Evidence map›Paper›PMID 12614196›Full record

ArticleThe Biochemical journal2003

Increased expression of the lipocalin 24p3 as an apoptotic mechanism for MK886.

Zhimin Tong, Xuli Wu, James P Kehrer

Open access · bronzeAbstract read
In one paragraph

Article in The Biochemical journal, 2003. 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
2.8field-weighted citation impact, top 10% 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, 48 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Lipocalin-2 is an autocrine mediator of reactive astrocytosis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009
    Article
  11. Mouse 24p3 protein has an effect on L929 cell viability.International journal of biological sciences · 2007
    Article
  12. Article
  13. 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.

Zhimin TongDivision of Pharmacology and Toxicology, College of Pharmacy, The University of Texas at Austin, Austin, TX 78712-0125, U.S.A.
Xuli Wu
James P Kehrer
Austin College · US

Funding

Pilot Project ProgramP30ES007784 · NIEHS · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI RICHIE, ELLEN R · 1996 to 2011
$16.4M
APOPTOSIS,5 LIPOXYGENASE ACTIVATING PROTEIN AND BCL XR01CA083701 · NCI · UNIVERSITY OF TEXAS AUSTIN · PI KEHRER, JAMES P · 2000 to 2004
$1.3M
NCI NIH HHS CA 83701NIEHS NIH HHS ES 07784
6 · The paper itself

Abstract

MK886, a strong proapoptotic agent, is an inhibitor of 5-lipoxygenase (LOX) through binding to the 5-LOX-activating protein (FLAP). Although MK886-induced apoptosis is through a FLAP-independent pathway, the precise mechanisms are not understood. In the present study, a possible role of 24p3, a lipocalin, in MK886-induced apoptosis was investigated. Exposure of murine prolymphoid progenitor cells (FL5.12) to 20 microM MK886 for 16 h dramatically increased 24p3 mRNA and protein expression. Induction could also be achieved with another FLAP inhibitor, MK591. The induction of 24p3 by MK886 was dose- and time-dependent. The up-regulated 24p3 mRNA expression by MK886 was enhanced a further 3.1-fold by WY14643, an activator of peroxisome-proliferator-activated receptor alpha, whereas ciglitazone, an activator of peroxisome-proliferator-activated receptor gamma attenuated the MK886-induced 24p3 expression by more than 50%. Neither WY14643 nor ciglitazone alone had any effect on the expression of 24p3. The induction of 24p3 by MK886 was dependent on the synthesis of new protein(s), since cycloheximide, an inhibitor of protein synthesis, prevented this effect. In all cases, including the inhibition of MK886-induced 24p3 protein expression by stable transfection with antisense cDNA of 24p3, the extent of apoptosis closely paralleled 24p3 levels. Apoptosis induced by MK886, or enhanced by WY14643, was accompanied by the cleavage and activation of caspase-3. The overexpression of bcl-2 or bcl-x(L) in FL5.12 cells inhibited apoptosis induced by MK886 as well as the enhancement of apoptosis by WY14643. Thus 24p3 is an MK886-inducible gene and may play an important role in MK886-induced apoptosis.

Indexed as

ThiazolidinedionesAcute-Phase ProteinsAnimalsApoptosisCarcinogensCaspase 3CaspasesChlorobenzenesGene Expression RegulationIndolesLipocalin-2LipocalinsLipoxygenase InhibitorsMiceOncogene ProteinsProto-Oncogene Proteins c-bcl-2Acute-Phase ProteinsCarcinogensCasp3 protein, mouseCaspase 3CaspasesChlorobenzenesciglitazoneIndolesLcn2 protein, mouseLipocalin-2LipocalinsLipoxygenase InhibitorsMK-886Oncogene Proteinspirinixic acidProto-Oncogene Proteins c-bcl-2PyrimidinesThiazolesThiazolidinediones

Identifiers

PMID12614196
PMCPMC1223388
OpenAlexW2020981505

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.