Evidence map›Paper›PMID 18299399›Full record

ArticleThe Journal of experimental medicine2008

Loss of the BH3-only protein Bmf impairs B cell homeostasis and accelerates gamma irradiation-induced thymic lymphoma development.

Verena Labi, Miriam Erlacher, Stephan Kiessling, Claudia Manzl, Anna Frenzel, Lorraine O'Reilly, Andreas Strasser, Andreas Villunger

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed, 1 pooled it
7.1field-weighted citation impact, top 3% 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

80 citing papers in PubMed, 1 synthesis or guideline pooled it, 121 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. BCL-2 protein family: attractive targets for cancer therapy.Apoptosis : an international journal on programmed cell death · 2023
    Review
  9. Regulation of Oocyte Apoptosis: A View from Gene Knockout Mice.International journal of molecular sciences · 2023
    Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article

20 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

8 authors at 2 institutions in 2 countries.

Verena LabiDivision of Developmental Immunology, Biocenter, Innsbruck Medical University, 6020 Innsbruck, Austria.
Miriam Erlacher
Stephan Kiessling
Claudia Manzl
Anna Frenzel
Lorraine O'Reilly
Andreas Strasser
Andreas Villunger
Innsbruck Medical University · ATWalter and Eliza Hall Institute of Medical Research · AU

Funding

Austrian Science Fund FWF Y 212Worldwide Cancer Research 06-0440
6 · The paper itself

Abstract

Members of the Bcl-2 protein family play crucial roles in the maintenance of tissue homeostasis by regulating apoptosis in response to developmental cues or exogenous stress. Proapoptotic BH3-only members of the Bcl-2 family are essential for initiation of cell death, and they function by activating the proapoptotic Bcl-2 family members Bax and/or Bak, either directly or indirectly through binding to prosurvival Bcl-2 family members. Bax and Bak then elicit the downstream events in apoptosis signaling. Mammals have at least eight BH3-only proteins and they are activated in a stimulus-specific, as well as a cell type-specific, manner. We have generated mice lacking the BH3-only protein Bcl-2-modifying factor (Bmf) to investigate its role in cell death signaling. Our studies reveal that Bmf is dispensable for embryonic development and certain forms of stress-induced apoptosis, including loss of cell attachment (anoikis) or UV irradiation. Remarkably, loss of Bmf protected lymphocytes against apoptosis induced by glucocorticoids or histone deacetylase inhibition. Moreover, bmf(-/-) mice develop a B cell-restricted lymphadenopathy caused by the abnormal resistance of these cells to a range of apoptotic stimuli. Finally, Bmf-deficiency accelerated the development of gamma irradiation-induced thymic lymphomas. Our results demonstrate that Bmf plays a critical role in apoptosis signaling and can function as a tumor suppressor.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsApoptosisApoptosis Regulatory ProteinsBcl-2-Like Protein 11B-LymphocytesGamma RaysHomeostasisLymphomaMembrane ProteinsMiceMice, Inbred C57BLMice, KnockoutProto-Oncogene ProteinsSignal TransductionThymus NeoplasmsAdaptor Proteins, Signal TransducingApoptosis Regulatory ProteinsBcl2l11 protein, mouseBcl-2-Like Protein 11Bmf protein, mouseMembrane ProteinsProto-Oncogene ProteinsPUMA protein, mouseTumor Suppressor Proteins

Identifiers

PMID18299399
PMCPMC2275386
OpenAlexW2158105676

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.