Evidence map›Paper›PMID 10072387›Full record

ArticleGenes & development1999

Binding of hnRNP H to an exonic splicing silencer is involved in the regulation of alternative splicing of the rat beta-tropomyosin gene.

C D Chen, R Kobayashi, D M Helfman

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 1999. 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
–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

102 citing papers in PubMed, 197 citations in OpenAlex.

  1. Article
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  3. Review
  4. Deciphering RNA splicing logic with interpretable machine learning.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
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  11. Pre-mRNA mis-splicing of sarcomeric genes in heart failure.Biochimica et biophysica acta. Molecular basis of disease · 2017
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. A day in the life of the spliceosome.Nature reviews. Molecular cell biology · 2014
    Review

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

3 authors at 2 institutions in 1 country.

C D ChenCold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724, USA.
R Kobayashi
D M Helfman
Cold Spring Harbor Laboratory · USStony Brook University · US

Funding

TROPOMYOSIN GENE STRUCTURE, EXPRESSION AND REGULATIONR01GM043049 · NIGMS · COLD SPRING HARBOR LABORATORY · PI HELFMAN, DAVID M · 1989 to 1997
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NCI NIH HHS CA95508NIGMS NIH HHS GM43049
6 · The paper itself

Abstract

In the rat beta-tropomyosin (beta-TM) gene, exons 6 and 7 are spliced alternatively in a mutually exclusive manner. Exon 6 is included in mRNA encoding nonmuscle TM-1, whereas exon 7 is used in mRNA encoding skeletal muscle beta-TM. Previously, we demonstrated that a six nucleotide mutation at the 5' end of exon 7, designated as ex-1, activated exon 7 splicing in nonmuscle cells. In this study, we show that the activating effect of this mutation is not the result of creating an exonic splicing enhancer (ESE) or disrupting a putative secondary structure. The sequence in exon 7 acts as a bona fide exonic splicing silencer (ESS), which is bound specifically by a trans-acting factor. Isolation and peptide sequencing reveal that this factor is hnRNP H, a member of the heterogeneous nuclear ribonucleoprotein (hnRNP) family. Binding of hnRNP H correlates with the ESS activity. Furthermore, addition of antibodies that specifically recognizes hnRNP H to the splicing reactions or partial depletion of hnRNP H from nuclear extract activates exon 7 splicing in vitro and this effect can be reversed by addition of purified recombinant hnRNP H. These results indicate that hnRNP H participates in exclusion of exon 7 in nonmuscle cells. The involvement of hnRNP H in the activity of an ESS may represent a prototype for the regulation of tissue- and developmental-specific alternative splicing.

Indexed as

Alternative SplicingExonsAnimalsBase SequenceGene Expression RegulationHeLa CellsHeterogeneous-Nuclear Ribonucleoprotein Group F-HHeterogeneous-Nuclear RibonucleoproteinsHumansMolecular Sequence DataMutagenesisRatsRecombinant ProteinsRibonucleoproteinsRNATropomyosinHeterogeneous-Nuclear Ribonucleoprotein Group F-HHeterogeneous-Nuclear RibonucleoproteinsRecombinant ProteinsRibonucleoproteinsRNATropomyosin

Identifiers

PMID10072387
PMCPMC316507
OpenAlexW2103065204

What OpenQuestion holds

Texttitle and abstract
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.