Evidence map›Paper›PMID 9553040›Full record

ArticleGenes & development1998

Cytokine rescue of p53-dependent apoptosis and cell cycle arrest is mediated by distinct Jak kinase signaling pathways.

F W Quelle, J Wang, J Feng, D Wang, J L Cleveland, J N Ihle, G P Zambetti

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
–field-weighted citation impact
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

31 citing papers in PubMed, 97 citations in OpenAlex.

  1. Review
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  14. Cytokine signaling to the cell cycle.Immunologic research · 2007
    Review
  15. Article
  16. Neuregulin 1-Beta cytoprotective role in AML 12 mouse hepatocytes exposed to pentachlorophenol.International journal of environmental research and public health · 2006
    Article
  17. Article
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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

7 authors at 4 institutions in 1 country.

F W QuelleDepartment of Biochemistry, St. Jude Children's Research Hospital, Memphis, Tennessee 38105, USA.
J Wang
J Feng
D Wang
J L Cleveland
J N Ihle
G P Zambetti
University of Tennessee Health Science Center · USSt. Jude Children's Research Hospital · USHoward Hughes Medical Institute · USUniversity of Iowa · US

Funding

Viral Vector Technology (VVTSR)P30CA021765 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI CHARLES ROBERTS · 1985 to 2026
$166.9M
Myc Role in Hematopoiesis, Vasculogenesis &AgiogenesisR01DK044158 · NIDDK · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI CLEVELAND, JOHN L. · 1991 to 2009
$2.8M
MUTANT P53 GAIN OF FUNCTION IN TURMORIGENISISR01CA063230 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI ZAMBETTI, GERARD PAUL · 1995 to 2007
$2.3M
NCI NIH HHS 5 P30 CA21765NCI NIH HHS CA63230NCI NIH HHS P30 CA021765NCI NIH HHS R01 CA063230NIDDK NIH HHS DK44158NIDDK NIH HHS R01 DK044158
6 · The paper itself

Abstract

Exposure of hematopoietic progenitors to gamma-irradiation (IR) induces p53-dependent apoptosis and a p53-independent G2/M cell cycle arrest. These responses to DNA-damage can be inhibited by treatment with cytokine growth factors. Here we report that gamma-IR-induced apoptosis and cell cycle arrest are suppressed by specific cytokines (e.g., erythropoietin and interleukin-3) and that activation of the Jak kinase is necessary and sufficient for these effects. Using myleoid cells expressing a series of erythropoietin receptor (EpoR) mutants, we have demonstrated that Jak kinase-dependent signals initiated from the membrane proximal domain of EpoR were sufficient to prevent IR-induced apoptotic cell death, but failed to prevent cell cycle arrest. Cell survival by Epo did not require activation of other known signaling pathways including PI-3 kinase, PLC-gamma, Ras or Stats. Signaling targets of Jak kinase pathways included members of the Bcl-2 family of anti-apoptotic proteins, and enforced expression of Bcl-2 or Bcl-xL was as effective as cytokine treatment in blocking IR-induced apoptosis but did not prevent growth arrest. A distinct signal derived from a membrane distal domain of EpoR is required to overcome growth arrest associated with DNA damage. These findings functionally link the Jak signaling pathway to suppression of p53-mediated cell death by cytokines and demonstrate that the apoptotic and growth arrest responses to DNA damage in hematopoietic cells are modulated by distinct, cytokine specific signal transduction pathways.

Indexed as

ApoptosisCell CycleProto-Oncogene ProteinsSignal TransductionAnimalsbcl-X ProteinCell DivisionCell LineDNA DamageEnzyme ActivationErythropoietinHumansInterleukin-3Janus Kinase 2MiceProtein-Tyrosine KinasesBCL2L1 protein, humanBcl2l1 protein, mousebcl-X ProteinErythropoietinInterleukin-3JAK2 protein, humanJak2 protein, mouseJanus Kinase 2Protein-Tyrosine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-bcl-2Receptors, ErythropoietinSerum Albumin, BovineTumor Suppressor Protein p53

Identifiers

PMID9553040
PMCPMC316716
OpenAlexW2168674846

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.