Evidence map›Paper›PMID 9461531›Full record

ArticleThe Biochemical journal1998

Roles for interleukin-1beta, phorbol ester and a post-transcriptional regulator in the control of bradykinin B1 receptor gene expression.

X Zhou, P Polgar, L Taylor

Open access · bronzeAbstract read
In one paragraph

Article in The Biochemical journal, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
8.4field-weighted citation impact, top 2% 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

15 citing papers in PubMed, 68 citations in OpenAlex.

  1. C-reactive protein levels in hereditary angioedema.Clinical and experimental immunology · 2014
    Trial
  2. Review
  3. Article
  4. Expression, distribution and function of kinin BBritish journal of pharmacology · 2018
    Article
  5. Hereditary Angioedema Attacks: Local Swelling at Multiple Sites.Clinical reviews in allergy & immunology · 2016
    Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Hypoalgesia and altered inflammatory responses in mice lacking kinin B1 receptors.Proceedings of the National Academy of Sciences of the United States of America · 2000
    Article
  14. Article
  15. 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

3 authors at 1 institution in 1 country.

X ZhouDepartment of Biochemistry, Boston University School of Medicine, 80 East Concord Street, Boston MA 02118, USA.
P Polgar
L Taylor
Boston University · US

Funding

REGULATION OF PROSTAGLANDIN SYNTHESIS BY LUNG CELLSR01HL025776 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI POLGAR, PETER RUDOLPH · 1985 to 2013
$4.6M
NHLBI NIH HHS HL 25776
6 · The paper itself

Abstract

Bradykinin B1 receptor (BKB1R) is involved in a variety of pathophysiological processes, particularly those related to inflammation. The gene for this receptor is known to be upregulated by interleukin (IL)-1beta, a proinflammatory cytokine. However, the molecular mechanisms involved in the regulation of the BKB1R gene expression have not been defined. We demonstrated that IL-1beta induces a rapid increase in BKB1R mRNA level and the binding of desArg10-kallidin in human embryo lung fibroblasts (IMR90). This increase in BKB1R mRNA level is protein synthesis-independent as indicated by treatment of cells with cycloheximide (CHX) or puromycin (PUR). By testing the IL-1beta effect on BKB1R mRNA degradation, we showed that the IL-1beta upregulation of BKB1R expression is achieved through both transcriptional activation and post-transcriptional mRNA stabilization. In addition to the IL-1beta effects, translation inhibitors, CHX and PUR increase the steady state BKB1R mRNA level by inhibiting BKB1R mRNA degradation. Removal of the CHX block with subsequent resumption of protein synthesis results in a sizable increase of desArg10-kallidin binding. Using signalling pathway inhibitors, we show that IL-1beta functions through a protein tyrosine kinase, not protein kinase C or protein kinase A. However, activation of protein kinase C by phorbol 12-myristate 13-acetate increases the level of BKB1R mRNA and the binding of desArg10-kallidin. This increase is blocked by NF-kappaB activation inhibitors.

Indexed as

Cell LineCyclic AMP-Dependent Protein KinasesCycloheximideEnzyme InhibitorsGene Expression RegulationHumansInterleukin-1NF-kappa BProtein BiosynthesisProtein Kinase CProtein Synthesis InhibitorsProtein-Tyrosine KinasesReceptor, Bradykinin B1Receptors, BradykininRNA, MessengerSignal TransductionCyclic AMP-Dependent Protein KinasesCycloheximideEnzyme InhibitorsInterleukin-1NF-kappa BProtein Kinase CProtein Synthesis InhibitorsProtein-Tyrosine KinasesReceptor, Bradykinin B1Receptors, BradykininRNA, MessengerTetradecanoylphorbol Acetate

Identifiers

PMID9461531
PMCPMC1219148
OpenAlexW2331353594

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.