Evidence map›Paper›PMID 29868029›Full record

ArticleFrontiers in immunology2018

STAT3-Mediated Transcriptional Regulation of Osteopontin in STAT3 Loss-of-Function Related Hyper IgE Syndrome.

Shubham Goel, Smrity Sahu, Ranjana W Minz, Surjit Singh, Deepti Suri, Young M Oh, Amit Rawat, Shobha Sehgal, Biman Saikia

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

16 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Hyper-IgE syndrome: A rare case report.The journal of allergy and clinical immunology. Global · 2025
    Article
  7. Article
  8. Article
  9. Role of Herbal Extracts of Catechu fromPharmaceuticals (Basel, Switzerland) · 2022
    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

9 authors at 2 institutions in 2 countries.

Shubham GoelDepartment of Immunopathology, Postgraduate Institute of Medical Education and Research, Chandigarh, India.
Smrity SahuDepartment of Immunopathology, Postgraduate Institute of Medical Education and Research, Chandigarh, India.
Ranjana W MinzDepartment of Immunopathology, Postgraduate Institute of Medical Education and Research, Chandigarh, India.
Surjit SinghDepartment of Pediatrics, Advanced Pediatrics Centre, Postgraduate Institute of Medical Education and Research, Chandigarh, India.
Deepti SuriDepartment of Pediatrics, Advanced Pediatrics Centre, Postgraduate Institute of Medical Education and Research, Chandigarh, India.
Young M OhCell Line Development Team, Bio Research Institute, Genexine Inc, Seongnam, South Korea.
Amit RawatDepartment of Pediatrics, Advanced Pediatrics Centre, Postgraduate Institute of Medical Education and Research, Chandigarh, India.
Shobha SehgalDepartment of Immunopathology, Postgraduate Institute of Medical Education and Research, Chandigarh, India.
Biman SaikiaDepartment of Immunopathology, Postgraduate Institute of Medical Education and Research, Chandigarh, India.
Post Graduate Institute of Medical Education and Research · INGenexine (South Korea) · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Hyper-IgE syndrome (HIES) caused by loss-of-function (LOF) mutations in STAT3 gene (STAT3 LOF HIES) is associated with dental and facial abnormalities in addition to immunological defects. The role of STAT3 in the pathogenesis of the dental/facial features is, however, poorly elucidated. Objectives: Since mechanism of cellular resorption of mineralized tissues such as bone and teeth are similar, we attempted to study the expression of genes involved in bone homeostasis in STAT3 LOF HIES. Methods: Peripheral blood mononuclear cells from healthy controls (HCs), STAT3 LOF HIES patients, STAT3 Results: Osteopontin (OPN) gene was seen to be significantly upregulated after IL-6 stimulation in HC (mean fold change 18.6, Conclusion: Regulation of OPN gene through IL-6-mediated STAT3 activation and its significant dysregulation in STAT3 LOF HIES subjects could make OPN a plausible candidate involved in the pathogenesis of dental/facial manifestations in HIES.

Indexed as

Gene Expression RegulationLoss of Function MutationTranscription, GeneticAdolescentAdultBinding SitesCell Line, TumorChild, PreschoolComputational BiologyEnhancer Elements, GeneticGene Expression ProfilingHumansInterleukin-6Job SyndromeLeukocytes, MononuclearMaleInterleukin-6OsteopontinSOCS3 protein, humanSTAT3 Transcription FactorSuppressor of Cytokine Signaling 3 Proteincraniosynostosisdental anomalieshyper-IgE syndromeosteopontinskeletal anomaliesSTAT3 signaling

Identifiers

PMID29868029
PMCPMC5966547
OpenAlexW2799625219

What OpenQuestion holds

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Registered trials

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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.