Evidence map›Paper›PMID 35163390›Full record

ReviewInternational journal of molecular sciences2022

The Discovery and Function of Filaggrin.

J Kenneth Hoober, Laura L Eggink

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
14.0field-weighted citation impact, top 1% 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

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 74 citations in OpenAlex.

  1. Pooled it
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  11. Co-morbid monogenic disorders at chromosome region 1q2: LMNA- and FLG-related disorders in a patient referred for assessment of joint hypermobility.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2025
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  16. Histological Comparison of Lipofilling and Hyaluronic Acid Filler Injection 30 Days after Simulation in Rats.Doklady biological sciences : proceedings of the Academy of Sciences of the USSR, Biological sciences sections · 2025
    Article
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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

2 authors.

J Kenneth HooberSusavion Biosciences, Inc., 1615 W University Drive, Suite 132, Tempe, AZ 85281, USA.ORCID 0000-0003-0250-9970
Laura L EgginkSusavion Biosciences, Inc., 1615 W University Drive, Suite 132, Tempe, AZ 85281, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Keratohyalin granules were discovered in the mid-19th century in cells that terminally differentiate to form the outer, cornified layer of the epidermis. The first indications of the composition of these structures emerged in the 1960s from a histochemical stain for histidine, followed by radioautographic evidence of a high incidence of histidine incorporation into newly synthesized proteins in cells containing the granules. Research during the next three decades revealed the structure and function of a major protein in these granules, which was initially called the 'histidine-rich protein'. Steinert and Dale named the protein 'filaggrin' in 1981 because of its ability to aggregate keratin intermediate filaments. The human gene for the precursor, 'profilaggrin,' was reported in 1991 to encode 10, 11 or 12 nearly identical repeats. Remarkably, the mouse and rat genes encode up to 20 repeats. The lifetime of filaggrin is the time required for keratinocytes in the granular layer to move into the inner cornified layer. During this transition, filaggrin facilitates the collapse of corneocytes into 'building blocks' that become an impermeable surface barrier. The subsequent degradation of filaggrin is as remarkable as its synthesis, and the end-products aid in maintaining moisture in the cornified layer. It was apparent that ichthyosis vulgaris and atopic dermatitis were associated with the absence of this protein. McLean's team in 2006 identified the cause of these diseases by discovering loss-of-function mutations in the profilaggrin gene, which led to dysfunction of the surface barrier. This story illustrates the complexity in maintaining a healthy, functional epidermis.

Indexed as

AnimalsCytoplasmic GranulesFilaggrin ProteinsHistidineHumansKeratinocytesMutationPublicationsFilaggrin ProteinsHistidineatopic dermatitiscorneodesmosomeseczemafilaggrinhistidine-rich proteinichthyosis vulgariskeratohyalin granulesloss-of-function mutationsprofilaggrintransglutaminase

Identifiers

PMID35163390
PMCPMC8835998
OpenAlexW4210295330

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.