Evidence map›Paper›PMID 41788573›Full record

ArticleJournal of ginseng research2026

The ectopic olfactory receptor OR7A17 regulates the proliferation and differentiation of human epidermal keratinocytes, and ginsenoside Rh3 acts as its antagonist.

Su Bin Han, Soyoon Baek, Eunbi Yu, Sae Woong Oh, Hyeyoun Kim, Seokhyeon Min, Gyeonghyeon Kim, Yeonsoo Kim, Koo Chul Kwon, Iseul Jo and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of ginseng research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

13 authors.

Su Bin HanMolecular Dermatology Laboratory, Department of Integrative Biotechnology, College of Biotechnology and Bioengineering, Sungkyunkwan University, Suwon-si, 16419, Gyunggi-do, South Korea.
Soyoon BaekKolmar Korea, R&D Complex, 06800, Seoul, South Korea.
Eunbi YuMolecular Dermatology Laboratory, Department of Integrative Biotechnology, College of Biotechnology and Bioengineering, Sungkyunkwan University, Suwon-si, 16419, Gyunggi-do, South Korea.
Sae Woong OhMolecular Dermatology Laboratory, Department of Integrative Biotechnology, College of Biotechnology and Bioengineering, Sungkyunkwan University, Suwon-si, 16419, Gyunggi-do, South Korea.
Hyeyoun KimMolecular Dermatology Laboratory, Department of Integrative Biotechnology, College of Biotechnology and Bioengineering, Sungkyunkwan University, Suwon-si, 16419, Gyunggi-do, South Korea.
Seokhyeon MinMolecular Dermatology Laboratory, Department of Integrative Biotechnology, College of Biotechnology and Bioengineering, Sungkyunkwan University, Suwon-si, 16419, Gyunggi-do, South Korea.
Gyeonghyeon KimMolecular Dermatology Laboratory, Department of Integrative Biotechnology, College of Biotechnology and Bioengineering, Sungkyunkwan University, Suwon-si, 16419, Gyunggi-do, South Korea.
Yeonsoo KimMolecular Dermatology Laboratory, Department of Integrative Biotechnology, College of Biotechnology and Bioengineering, Sungkyunkwan University, Suwon-si, 16419, Gyunggi-do, South Korea.
Koo Chul KwonMolecular Immunology Laboratory, SEORIN COMPANY Co., Ltd., Chuncheon-si, Gangwon-do, South Korea.
Iseul JoMolecular Immunology Laboratory, SEORIN COMPANY Co., Ltd., Chuncheon-si, Gangwon-do, South Korea.
Jae Youl ChoMolecular Immunology Laboratory, Department of Integrative Biotechnology, College of Biotechnology and Bioengineering, Sungkyunkwan University, Suwon-si, 16419, Gyunggi-do, South Korea.
In Ki HongKolmar Korea, R&D Complex, 06800, Seoul, South Korea.
Jongsung LeeMolecular Dermatology Laboratory, Department of Integrative Biotechnology, College of Biotechnology and Bioengineering, Sungkyunkwan University, Suwon-si, 16419, Gyunggi-do, South Korea.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Olfactory receptors perform diverse functions in many cell types and are ectopically expressed in human epidermis. Purpose: This study aimed to examine the role of OR7A17 in keratinocyte biology, its signaling pathway and the potential of ginsenosides as its antagonist. Methods: OR7A17 function was examined in stably OR7A17-overexpressing HaCaT cells using western blots, image analysis, flow cytometric and qPCR. Results: We found that OR7A17 overexpression promoted keratinocyte proliferation through MAPK signaling pathway, accompanied by elevated cAMP and cytosolic Ca Conclusion: In summary, OR7A17 promoted keratinocyte proliferation by activating PKA/MAPK, Ca

Indexed as

Cell proliferationDifferentiationG-protein-coupled receptorMitogen-activated protein kinaseOlfactory receptorOverexpression

Identifiers

PMID41788573
PMCPMC12959293

What Socratic 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 Socratic graph.