Evidence map›Paper›PMID 35596832›Full record

ArticleCellular and molecular life sciences : CMLS2022

Nuclear receptor Nr1d1 alleviates asthma by abating GATA3 gene expression and Th2 cell differentiation.

Drishti Tiwari, Nancy Ahuja, Sumit Kumar, Rashi Kalra, Ravikanth Nanduri, Shalini Gupta, Asheesh Kumar Khare, Ella Bhagyaraj, Rashmi Arora, Pawan Gupta

Open access · greenAbstract read
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

13 citing papers in PubMed, 14 citations in OpenAlex.

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  7. Daily Supplementation withFoods (Basel, Switzerland) · 2024
    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

10 authors at 4 institutions in 2 countries.

Drishti TiwariDepartment of Molecular Immunology, Council of Scientific and Industrial Research, Institute of Microbial Technology, Sector 39A, Chandigarh, 160036, India. t.drishti@imtech.res.in.
Nancy AhujaDepartment of Molecular Immunology, Council of Scientific and Industrial Research, Institute of Microbial Technology, Sector 39A, Chandigarh, 160036, India.
Sumit KumarDepartment of Molecular Immunology, Council of Scientific and Industrial Research, Institute of Microbial Technology, Sector 39A, Chandigarh, 160036, India.
Rashi KalraDepartment of Molecular Immunology, Council of Scientific and Industrial Research, Institute of Microbial Technology, Sector 39A, Chandigarh, 160036, India.
Ravikanth NanduriDepartment of Molecular Immunology, Council of Scientific and Industrial Research, Institute of Microbial Technology, Sector 39A, Chandigarh, 160036, India.
Shalini GuptaDepartment of Molecular Immunology, Council of Scientific and Industrial Research, Institute of Microbial Technology, Sector 39A, Chandigarh, 160036, India.
Asheesh Kumar KhareDepartment of Molecular Immunology, Council of Scientific and Industrial Research, Institute of Microbial Technology, Sector 39A, Chandigarh, 160036, India.
Ella BhagyarajDepartment of Molecular Immunology, Council of Scientific and Industrial Research, Institute of Microbial Technology, Sector 39A, Chandigarh, 160036, India.
Rashmi AroraDepartment of Molecular Immunology, Council of Scientific and Industrial Research, Institute of Microbial Technology, Sector 39A, Chandigarh, 160036, India.
Pawan GuptaDepartment of Molecular Immunology, Council of Scientific and Industrial Research, Institute of Microbial Technology, Sector 39A, Chandigarh, 160036, India. pawan@imtech.res.in.ORCID http://orcid.org/0000-0001-6692-7237
Institute of Microbial Technology · INBaylor College of Medicine · USNational Cancer Institute · USUniversity of Florida · US

Funding

Council of Scientific and Industrial Research, India BSC0211Council of Scientific and Industrial Research, India OLP0704
6 · The paper itself

Abstract

Nuclear receptors are a unique family of transcription factors that play cardinal roles in physiology and plethora of human diseases. The adopted orphan nuclear receptor Nr1d1 is a constitutive transcriptional repressor known to modulate several biological processes. In this study, we found that Nr1d1 plays a decisive role in T helper (Th)-cell polarization and transcriptionally impedes the formation of Th2 cells by directly binding to the promoter region of GATA binding protein 3 (GATA3) gene. Nr1d1 interacts with its cellular companion, the nuclear receptor corepressor and histone deacetylase 3 to form a stable repression complex on the GATA3 promoter. The presence of Nr1d1 also imparts protection against associated inflammatory responses in murine model of asthma and its ligand SR9011 eased disease severity by suppressing Th2 responses. Moreover, Chip-seq profiling uncovered Nr1d1 interactions with other gene subsets that impedes Th2-linked pathways and regulates metabolism, immunity and brain functions, therefore, providing empirical evidence regarding the genetic link between asthma and other comorbid conditions. Thus, Nr1d1 emerges as a molecular switch that could be targeted to subdue asthma.

Indexed as

AsthmaTh2 CellsAnimalsCell DifferentiationGATA3 Transcription FactorGene ExpressionHumansMiceNuclear Receptor Subfamily 1, Group D, Member 1Th1 CellsGATA3 protein, humanGata3 protein, mouseGATA3 Transcription FactorNR1D1 protein, humanNr1d1 protein, mouseNuclear Receptor Subfamily 1, Group D, Member 1AsthmaGATA3Nuclear receptorT-betT lymphocytes

Identifiers

PMID35596832
PMCPMC11073070
OpenAlexW4281258036

What Socratic 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 Socratic graph.