Analysis of mechanisms involved in the prevention of gamma irradiation-induced apoptosis by hGM-CSF.

R Liu, C B Liu, M G Mohi, K Arai, S Watanabe

Abstract read

In one paragraph

Article in Oncogene, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it

0cells of the map it votes in

4citing papers in PubMed

0.8field-weighted citation impact, top 26% 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

4 citing papers in PubMed, 14 citations in OpenAlex.

JAK2(V617F) negatively regulates p53 stabilization by enhancing MDM2 via La expression in myeloproliferative neoplasms.Oncogene · 2012
Article
Design and Applications of Bifunctional Small Molecules: Why Two Heads Are Better Than One.ACS chemical biology · 2008
Review
Enforced granulocyte/macrophage colony-stimulating factor signals do not support lymphopoiesis, but instruct lymphoid to myelomonocytic lineage conversion.The Journal of experimental medicine · 2003
Article
Evidence of a possible epigenetic inactivation mechanism operating on a region of mouse chromosome 19 in gamma-radiation-induced thymic lymphomas.Oncogene · 2001
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

5 authors at 2 institutions in 1 country.

R LiuDepartment of Molecular and Developmental Biology, Institute of Medical Science, University of Tokyo, Japan.

C B Liu

M G Mohi

K Arai

S Watanabe

The University of Tokyo · JPTokyo University of Science · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human granulocyte-macrophage colony-stimulating factor (hGM-CSF) induces proliferation and sustains viability of the mouse interleukin (IL)-3 dependent lymphoid cell line BA/F3 expressing the hGM-CSF receptor. Caspase-3 like enzyme activity and DNA fragmentation were augmented by depletion of this factor from the cell, and exposure to gamma irradiation accelerated kinetics of these events. Anti gamma irradiation-induced apoptosis occurred through various mutant GM-CSF receptors and only the box1 region was essential while the C terminal region, including tyrosine residues which are required for MAPK cascade activation, was dispensable. Consistent with this notion, the addition of PD98059 had no effect on this activity thereby indicating that activation of MAPK is not essential for the activity. As expected, gamma irradiation increased p53 protein and bax mRNA levels and the presence of hGM-CSF dramatically modulated bax/bcl-X(L) ratio. The PI-3K specific inhibitor wortmannin did not affect hGM-CSF dependent anti gamma irradiation induced apoptosis nor bcl-X(L) induction, thus bcl-X(L) but not PI-3K pathway seems to be involved in hGM-CSF dependent anti gamma irradiation-induced apoptosis. It is well documented that the boxl region is essential for GM-CSF dependent activation of JAK2 and JAK2 specific inhibitor AG490 suppressed anti gamma, irradiation-induced apoptosis by hGM-CSF. An artificial JAK2 activating molecule in which extracellular and the transmembrane of beta(c) fused with whole JAK2 can sustain BA/F3 cells survival and proliferation mIL-3 independently, but these cells are susceptible to gamma irradiation. Furthermore GyrB/Jak2, which can activate STAT5 but not the MAPK cascade nor survival of BA/F3 cells, also could not prevent gamma irradiation-induced apoptosis. Although JAK2 is essential for hGM-CSF dependent anti gamma irradiation-induced apoptosis, it appeared that JAK2 does not seem sufficient for the activity.

Indexed as

Milk ProteinsProto-Oncogene ProteinsAnimalsApoptosisbcl-X ProteinCaspasesCell LineDNA-Binding ProteinsDNA DamageDNA FragmentationEnzyme InductionEnzyme InhibitorsFlavonoidsGamma RaysGenisteinGranulocyte-Macrophage Colony-Stimulating Factor2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-oneBCL2L1 protein, humanBcl2l1 protein, mousebcl-X ProteinCaspasesDNA-Binding ProteinsEnzyme InhibitorsFlavonoidsGenisteinGranulocyte-Macrophage Colony-Stimulating FactorInterleukin-3JAK2 protein, humanJak2 protein, mouseJanus Kinase 2Milk ProteinsProtein-Tyrosine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-bcl-2Radiation-Protective AgentsReceptors, Granulocyte-Macrophage Colony-Stimulating FactorRecombinant Fusion ProteinsSTAT5 Transcription FactorTrans-Activators

Identifiers

PMID10698527

DOI10.1038/sj.onc.1203364

OpenAlexW2318390744

What OpenQuestion holds

Textmetadata

Read underepoch 390

Registered trials

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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.