Evidence map›Paper›PMID 29510724›Full record

ReviewSkeletal muscle2018

Diversification of the muscle proteome through alternative splicing.

Kiran Nakka, Claudia Ghigna, Davide Gabellini, F Jeffrey Dilworth

Open access · goldAbstract readReview
In one paragraph

Review in Skeletal muscle, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

55 citing papers in PubMed, 98 citations in OpenAlex.

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  13. Differential inclusion ofmedRxiv : the preprint server for health sciences · 2024
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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

4 authors at 4 institutions in 2 countries.

Kiran NakkaSprott Centre for Stem Cell Research, Regenerative Medicine Program, Ottawa Hospital Research Institute, Ottawa, ON, K1H 8L6, Canada.
Claudia GhignaIstituto di Genetica Molecolare-Consiglio Nazionale delle Ricerche (IGM-CNR), Pavia, Italy.
Davide GabelliniUnit of Gene Expression and Muscular Dystrophy, Division of Genetics and Cell Biology, IRCCS San Raffaele Scientific Institute, DIBIT2, 5A3-44, via Olgettina 58, 20132, Milan, Italy. gabellini.davide@hsr.it.
F Jeffrey DilworthSprott Centre for Stem Cell Research, Regenerative Medicine Program, Ottawa Hospital Research Institute, Ottawa, ON, K1H 8L6, Canada. jdilworth@ohri.ca.ORCID 0000-0002-6265-8102
Istituto di Genetica Molecolare · ITOttawa Hospital · CAUniversity of Ottawa · CAVita-Salute San Raffaele University · IT

Funding

CIHR FDN-143330Fondazione Telethon TCR13001
6 · The paper itself

Abstract

backgroundSkeletal muscles express a highly specialized proteome that allows the metabolism of energy sources to mediate myofiber contraction. This muscle-specific proteome is partially derived through the muscle-specific transcription of a subset of genes. Surprisingly, RNA sequencing technologies have also revealed a significant role for muscle-specific alternative splicing in generating protein isoforms that give specialized function to the muscle proteome. MAIN BODY: In this review, we discuss the current knowledge with respect to the mechanisms that allow pre-mRNA transcripts to undergo muscle-specific alternative splicing while identifying some of the key trans-acting splicing factors essential to the process. The importance of specific splicing events to specialized muscle function is presented along with examples in which dysregulated splicing contributes to myopathies. Though there is now an appreciation that alternative splicing is a major contributor to proteome diversification, the emergence of improved "targeted" proteomic methodologies for detection of specific protein isoforms will soon allow us to better appreciate the extent to which alternative splicing modifies the activity of proteins (and their ability to interact with other proteins) in the skeletal muscle. In addition, we highlight a continued need to better explore the signaling pathways that contribute to the temporal control of trans-acting splicing factor activity to ensure specific protein isoforms are expressed in the proper cellular context.

conclusionsAn understanding of the signal-dependent and signal-independent events driving muscle-specific alternative splicing has the potential to provide us with novel therapeutic strategies to treat different myopathies.

Indexed as

Alternative SplicingContractile ProteinsExcitation Contraction CouplingHumansMEF2 Transcription FactorsMitochondria, MuscleMuscle ProteinsMuscle, SkeletalMuscular DiseasesProtein IsoformsProteomeTranscription FactorsContractile ProteinsMEF2 Transcription FactorsMuscle ProteinsProtein IsoformsProteomeTranscription FactorsAlternative splicingCo-transcriptional splicingMuscle disordersMuscular dystrophyMyogenesisProteomeRNA-binding proteins

Identifiers

PMID29510724
PMCPMC5840707
OpenAlexW2800540195

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.