Evidence map›Paper›PMID 28687747›Full record

ArticleScientific reports2017

Lamin B1 levels modulate differentiation into neurons during embryonic corticogenesis.

Sameehan Mahajani, Caterina Giacomini, Federica Marinaro, Davide De Pietri Tonelli, Andrea Contestabile, Laura Gasparini

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

24 citing papers in PubMed, 43 citations in OpenAlex.

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  8. Lamin B1 as a key modulator of the developing and aging brain.Frontiers in cellular neuroscience · 2023
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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

6 authors at 2 institutions in 3 countries.

Sameehan MahajaniDept. of Neuroscience and Brain Technologies, Istituto Italiano di Tecnologia, Genova, Italy.
Caterina GiacominiDept. of Neuroscience and Brain Technologies, Istituto Italiano di Tecnologia, Genova, Italy.
Federica MarinaroDept. of Neuroscience and Brain Technologies, Istituto Italiano di Tecnologia, Genova, Italy.
Davide De Pietri TonelliDept. of Neuroscience and Brain Technologies, Istituto Italiano di Tecnologia, Genova, Italy.ORCID 0000-0001-9537-8900
Andrea ContestabileDept. of Neuroscience and Brain Technologies, Istituto Italiano di Tecnologia, Genova, Italy.ORCID 0000-0002-5417-4722
Laura GaspariniDept. of Neuroscience and Brain Technologies, Istituto Italiano di Tecnologia, Genova, Italy. laura.gasparini@abbvie.com.
Italian Institute of Technology · ITKing's College London · GB

Funding

UCD Mutant Mouse Regional Resource CenterU42OD012210 · OD · UNIVERSITY OF CALIFORNIA AT DAVIS · PI KC KENT LLOYD · 2012 to 2026
$29.2M
NIH HHS U42 OD012210
6 · The paper itself

Abstract

Lamin B1, a key component of the nuclear lamina, plays an important role in brain development. Ablation of endogenous Lamin B1 (Lmnb1) in the mouse strongly impairs embryonic brain development and corticogenesis. However, the mechanisms underlying these neurodevelopmental effects are unknown. Here, we report that Lamin B1 levels modulate the differentiation of murine neural stem cells (NSCs) into neurons and astroglial-like cells. In vitro, endogenous Lmnb1 depletion favors NSC differentiation into glial fibrillar acidic protein (GFAP)-immunoreactive cells over neurons, while overexpression of human Lamin B1 (LMNB1) increases the proportion of neurons. In Lmnb1-null embryos, neurogenesis is reduced, while in vivo Lmnb1 silencing in mouse embryonic brain by in utero electroporation of a specific Lmnb1 sh-RNA results in aberrant cortical positioning of neurons and increased expression of the astrocytic marker GFAP in the cortex of 7-day old pups. Together, these results indicate that finely tuned levels of Lamin B1 are required for NSC differentiation into neurons, proper expression of the astrocytic marker GFAP and corticogenesis.

Indexed as

AnimalsAnimals, NewbornAstrocytesCell DifferentiationCerebral CortexEmbryo, MammalianFemaleGene Expression Regulation, DevelopmentalGlial Fibrillary Acidic ProteinLamin Type BMiceMice, Inbred C57BLNeural Stem CellsNeurogenesisNeuronsPregnancyGlial Fibrillary Acidic Proteinglial fibrillary astrocytic protein, mouseLamin Type BRNA, Small Interfering

Identifiers

PMID28687747
PMCPMC5501862
OpenAlexW2732859689

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.