Evidence map›Paper›PMID 25744027›Full record

ArticleCell death and differentiation2015

Bak apoptotic pores involve a flexible C-terminal region and juxtaposition of the C-terminal transmembrane domains.

S Iyer, F Bell, D Westphal, K Anwari, J Gulbis, B J Smith, G Dewson, R M Kluck

Open access · bronzeAbstract read
In one paragraph

Article in Cell death and differentiation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

43 citing papers in PubMed, 62 citations in OpenAlex.

  1. Article
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  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Apoptotic mitochondrial poration by a growing list of pore-forming BCL-2 family proteins.BioEssays : news and reviews in molecular, cellular and developmental biology · 2023
    Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. BAK core dimers bind lipids and can be bridged by them.Nature structural & molecular biology · 2020
    Article
  18. Article
  19. Article
  20. BAX, BAK, and BOK: A Coming of Age for the BCL-2 Family Effector Proteins.Cold Spring Harbor perspectives in biology · 2020
    Review
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 3 institutions in 1 country.

S IyerThe Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria 3050, Australia.
F BellThe Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria 3050, Australia.
D WestphalThe Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria 3050, Australia.
K AnwariThe Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria 3050, Australia.
J GulbisThe Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria 3050, Australia.
B J SmithDepartment of Chemistry and Physics, La Trobe Institute for Molecular Sciences, La Trobe University, Melbourne, Victoria 3086, Australia.
G DewsonThe Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria 3050, Australia.
R M KluckThe Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria 3050, Australia.
Walter and Eliza Hall Institute of Medical Research · AUUniversity of Melbourne · AULa Trobe University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bak and Bax mediate apoptotic cell death by oligomerizing and forming a pore in the mitochondrial outer membrane. Both proteins anchor to the outer membrane via a C-terminal transmembrane domain, although its topology within the apoptotic pore is not known. Cysteine-scanning mutagenesis and hydrophilic labeling confirmed that in healthy mitochondria the Bak α9 segment traverses the outer membrane, with 11 central residues shielded from labeling. After pore formation those residues remained shielded, indicating that α9 does not line a pore. Bak (and Bax) activation allowed linkage of α9 to neighboring α9 segments, identifying an α9:α9 interface in Bak (and Bax) oligomers. Although the linkage pattern along α9 indicated a preferred packing surface, there was no evidence of a dimerization motif. Rather, the interface was invoked in part by Bak conformation change and in part by BH3:groove dimerization. The α9:α9 interaction may constitute a secondary interface in Bak oligomers, as it could link BH3:groove dimers to high-order oligomers. Moreover, as high-order oligomers were generated when α9:α9 linkage in the membrane was combined with α6:α6 linkage on the membrane surface, the α6-α9 region in oligomerized Bak is flexible. These findings provide the first view of Bak carboxy terminus (C terminus) membrane topology within the apoptotic pore.

Indexed as

Amino Acid MotifsAnimalsApoptosisbcl-2-Associated X Proteinbcl-2 Homologous Antagonist-Killer ProteinHumansMiceMitochondrial MembranesProtein Multimerizationbcl-2-Associated X Proteinbcl-2 Homologous Antagonist-Killer Protein

Identifiers

PMID25744027
PMCPMC4563781
OpenAlexW2064538146

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.