Evidence map›Paper›PMID 33554442›Full record

ArticleThe Kaohsiung journal of medical sciences2021

LncRNA UCA1 negatively regulates NF-kB activity in psoriatic keratinocytes through the miR125a-A20 axis.

Xiao-Lei Ma, Guang-Dong Wen, Cong Yu, Zheng Zhao, Na Gao, Zheng-Yi Liu

Open access · goldAbstract read
In one paragraph

Article in The Kaohsiung journal of medical sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.2field-weighted citation impact, top 24% 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

9 citing papers in PubMed, 15 citations in OpenAlex.

  1. Review
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  3. Review
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  5. Review
  6. Repressive Control of Keratinocyte Cytoplasmic Inflammatory Signaling.International journal of molecular sciences · 2023
    Review
  7. Article
  8. Review
  9. 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

6 authors at 1 institution in 1 country.

Xiao-Lei MaDepartment of Dermatology, Peking University International Hospital, Beijing, China.ORCID https://orcid.org/0000-0001-7108-3956
Guang-Dong WenDepartment of Dermatology, Peking University People's Hospital, Beijing, China.
Cong YuDepartment of Dermatology, Peking University People's Hospital, Beijing, China.
Zheng ZhaoDepartment of Dermatology, Peking University International Hospital, Beijing, China.
Na GaoDepartment of Dermatology, Peking University International Hospital, Beijing, China.
Zheng-Yi LiuDepartment of Dermatology, Peking University International Hospital, Beijing, China.
Peking University · CN

Funding

Grant from Peking University International Hospital YN2018QN04National Natural Science Foundation of China 81773311
6 · The paper itself

Abstract

Psoriasis is one of the most common chronic inflammatory skin diseases that affects approximately 3% of the world's population. Hyper proliferation, infiltration of inflammatory cells and aberrant differentiation of keratinocytes are the three most important characteristics of psoriasis. Previous reports showed that NF-κBis the crucial mediator linking psoriatic keratinocytes and immune cell states through its effects on chemokine and cytokine production. To identify the role of NF-κB in psoriasis, we conducted ELISA assay to detect the activity of NF-κB in lesional skin and nonlesional skin of patients with psoriasis. Mounting evidence suggests that the interaction between long noncoding RNAs (lncRNAs) and microRNAs plays important role in the regulation of the initiation and development of various diseases. In this article, we identified that lncRNA UCA1 was down-regulated in lesional skin of patients with psoriasis. Further studies showed that lncRNA UCA1 could promote the expression of A20 by inhibitingmiR125a, and up-regulated A20 decreased the activity of NF-κB through its ubiquitin editing function. Taken together, we identified and demonstrated that lncRNA UCA1 negatively regulated NF-κB activity in psoriasis through the miR125a-A20 axis.

Indexed as

Signal TransductionAdultAgedBase SequenceDown-RegulationFemaleHaCaT CellsHumansKeratinocytesMaleMicroRNAsMiddle AgedNF-kappa BPsoriasisRNA, Long NoncodingTumor Necrosis Factor alpha-Induced Protein 3MicroRNAsMIRN125 microRNA, humanNF-kappa BRNA, Long NoncodingTNFAIP3 protein, humanTumor Necrosis Factor alpha-Induced Protein 3UCA1 RNA, humanA20lncRNA UCA1miR125aNF-κBpsoriasis

Identifiers

PMID33554442
PMCPMC11896314
OpenAlexW3126759242

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.