Evidence map›Paper›PMID 15630138›Full record

ArticleThe Journal of experimental medicine2005

Spred-1 negatively regulates allergen-induced airway eosinophilia and hyperresponsiveness.

Hiromasa Inoue, Reiko Kato, Satoru Fukuyama, Atsushi Nonami, Kouji Taniguchi, Koichiro Matsumoto, Takako Nakano, Miyuki Tsuda, Mikiko Matsumura, Masato Kubo and 5 more

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The Journal of experimental medicine, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

38 citing papers in PubMed, 118 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. The molecular genetics of RASopathies: An update on novel disease genes and new disorders.American journal of medical genetics. Part C, Seminars in medical genetics · 2022
    Review
  5. The RASopathies: from pathogenetics to therapeutics.Disease models & mechanisms · 2022
    Review
  6. Article
  7. Article
  8. Article
  9. SOCS, SPRED, and NR4a: Negative regulators of cytokine signaling and transcription in immune tolerance.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2021
    Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Strand and Cell Type-specific Function of microRNA-126 in Angiogenesis.Molecular therapy : the journal of the American Society of Gene Therapy · 2016
    Article
  19. Article
  20. 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

15 authors at 4 institutions in 2 countries.

Hiromasa InoueResearch Institute for Diseases of the Chest, Graduate School of Medical Sciences, Kyushu University, Higashi-ku, Fukuoka, Japan. inoue@kokyu.med.kyushu-u.ac.jp
Reiko Kato
Satoru Fukuyama
Atsushi Nonami
Kouji Taniguchi
Koichiro Matsumoto
Takako Nakano
Miyuki Tsuda
Mikiko Matsumura
Masato Kubo
Fumihiko Ishikawa
Byoung-gon Moon
Kiyoshi Takatsu
Yoichi Nakanishi
Akihiko Yoshimura
St. Petersburg Institute of Bioregulation and Gerontology · RUTokyo University of Science · JPKyushu University · JPRIKEN Center for Integrative Medical Sciences · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

T helper 2 cytokines, including interleukin (IL)-4, IL-5, and IL-13, play a critical role in allergic asthma. These cytokines transmit signals through the Janus kinase/signal transducer and activator of transcription (STAT) and the Ras-extracellular signal-regulated kinase (ERK) signaling pathways. Although the suppressor of cytokine signaling (SOCS) family proteins have been shown to regulate the STAT pathway, the mechanism regulating the ERK pathway has not been clarified. The Sprouty-related Ena/VASP homology 1-domain-containing protein (Spred)-1 has recently been identified as a negative regulator of growth factor-mediated, Ras-dependent ERK activation. Here, using Spred-1-deficient mice, we demonstrated that Spred-1 negatively regulates allergen-induced airway eosinophilia and hyperresponsiveness, without affecting helper T cell differentiation. Biochemical assays indicate that Spred-1 suppresses IL-5-dependent cell proliferation and ERK activation. These data indicate that Spred-1 negatively controls eosinophil numbers and functions by modulating IL-5 signaling in allergic asthma.

Indexed as

Signal TransductionAdaptor Proteins, Signal TransducingAirway ResistanceAnimalsAsthmaCell DifferentiationCell LineCytokinesDNA PrimersEosinophiliaExtracellular Signal-Regulated MAP KinasesHypersensitivityImmunohistochemistryInterleukin-5LungMiceAdaptor Proteins, Signal TransducingCytokinesDNA PrimersExtracellular Signal-Regulated MAP KinasesInterleukin-5Repressor ProteinsSpred1 protein, mouse

Identifiers

PMID15630138
PMCPMC2212755
OpenAlexW2119008404

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.