Evidence map›Paper›PMID 18276794›Full record

ArticleAmerican journal of respiratory cell and molecular biology2008

SHP-1 inhibition by 4-hydroxynonenal activates Jun N-terminal kinase and glutamate cysteine ligase.

Alessandra Rinna, Henry Jay Forman

Abstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

22 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Review
  3. Redox signaling: An evolution from free radicals to aging.Free radical biology & medicine · 2016
    Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Antioxidant therapeutics: Pandora's box.Free radical biology & medicine · 2014
    Review
  9. Article
  10. Glutathione synthesis and its role in redox signaling.Seminars in cell & developmental biology · 2012
    Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Disruption of the mGsta4 gene increases life span of C57BL mice.The journals of gerontology. Series A, Biological sciences and medical sciences · 2010
    Article
  18. Article
  19. Article
  20. Surfactant-associated protein B is critical to survival in nickel-induced injury in mice.American journal of respiratory cell and molecular biology · 2009
    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

2 authors at 2 institutions in 2 countries.

Alessandra RinnaSchool of Natural Sciences, University of California Merced, Merced, CA 95344, USA.
Henry Jay Forman
University of California, Merced · USUniversity of Messina · IT

Funding

REGULATION OF GLUTATHIONE SYNTHESIS IN OXIDATIVE STRESSR01ES005511 · NIEHS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI FORMAN, HENRY JAY · 1991 to 2010
$2.9M
Hydroxynonenal induces glutathione synthesis through JNKR56ES005511 · NIEHS · UNIVERSITY OF CALIFORNIA, MERCED · PI FORMAN, HENRY JAY · 2006 to 2006
$75k
NIEHS NIH HHS ES 05511
6 · The paper itself

Abstract

4-Hydroxy-2-nonenal (HNE), a major lipid peroxidation product, is toxic at high concentrations, but at near-physiological concentrations it induces detoxifying enzymes. Previous data established that in human bronchial epithelial (HBE1) cells, both genes for glutamate cysteine ligase (GCL) are induced by HNE through the c-Jun N-terminal kinase (JNK) pathway. The protein-tyrosine phosphatase SH2 domain containing phosphatase-1 (SHP-1) is thought to play a role as a negative regulator of cell signaling, and has been implicated as such in the JNK pathway. In the present study, SHP-1 was demonstrated to contribute to HNE-induced-gclc expression via regulation of the JNK pathway in HBE1 cells. Treatment of HBE1 cells with HNE induced phosphorylation of mitogen-activated protein kinase kinase 4 (MKK4), JNK, and c-Jun. HNE was able to inhibit protein tyrosine phosphatase activity of SHP-1 through increased degradation of the protein. Furthermore, transfection with small interference RNA SHP-1 showed an enhancement of JNK and c-Jun phosphorylation, but not of MKK4, leading to increased gclc expression. These results demonstrate that SHP-1 plays a role as a negative regulator of the JNK pathway and that HNE activated the JNK pathway by inhibiting SHP-1. Thus, SHP-1 acts as a sensor for HNE and is responsible for an important adaptive response to oxidative stress.

Indexed as

AldehydesCell SurvivalEnzyme ActivationEpidermal Growth FactorGlutamate-Cysteine LigaseHumansHydrocortisoneInsulinJNK Mitogen-Activated Protein KinasesPhosphorylationProtein Tyrosine Phosphatase, Non-Receptor Type 6Respiratory MucosaRNA, Small InterferingTransfectionTransferrinTriiodothyronine4-hydroxy-2-nonenalAldehydesEpidermal Growth FactorGlutamate-Cysteine LigaseHydrocortisoneInsulinJNK Mitogen-Activated Protein KinasesProtein Tyrosine Phosphatase, Non-Receptor Type 6PTPN6 protein, humanRNA, Small InterferingTransferrinTriiodothyronine

Identifiers

PMID18276794
PMCPMC2438451
OpenAlexW2002307866

What OpenQuestion 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 OpenQuestion graph.