Evidence map›Paper›PMID 21498514›Full record

ArticleThe Journal of biological chemistry2011

Identification of a novel muscle A-type lamin-interacting protein (MLIP).

Elmira Ahmady, Shelley A Deeke, Seham Rabaa, Lara Kouri, Laura Kenney, Alexandre F R Stewart, Patrick G Burgon

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

23 citing papers in PubMed, 36 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Cells · 2024
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Cardiac CIP protein regulates dystrophic cardiomyopathy.Molecular therapy : the journal of the American Society of Gene Therapy · 2022
    Article
  10. Neuromuscular disease: 2022 update.Free neuropathology · 2022
    Article
  11. Article
  12. Article
  13. Article
  14. Regulation of myonuclear positioning and muscle function by the skeletal muscle-specific CIP protein.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review
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 1 institution in 1 country.

Elmira AhmadyUniversity of Ottawa Heart Institute, Ottawa, Ontario, Canada.
Shelley A Deeke
Seham Rabaa
Lara Kouri
Laura Kenney
Alexandre F R Stewart
Patrick G Burgon
University of Ottawa · CA

Funding

Canadian Institutes of Health Research MOP77682Canadian Institutes of Health Research MOP82748
6 · The paper itself

Abstract

Mutations in the A-type lamin (LMNA) gene are associated with age-associated degenerative disorders of mesenchymal tissues, such as dilated cardiomyopathy, Emery-Dreifuss muscular dystrophy, and limb-girdle muscular dystrophy. The molecular mechanisms that connect mutations in LMNA with different human diseases are poorly understood. Here, we report the identification of a Muscle-enriched A-type Lamin-interacting Protein, MLIP (C6orf142 and 2310046A06rik), a unique single copy gene that is an innovation of amniotes (reptiles, birds, and mammals). MLIP encodes alternatively spliced variants (23-57 kDa) and possesses several novel structural motifs not found in other proteins. MLIP is expressed ubiquitously and most abundantly in heart, skeletal, and smooth muscle. MLIP interacts directly and co-localizes with lamin A and C in the nuclear envelope. MLIP also co-localizes with promyelocytic leukemia (PML) bodies within the nucleus. PML, like MLIP, is only found in amniotes, suggesting that a functional link between the nuclear envelope and PML bodies may exist through MLIP. Down-regulation of lamin A/C expression by shRNA results in the up-regulation and mislocalization of MLIP. Given that MLIP is expressed most highly in striated and smooth muscle, it is likely to contribute to the mesenchymal phenotypes of laminopathies.

Indexed as

Alternative SplicingAnimalsCarrier ProteinsCo-Repressor ProteinsGene Expression RegulationHumansLamin Type AMiceMuscle ProteinsMusclesNuclear EnvelopeNuclear ProteinsOrgan SpecificityPromyelocytic Leukemia ProteinTranscription FactorsTumor Suppressor ProteinsCarrier ProteinsCo-Repressor ProteinsLamin Type AMLIP protein, mouseMuscle ProteinsNuclear ProteinsPml protein, mousePromyelocytic Leukemia ProteinTranscription FactorsTumor Suppressor Proteins

Identifiers

PMID21498514
PMCPMC3103349
OpenAlexW2028647555

What OpenQuestion holds

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LicenceCC BY-NC
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.