Evidence map›Paper›PMID 17178918›Full record

ArticleThe Journal of experimental medicine2006

Puma cooperates with Bim, the rate-limiting BH3-only protein in cell death during lymphocyte development, in apoptosis induction.

Miriam Erlacher, Verena Labi, Claudia Manzl, Günther Böck, Alexandar Tzankov, Georg Häcker, Ewa Michalak, Andreas Strasser, Andreas Villunger

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 142 papers.

0numbers the graph read from it
0cells of the map it votes in
142citing papers in PubMed
9.2field-weighted citation impact, top 1% 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

142 citing papers in PubMed, 228 citations in OpenAlex.

  1. Article
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  5. Article
  6. Review
  7. Review
  8. Review
  9. Review
  10. Updated mechanisms of MASLD pathogenesis.Lipids in health and disease · 2024
    Review
  11. Review
  12. Review
  13. BCL-2 protein family: attractive targets for cancer therapy.Apoptosis : an international journal on programmed cell death · 2023
    Review
  14. Article
  15. Article
  16. Review
  17. Bcl-2 Is Necessary to Counteract Bim and Promote Survival of TCRαβJournal of immunology (Baltimore, Md. : 1950) · 2022
    Article
  18. BH3-mimetics: recent developments in cancer therapy.Journal of experimental & clinical cancer research : CR · 2021
    Review
  19. SNAI2-Mediated Repression ofCancer research · 2021
    Article
  20. Article

82 more citing papers are in PubMed but not listed here.

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

9 authors at 5 institutions in 5 countries.

Miriam ErlacherDivision of Developmental Immunology, Biocenter, Innsbruck Medical University, A-6020 Innsbruck, Austria.
Verena Labi
Claudia Manzl
Günther Böck
Alexandar Tzankov
Georg Häcker
Ewa Michalak
Andreas Strasser
Andreas Villunger
Institut thématique Génétique, génomique et bioinformatique · FRWalter and Eliza Hall Institute of Medical Research · AUInnsbruck Medical University · ATTechnical University of Munich · DEUniversity of Basel · CH

Funding

ONCOGENE-INDUCED LEUKEMOGENESIS IN TRANSGENIC MICER01CA043540 · NCI · WALTER AND ELIZA HALL INST MEDICAL RES · PI CORY, SUZANNE · 1987 to 2009
$1.7M
MECHANISMS IN THE REGULATION OF APOPTOSISR01CA080188 · NCI · WALTER AND ELIZA HALL INST MEDICAL RES · PI ADAMS, JERRY M · 1999 to 2006
$1.1M
NCI NIH HHS CA43540NCI NIH HHS CA 80188NCI NIH HHS R01 CA043540NCI NIH HHS R01 CA080188
6 · The paper itself

Abstract

The physiological role of B cell lymphoma 2 (Bcl-2) homology 3-only proteins has been investigated in mice lacking the individual genes identifying rate-limiting roles for Bim (Bcl-2-interacting mediator of cell death) and Puma (p53-up-regulated modulator of apoptosis) in apoptosis induction. The loss of Bim protects lymphocytes from apoptosis induced by cytokine deprivation and deregulated Ca++ flux and interferes with the deletion of autoreactive lymphocytes and the shutdown of immune responses. In contrast, Puma is considered the key mediator of p53-induced apoptosis. To investigate the hypothesis that Bim and Puma have overlapping functions, we generated mice lacking both genes and found that bim-/-/puma-/- animals develop multiple postnatal defects that are not observed in the single knockout mice. Most strikingly, hyperplasia of lymphatic organs is comparable with that observed in mice overexpressing Bcl-2 in all hemopoietic cells exceeding the hyperplasia observed in bim-/- mice. Bim and Puma also have clearly overlapping functions in p53-dependent and -independent apoptosis. Their combined loss promotes spontaneous tumorigenesis, causing the malignancies observed in Bcl-2 transgenic mice, but does not exacerbate the autoimmunity observed in the absence of Bim.

Indexed as

AnimalsAntigens, CDApoptosisApoptosis Regulatory ProteinsAutoantibodiesBcl-2-Like Protein 11B-Lymphocyte SubsetsCell DifferentiationEnzyme-Linked Immunosorbent AssayFlow CytometryImmune SeraImmunoglobulin GImmunoglobulin MLymphocytesLymphomaMembrane ProteinsAntigens, CDApoptosis Regulatory ProteinsAutoantibodiesBcl2l11 protein, mouseBcl-2-Like Protein 11Immune SeraImmunoglobulin GImmunoglobulin MMembrane ProteinsProto-Oncogene ProteinsProto-Oncogene Proteins c-bcl-2PUMA protein, mouseTumor Suppressor Proteins

Identifiers

PMID17178918
PMCPMC2118188
OpenAlexW2000686057

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.