Evidence map›Paper›PMID 26701887›Full record

ArticleOncotarget2016

Barrier-to-autointegration factor (BAF) involvement in prelamin A-related chromatin organization changes.

Manuela Loi, Vittoria Cenni, Serena Duchi, Stefano Squarzoni, Carlos Lopez-Otin, Roland Foisner, Giovanna Lattanzi, Cristina Capanni

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

34 citing papers in PubMed, 53 citations in OpenAlex.

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  18. Survival ofDevelopment (Cambridge, England) · 2020
    Article
  19. Review
  20. The Cutting Edge: The Role of mTOR Signaling in Laminopathies.International journal of molecular sciences · 2019
    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

8 authors at 4 institutions in 3 countries.

Manuela LoiCNR-National Research Council of Italy, Institute of Molecular Genetics, Unit of Bologna, 40136 Bologna, Italy.
Vittoria CenniCNR-National Research Council of Italy, Institute of Molecular Genetics, Unit of Bologna, 40136 Bologna, Italy.
Serena DuchiOsteoarticolar Regeneration Laboratory, Rizzoli Orthopaedic Institute, 40136 Bologna, Italy.
Stefano SquarzoniCNR-National Research Council of Italy, Institute of Molecular Genetics, Unit of Bologna, 40136 Bologna, Italy.
Carlos Lopez-OtinDepartment of Biochemistry and Molecular Biology, Medical Faculty, Oviedo University, 33006 Oviedo, Spain.
Roland FoisnerMax F. Perutz Laboratories, Medical University of Vienna, A-1030 Vienna, Austria.
Giovanna LattanziCNR-National Research Council of Italy, Institute of Molecular Genetics, Unit of Bologna, 40136 Bologna, Italy.
Cristina CapanniCNR-National Research Council of Italy, Institute of Molecular Genetics, Unit of Bologna, 40136 Bologna, Italy.
National Research Council · ITIstituto Ortopedico Rizzoli · ITMedical University of Vienna · ATUniversidad de Oviedo · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chromatin disorganization is one of the major alterations linked to prelamin A processing impairment. In this study we demonstrate that BAF is necessary to modulate prelamin A effects on chromatin structure. We show that when prelamin A and BAF cannot properly interact no prelamin A-dependent effects on chromatin occur; similar to what is observed in human Nestor Guillermo Progeria Syndrome cells harboring a BAF mutation, in HEK293 cells expressing a BAF mutant unable to bind prelamin A, or in siRNA mediated BAF-depleted HEK293 cells expressing prelamin A. BAF is necessary to induce histone trimethyl-H3K9 as well as HP1-alpha and LAP2-alpha nuclear relocalization in response to prelamin A accumulation. These findings are enforced by electron microscopy evaluations showing how the prelamin A-BAF interaction governs overall chromatin organization. Finally, we demonstrate that the LAP2-alpha nuclear localization defect observed in HGPS cells involves the progerin-BAF interaction, thus establishing a functional link between BAF and prelamin A pathological forms.

Indexed as

ChromatinDNA-Binding ProteinsHEK293 CellsHumansLamin Type AMutationNuclear ProteinsProgeriaBANF1 protein, humanChromatinDNA-Binding ProteinsLamin Type ANuclear Proteinsprelamin Abarrier-to-autointegration factorchromatinHutchinson-Gilford progeria syndromeNestor-Guillermo progeriaprelamin A

Identifiers

PMID26701887
PMCPMC4941268
OpenAlexW2284169692

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.