Evidence map›Paper›PMID 28055293›Full record

ReviewSmall GTPases2019

Epidermal activation of the small GTPase Rac1 in psoriasis pathogenesis.

Mårten C G Winge, M Peter Marinkovich

Open access · bronzeAbstract readReviewVideo-Audio Media
In one paragraph

Review in Small GTPases, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.3field-weighted citation impact, top 44% 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

10 citing papers in PubMed, 11 citations in OpenAlex.

  1. 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 at 1 institution in 1 country.

Mårten C G Wingea Program in Epithelial Biology , Stanford University School of Medicine , Stanford , CA , USA.
M Peter Marinkovicha Program in Epithelial Biology , Stanford University School of Medicine , Stanford , CA , USA.
Stanford University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The small GTPase Ras-related C3 botulinum toxin substrate 1 (RAC1) plays a central role in skin homeostasis, including barrier function, wound healing and inflammatory responses. Psoriasis is a common skin disease characterized by deregulation of these functions, and affected skin exhibit keratinocyte hyperproliferation, inflammation and immune cell infiltration. Although psoriasis is often triggered by environmental stimulus, there is a strong genetic association with genes expressed in both immune cells and keratinocytes, of which several are linked to Rac1 signaling. Rac1 is highly active in human psoriatic lesional skin and keratinocytes, and keratinocyte-specific overexpression of an activated mutant of Rac1, Rac1

Indexed as

Cell ProliferationAnimalsDisease Models, AnimalEnzyme ActivationEpidermisHumansKeratinocytesMiceMice, TransgenicMutationPsoriasisrac1 GTP-Binding Proteinrac1 GTP-Binding ProteinRAC1 protein, humancrosstalkepidermis-immunekeratinocytepsoriasisRac1

Identifiers

PMID28055293
PMCPMC6548294
OpenAlexW2568120864

What OpenQuestion holds

Textmetadata
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.