Evidence map›Paper›PMID 18824513›Full record

ArticleRNA (New York, N.Y.)2008

Mutational analysis of the U12-dependent branch site consensus sequence.

Jay E Brock, Rosemary C Dietrich, Richard A Padgett

Open access · bronzeAbstract read
In one paragraph

Article in RNA (New York, N.Y.), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.6field-weighted citation impact, top 32% 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

6 citing papers in PubMed, 13 citations in OpenAlex.

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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 at 1 institution in 1 country.

Jay E BrockDepartment of Molecular Genetics, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA.
Rosemary C Dietrich
Richard A Padgett
Cleveland Clinic · US

Funding

Mechanism of U12-dependent spliceosomal splicingR01GM079527 · NIGMS · CLEVELAND CLINIC LERNER COM-CWRU · PI PADGETT, RICHARD A · 2007 to 2010
$1.2M
NIGMS NIH HHS GM079527NIGMS NIH HHS R01 GM079527
6 · The paper itself

Abstract

Highly conserved sequences at the 5' splice site and branch site of U12-dependent introns are important determinants for splicing by U12-dependent spliceosomes. This study investigates the in vivo splicing phenotypes of mutations in the branch site consensus sequence of the U12-dependent intron F from a human NOL1 (P120) minigene. Intron F contains a fully consensus branch site sequence (UUCCUUAAC). Mutations at each position were analyzed for their effects on U12-dependent splicing in vivo. Mutations at most positions resulted in a significant reduction of correct U12-dependent splicing. Defects observed included increased unspliced RNA levels, the activation of cryptic U2-dependent 5' and 3' splice sites, and the activation of cryptic U12-dependent branch/3' splice sites. A strong correlation was observed between the predicted thermodynamic stability of the branch site: U12 snRNA interaction and correct U12-dependent splicing. The lack of a polypyrimidine tract between the branch site and 3' splice site of U12-dependent introns and the observed reliance on base-pairing interactions for correct U12-dependent splicing emphasize the importance of RNA/RNA interactions during U12-dependent intron recognition and proper splice site selection.

Indexed as

Alternative SplicingIntronsRNA Splice SitesBase SequenceConsensus SequenceHumansMutationNuclear ProteinsRNA, Small NuclearSpliceosomestRNA MethyltransferasesNOP2 protein, humanNuclear ProteinsRNA, Small NuclearRNA Splice SitestRNA MethyltransferasesU12 small nuclear RNA

Identifiers

PMID18824513
PMCPMC2578861
OpenAlexW2169681147

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.