Evidence map›Paper›PMID 28296893›Full record

ArticlePLoS genetics2017

hnRNP I regulates neonatal immune adaptation and prevents colitis and colorectal cancer.

Zhigang Jin, Feng Liang, Jing Yang, Wenyan Mei

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

18 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. High expression of HNRNPR in ESCA combined withJournal of translational medicine · 2022
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
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

4 authors at 1 institution in 1 country.

Zhigang JinDepartment of comparative Biosciences, College of veterinary medicine, University of Illinois at Urbana-Champaign, Urbana, Illinois, United States of America.ORCID 0000-0001-7557-2968
Feng LiangDepartment of statistics, University of Illinois at Urbana-Champaign, Champaign, Illinois, United States of America.
Jing YangDepartment of comparative Biosciences, College of veterinary medicine, University of Illinois at Urbana-Champaign, Urbana, Illinois, United States of America.ORCID 0000-0002-4983-1660
Wenyan MeiDepartment of comparative Biosciences, College of veterinary medicine, University of Illinois at Urbana-Champaign, Urbana, Illinois, United States of America.ORCID 0000-0001-5270-7727
University of Illinois Urbana-Champaign · US

Funding

Maternal control of germline developmentR35GM131810 · NIGMS · UNIVERSITY OF ILLINOIS AT URBANA-CHAMPAIGN · PI Jing Yang · 2019 to 2026
$3.2M
Dnd1 and repression of transcription in primordial germ cellsR01GM111816 · NIGMS · UNIVERSITY OF ILLINOIS AT URBANA-CHAMPAIGN · PI YANG, JING · 2015 to 2018
$1.2M
NIGMS NIH HHS R01 GM111816NIGMS NIH HHS R35 GM131810
6 · The paper itself

Abstract

The intestinal epithelium plays a critical role in host-microbe homeostasis by sensing gut microbes and subsequently initiating proper immune responses. During the neonatal stage, the intestinal epithelium is under immune repression, allowing the transition for newborns from a relatively sterile intra-uterine environment to one that is rich in foreign antigens. The mechanism underlying such immune repression remains largely unclear, but involves downregulation of IRAK1 (interleukin-1 receptor-associated kinase), an essential component of toll-like receptor-mediated NF-κB signaling. We report here that heterogeneous nuclear ribonucleoprotein I (hnRNPI), an RNA binding protein, is essential for regulating neonatal immune adaptation. We generated a mouse model in which hnRNPI is ablated specifically in the intestinal epithelial cells, and characterized intestinal defects in the knockout mice. We found that loss of hnRNPI function in mouse intestinal epithelial cells results in early onset of spontaneous colitis followed by development of invasive colorectal cancer. Strikingly, the epithelium-specific hnRNPI knockout neonates contain aberrantly high IRAK1 protein levels in the colons and fail to develop immune tolerance to environmental microbes. Our results demonstrate that hnRNPI plays a critical role in establishing neonatal immune adaptation and preventing colitis and colorectal cancer.

Indexed as

Adaptive ImmunityAnimalsAnimals, NewbornBlotting, WesternColitisColorectal NeoplasmsEpithelial CellsFemaleGene ExpressionHeterogeneous-Nuclear RibonucleoproteinsImmunohistochemistryIn Situ Hybridization, FluorescenceInterleukin-1 Receptor-Associated KinasesIntestinal MucosaMaleMice, Inbred C57BLHeterogeneous-Nuclear RibonucleoproteinsInterleukin-1 Receptor-Associated KinasesIrak1 protein, mouseNF-kappa BPolypyrimidine Tract-Binding ProteinPtbp1 protein, mouse

Identifiers

PMID28296893
PMCPMC5371387
OpenAlexW2603103900

What OpenQuestion holds

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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 OpenQuestion graph.