Evidence map›Paper›PMID 26045045›Full record

ArticleCell death and differentiation2015

AKT1-mediated Lamin A/C degradation is required for nuclear degradation and normal epidermal terminal differentiation.

A S Naeem, Y Zhu, W L Di, S Marmiroli, R F L O'Shaughnessy

Open access · bronzeAbstract read
In one paragraph

Article in Cell death and differentiation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
3.8field-weighted citation impact, top 7% 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

45 citing papers in PubMed, 72 citations in OpenAlex.

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  14. Frontiers in molecular biosciences · 2023
    Article
  15. Article
  16. Post-Translational Modification of Lamins: Mechanisms and Functions.Frontiers in cell and developmental biology · 2022
    Review
  17. Article
  18. ATM Modulates Nuclear Mechanics by Regulating Lamin A Levels.Frontiers in cell and developmental biology · 2022
    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

5 authors at 2 institutions in 2 countries.

A S NaeemImmunobiology and Dermatology, UCL Institute of Child Health, London, UK.
Y ZhuImmunobiology and Dermatology, UCL Institute of Child Health, London, UK.
W L DiImmunobiology and Dermatology, UCL Institute of Child Health, London, UK.
S MarmiroliDepartment of Surgery, Medicine and Dentistry, Università degli Studi di Modena e Reggio Emilia, Modena, Italy.
R F L O'ShaughnessyImmunobiology and Dermatology, UCL Institute of Child Health, London, UK.
University College London · GBUniversity of Modena and Reggio Emilia · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nuclear degradation is a key stage in keratinocyte terminal differentiation and the formation of the cornified envelope that comprises the majority of epidermal barrier function. Parakeratosis, the retention of nuclear material in the cornified layer of the epidermis, is a common histological observation in many skin diseases, notably in atopic dermatitis and psoriasis. Keratinocyte nuclear degradation is not well characterised, and it is unclear whether the retained nuclei contribute to the altered epidermal differentiation seen in eczema and psoriasis. Loss of AKT1 function strongly correlated with parakeratosis both in eczema samples and in organotypic culture models. Although levels of DNAses, including DNase1L2, were unchanged, proteomic analysis revealed an increase in Lamin A/C. AKT phosphorylates Lamin A/C, targeting it for degradation. Consistent with this, Lamin A/C degradation was inhibited and Lamin A/C was observed in the cornified layer of AKT1 knockdown organotypic cultures, surrounding retained nuclear material. Using AKT-phosphorylation-dead Lamin A constructs we show that the retention of nuclear material is sufficient to cause profound changes in epidermal terminal differentiation, specifically a reduction in Loricrin, Keratin 1, Keratin 10, and filaggrin expression. We show that preventing nuclear degradation upregulates BMP2 expression and SMAD1 signalling. Consistent with these data, we observe both parakeratosis and evidence of increased SMAD1 signalling in atopic dermatitis. We therefore present a model that, in the absence of AKT1-mediated Lamin A/C degradation, DNA degradation processes, such as those mediated by DNAse 1L2, are prevented, leading to parakeratosis and changes in epidermal differentiation.

Indexed as

Cell DifferentiationAnimalsBone Morphogenetic Protein 2Filaggrin ProteinsIntermediate Filament ProteinsKeratin-1Keratin-10KeratinocytesLamin Type AMembrane ProteinsMicePhosphorylationProto-Oncogene Proteins c-aktRatsRNA InterferenceRNA, Small InterferingAkt1 protein, mouseBmp2 protein, mouseBone Morphogenetic Protein 2Filaggrin ProteinsIntermediate Filament ProteinsKeratin-1Keratin-10Lamin Type AloricrinMembrane ProteinsProto-Oncogene Proteins c-aktRNA, Small InterferingSmad1 Protein

Identifiers

PMID26045045
PMCPMC4816115
OpenAlexW1571783785

What OpenQuestion holds

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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.