Evidence map›Paper›PMID 30623117›Full record

ArticleBiochemistry and biophysics reports2019

Konjac ceramide (kCer) regulates keratinocyte migration by Sema3A-like repulsion mechanism.

Seigo Usuki, Noriko Tamura, Tomohiro Tamura, Shigeki Higashiyama, Kunikazu Tanji, Susumu Mitsutake, Asuka Inoue, Junken Aoki, Katsuyuki Mukai, Yasuyuki Igarashi

Open access · goldAbstract read
In one paragraph

Article in Biochemistry and biophysics reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.2field-weighted citation impact, top 16% 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

4 citing papers in PubMed, 5 citations in OpenAlex.

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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

10 authors at 7 institutions in 1 country.

Seigo UsukiLipid Biofunction Section, Frontier Research Center for Advanced Material and Life Science, Faculty of Advanced Life Science, Hokkaido University, Sapporo, Hokkaido, Japan.
Noriko TamuraBioproduction Research Institute, National Institute of Advanced Industrial Science and Technology (AIST), Sapporo, Hokkaido, Japan.
Tomohiro TamuraBioproduction Research Institute, National Institute of Advanced Industrial Science and Technology (AIST), Sapporo, Hokkaido, Japan.
Shigeki HigashiyamaDepartment of Biochemistry and Molecular Genetics, Ehime University Graduate School of Medicine, Shitsukawa, Ehime, Japan.
Kunikazu TanjiDepartment of Neuropathology, Institute of Brain Science, Hirosaki University Graduate School of Medicine, Hirosaki, Aomori, Japan.
Susumu MitsutakeDepartment of Applied Biochemistry and Food Science, Faculty of Agriculture, Saga University, Saga, Japan.
Asuka InoueGraduate School of Pharmaceutical Sciences, Tohoku University, Sendai, Miyagi, Japan.
Junken AokiGraduate School of Pharmaceutical Sciences, Tohoku University, Sendai, Miyagi, Japan.
Katsuyuki MukaiR&D Headquarters, Daicel Corporation, Tokyo, Japan.
Yasuyuki IgarashiLipid Biofunction Section, Frontier Research Center for Advanced Material and Life Science, Faculty of Advanced Life Science, Hokkaido University, Sapporo, Hokkaido, Japan.
Hokkaido University · JPNational Institute of Advanced Industrial Science and Technology · JPTohoku University · JPDaicel (Japan) · JPEhime University · JPHirosaki University · JPSaga University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Previously, we proposed the following mechanism for konjac ceramide (kCer)-mediated neurite outgrowth inhibition: kCer binds to Nrp as a Sema3A agonist, resulting in Nrp1/PlexA complex formation and activation of the Sema3A signaling pathway to induce phosphorylation of CRMP2 and microtubule depolymerization. The Sema3A/Nrp1 signaling pathway is known to be also expressed in normal human keratinocytes. To determine whether kCer can function in human keratinocytes as it does in neurites, that is, if it can bind to Nrp1 in place of Sema3A, we studied the effect of kCer on HaCaT cell migration activity. Using a trans-well chamber assay, we compared the effects of Sema3A and kCer on serum-derived cell migration activity. kCer showed Sema3A-like suppression of cell migration activity and induction of cellular Cofilin phosphorylation. In addition, kCer and Sema3A inhibited histamine (His)-enhanced migration of immature HaCaT cells. We have demonstrated that kCer does not interact with histaime receptors H1R or H4R directly, but we speculate that kCer may transduce a signal downstream of the His signaling pathway.

Indexed as

AP-Sema3A, alkaline phosphatase-fused Sema3ABSA, bovine serum albuminC16Cer, N-hexadecanoyl-D-erythro-sphingosineC18Cer, N-octadecanoyl-D-erythro-sphingosineC24Cer, N-tetracosanoyl-D-erythro-sphingosineCer, ceramideCRMP2, collapsin response mediator protein 2DMEM, Dulbecco's modified Eagle's mediumEGCase I, endoglycoceramidase IGAPDH, Glyceraldehyde 3-phosphate dehydrogenaseGlcCer, glucosylceramideH1R, histamine G-coupled receptor 1H4R, histamine G-coupled receptor 4hGPCR, histamine G-coupled receptorHis, histamineHRs, histamine G-coupled receptorskCer, konjac ceramideNGF, nerve growth factorNrp1, neuropilin1PBS, phosphate-buffered salinep-Cofilin, phospho-Cofilinp-CRMP2, phospho-collapsin response mediator protein 2Sema3A, semaphorin 3A

Identifiers

PMID30623117
PMCPMC6319021
OpenAlexW2907149018

What OpenQuestion holds

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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.