Evidence map›Paper›PMID 29257328›Full record

ArticleMolecular medicine reports2018

Role of protein delta homolog 1 in the proliferation and differentiation of ameloblasts.

Shengcai Qi, Xueqin Zhu, Xiaoning Wang, Fubo Chen, Yanhong Yan, Guangwei Shang, Wantao Chen

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.1field-weighted citation impact, top 47% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. 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

7 authors at 4 institutions in 1 country.

Shengcai Qi *Department of Oral and Maxillofacial‑Head and Neck Oncology, and Faculty of Oral and Maxillofacial Surgery, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200011, P.R. China.
Xueqin Zhu *Department of Oral and Maxillofacial‑Head and Neck Oncology, and Faculty of Oral and Maxillofacial Surgery, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200011, P.R. China.
Xiaoning WangDepartment of Oral and Maxillofacial‑Head and Neck Oncology, and Faculty of Oral and Maxillofacial Surgery, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200011, P.R. China.
Fubo ChenDepartment of Stomatology, Shanghai Tenth People's Hospital, Tongji University, Shanghai 200072, P.R. China.
Yanhong YanDepartment of Pediatric Dentistry, School and Hospital of Stomatology, Tongji University, Shanghai Engineering Research Center of Tooth Restoration and Regeneration, Shanghai 200072, P.R. China.
Guangwei ShangDepartment of Stomatology, Shanghai Tenth People's Hospital, Tongji University, Shanghai 200072, P.R. China.
Wantao ChenDepartment of Oral and Maxillofacial‑Head and Neck Oncology, and Faculty of Oral and Maxillofacial Surgery, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200011, P.R. China.
Shanghai Ninth People's Hospital · CNTongji University · CNShanghai Jiao Tong University · CNShanghai Tenth People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Protein delta homolog 1 (DLK1) regulates the odontoblastic differentiation of human dental pulp stem cells. It was hypothesized that DLK1 may exert regulatory effects on epithelial‑mesenchymal interactions in tooth development. The present study investigated the expression of DLK1 during the development of mouse enamel and its role in the proliferation and differentiation of ameloblast‑lineage cells (ALCs). DLK1 expression was upregulated in ameloblasts in the first mandibular molar during the entire process of enamel development. The mRNA and protein levels of DLK1 were significantly upregulated following ameloblastic induction in ALCs. In addition, overexpression of DLK1 promoted the proliferation of ALCs, inhibited ameloblastic differentiation, upregulated the expression of amelogenin and enamelin, and downregulated the expression of odontogenic ameloblast‑associated protein and kallikrein 4. The results of the present study suggested that DLK1 may be a potent regulator of ameloblast proliferation and differentiation, and may regulate enamel formation during tooth development.

Indexed as

Cell DifferentiationCell ProliferationAmeloblastsAmelogeninAnimalsCalcium-Binding ProteinsCell LineDental EnamelDental Enamel ProteinsFemaleIntercellular Signaling Peptides and ProteinsKallikreinsMaleMiceMice, Inbred C57BLRNA, MessengerAmelogeninAmelx protein, mouseCalcium-Binding ProteinsDental Enamel ProteinsDlk1 protein, mouseIntercellular Signaling Peptides and Proteinskallikrein 4KallikreinsRNA, Messengertuftelinameloblastic differentiationameloblast-lineage cellenamelproliferationprotein delta homolog 1

Identifiers

PMID29257328
PMCPMC5802151
OpenAlexW2777594362

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.