Evidence map›Paper›PMID 29784039›Full record

ArticleHuman genomics2018

Mutational analysis of epidermal and hyperproliferative type I keratins in mild and moderate psoriasis vulgaris patients: a possible role in the pathogenesis of psoriasis along with disease severity.

Tamilselvi Elango, Jingying Sun, Caihong Zhu, Fusheng Zhou, Yaohua Zhang, Liangdan Sun, Sen Yang, Xuejun Zhang

Open access · goldAbstract read
In one paragraph

Article in Human genomics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing 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

18 citing papers in PubMed, 31 citations in OpenAlex.

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  13. Skin Barrier Dysregulation in Psoriasis.International journal of molecular sciences · 2021
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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

8 authors at 3 institutions in 1 country.

Tamilselvi ElangoInstitute and Department of Dermatology, The First Affiliated Hospital, Anhui Medical University, Hefei, China. tami24684@gmail.com.
Jingying SunInstitute and Department of Dermatology, The First Affiliated Hospital, Anhui Medical University, Hefei, China.
Caihong ZhuInstitute and Department of Dermatology, The First Affiliated Hospital, Anhui Medical University, Hefei, China.
Fusheng ZhouInstitute and Department of Dermatology, The First Affiliated Hospital, Anhui Medical University, Hefei, China.
Yaohua ZhangInstitute of Dermatology, Huashan Hospital, Fudan University, Shanghai, China.
Liangdan SunInstitute and Department of Dermatology, The First Affiliated Hospital, Anhui Medical University, Hefei, China.
Sen YangInstitute and Department of Dermatology, The First Affiliated Hospital, Anhui Medical University, Hefei, China.
Xuejun ZhangInstitute and Department of Dermatology, The First Affiliated Hospital, Anhui Medical University, Hefei, China. ayzxj@vip.sina.com.
Anhui Medical University · CNFirst Affiliated Hospital of Anhui Medical University · CNFudan University · CN

Funding

National Natural Science Foundation of China 81602397Natural Science Foundation of Shanghai 15ZR1405700
6 · The paper itself

Abstract

backgroundMutations in keratin proteins have been vastly associated with a wide array of genodermatoses; however, mutations of keratins in psoriasis have not been fully investigated. The main aim of the current research was to identify the mutation in K14, K10, K16, and K17 genes in two stages of psoriasis patients.

methodsNinety-six psoriatic skin biopsies were collected. mRNA transcript of K14, K10, K16, and K17 was prepared, amplified, and sequenced. Sanger sequences of all keratins were further validated for mutational analysis using Mutation Surveyor and Alamut Visual. Then, in silico analysis of protein stability and protein and gene expression of all keratins was performed and validated.

resultsOut of 44 mutations, about 75% of keratins are highly pathogenic and deleterious. Remaining 25% mutations are less pathogenic and tolerated in nature. In these 33 deleterious mutations were immensely found to decrease keratin protein stability. We also found a correlation between keratin and Psoriasis Area and Severity Index score which added that alteration in keratin gene in skin causes severity of psoriasis.

conclusionsWe strongly concluded that acanthosis and abnormal terminal differentiation was mainly due to the mutation in epidermal keratins. In turn, disease severity and relapsing of psoriasis are mainly due to the mutation of hyperproliferative keratins. These novel keratin mutations in psoriatic epidermis might be one of the causative factors for psoriasis.

Indexed as

Acanthosis NigricansAdolescentAdultAgedBiopsyCell DifferentiationCell ProliferationDNA Mutational AnalysisEpidermisFemaleHumansKeratinsKeratins, Type IMaleMiddle AgedMutationKeratinsKeratins, Type IEpidermal keratinsHyperproliferative keratinsImmunofluorescenceMutationPsoriasisSanger sequence

Identifiers

PMID29784039
PMCPMC5963134
OpenAlexW2806750372

What OpenQuestion holds

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LicenceCC BY
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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.