Evidence map›Paper›PMID 21135118›Full record

ArticleMolecular and cellular biology2011

SR proteins induce alternative exon skipping through their activities on the flanking constitutive exons.

Joonhee Han, Jian-Hua Ding, Cheol W Byeon, Jee H Kim, Klemens J Hertel, Sunjoo Jeong, Xiang-Dong Fu

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

51 citing papers in PubMed, 87 citations in OpenAlex.

  1. Review
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  13. miRNA-Based Regulation of Alternative RNA Splicing in Metazoans.International journal of molecular sciences · 2021
    Review
  14. Article
  15. Article
  16. CaMKIIδ Splice Variants in the Healthy and Diseased Heart.Frontiers in cell and developmental biology · 2021
    Review
  17. Article
  18. Article
  19. Article
  20. 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

7 authors at 3 institutions in 2 countries.

Joonhee HanDepartment of Cellular and Molecular Medicine, University of California, San Diego, La Jolla, CA 92093-0651, USA.
Jian-Hua Ding
Cheol W Byeon
Jee H Kim
Klemens J Hertel
Sunjoo Jeong
Xiang-Dong Fu
Dankook University · KRUniversity of California, San Diego · USUniversity of California, Irvine · US

Funding

FUNCTION &REGULATION OF THE HUMAN SPLICING FACTOR SC35R01GM049369 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI FU, XIANG-DONG · 1993 to 2018
$7.2M
MECHANISMS OF ENHANCER DEPENDENT SPLICE SITE ACTIVATIONR01GM062287 · NIGMS · UNIVERSITY OF CALIFORNIA-IRVINE · PI HERTEL, KLEMENS J · 2001 to 2019
$4.8M
NIGMS NIH HHS GM49369NIGMS NIH HHS R01 GM049369NIGMS NIH HHS R01 GM062287
6 · The paper itself

Abstract

SR proteins are well known to promote exon inclusion in regulated splicing through exonic splicing enhancers. SR proteins have also been reported to cause exon skipping, but little is known about the mechanism. We previously characterized SRSF1 (SF2/ASF)-dependent exon skipping of the CaMKIIδ gene during heart remodeling. By using mouse embryo fibroblasts derived from conditional SR protein knockout mice, we now show that SR protein-induced exon skipping depends on their prevalent actions on a flanking constitutive exon and requires collaboration of more than one SR protein. These findings, coupled with other established rules for SR proteins, provide a theoretical framework to understand the complex effect of SR protein-regulated splicing in mammalian cells. We further demonstrate that heart-specific CaMKIIδ splicing can be reconstituted in fibroblasts by downregulating SR proteins and upregulating a RBFOX protein and that SR protein overexpression impairs regulated CaMKIIδ splicing and neuronal differentiation in P19 cells, illustrating that SR protein-dependent exon skipping may constitute a key strategy for synergism with other splicing regulators in establishing tissue-specific alternative splicing critical for cell differentiation programs.

Indexed as

Alternative SplicingExonsAnimalsBase SequenceCalcium-Calmodulin-Dependent Protein Kinase Type 2Cell DifferentiationCells, CulturedMiceMice, KnockoutModels, BiologicalMutagenesisNeuronsNuclear ProteinsRecombinant ProteinsRNA-Binding ProteinsSerine-Arginine Splicing FactorsCalcium-Calmodulin-Dependent Protein Kinase Type 2Nuclear ProteinsRecombinant ProteinsRNA-Binding ProteinsSerine-Arginine Splicing Factors

Identifiers

PMID21135118
PMCPMC3028638
OpenAlexW2103521510

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.