Evidence map›Paper›PMID 11163212›Full record

ArticleMolecular cell2000

The combined functions of proapoptotic Bcl-2 family members bak and bax are essential for normal development of multiple tissues.

T Lindsten, A J Ross, A King, W X Zong, J C Rathmell, H A Shiels, E Ulrich, K G Waymire, P Mahar, K Frauwirth and 11 more

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cell, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 630 papers.

0numbers the graph read from it
0cells of the map it votes in
630citing papers in PubMed
23.8field-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

630 citing papers in PubMed, 1,468 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Review
  6. Relationship between different modes of death and premature ovarian insufficiency: a literature review.Apoptosis : an international journal on programmed cell death · 2026
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Apoptosis promotes fertility inbioRxiv : the preprint server for biology · 2025
    Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article

570 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

21 authors at 5 institutions in 1 country.

T LindstenDepartment of Medicine, Abramson Family Cancer Research Institute, University of Pennsylvania, Philadelphia, PA 19104, USA.
A J Ross
A King
W X Zong
J C Rathmell
H A Shiels
E Ulrich
K G Waymire
P Mahar
K Frauwirth
Y Chen
M Wei
V M Eng
D M Adelman
M C Simon
A Ma
J A Golden
G Evan
S J Korsmeyer
G R MacGregor
C B Thompson
Cancer Research Institute · USUniversity of Pennsylvania · USEmory University · USUniversity of Chicago · USHoward Hughes Medical Institute · US

Funding

FUNCTION OF BCL-W IN MURINE DEVELOPMENTR01HD036437 · NICHD · UNIVERSITY OF CALIFORNIA IRVINE · PI MACGREGOR, GRANT R · 1998 to 2001
$466k
NICHD NIH HHS R01 HD036437
6 · The paper itself

Abstract

Proapoptotic Bcl-2 family members have been proposed to play a central role in regulating apoptosis. However, mice lacking bax display limited phenotypic abnormalities. As presented here, bak(-/-) mice were found to be developmentally normal and reproductively fit and failed to develop any age-related disorders. However, when Bak-deficient mice were mated to Bax-deficient mice to create mice lacking both genes, the majority of bax(-/-)bak(-/-) animals died perinatally with fewer than 10% surviving into adulthood. bax(-/-)bak(-/-) mice displayed multiple developmental defects, including persistence of interdigital webs, an imperforate vaginal canal, and accumulation of excess cells within both the central nervous and hematopoietic systems. Thus, Bax and Bak have overlapping roles in the regulation of apoptosis during mammalian development and tissue homeostasis.

Indexed as

ApoptosisGene DeletionAbnormalities, MultipleAnimalsbcl-2-Associated X Proteinbcl-2 Homologous Antagonist-Killer ProteinBrainCells, CulturedCrosses, GeneticEmbryonic and Fetal DevelopmentEtoposidefas ReceptorFemaleGenes, EssentialGene TargetingHematopoietic Stem CellsBak1 protein, mouseBax protein, mousebcl-2-Associated X Proteinbcl-2 Homologous Antagonist-Killer ProteinEtoposidefas ReceptorMembrane ProteinsProto-Oncogene ProteinsProto-Oncogene Proteins c-bcl-2

Identifiers

PMID11163212
PMCPMC3057227
OpenAlexW2026873116

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.