Evidence map›Paper›PMID 23533418›Full record

ArticleInternational journal of cell biology2013

Functions of BCL-X L at the Interface between Cell Death and Metabolism.

Judith Michels, Oliver Kepp, Laura Senovilla, Delphine Lissa, Maria Castedo, Guido Kroemer, Lorenzo Galluzzi

Open access · goldAbstract read
In one paragraph

Article in International journal of cell biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed, 1 pooled it
5.8field-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

54 citing papers in PubMed, 1 synthesis or guideline pooled it, 92 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Kynurenic acid protects against ischemia/reperfusion injury by modulating apoptosis in cardiomyocytes.Apoptosis : an international journal on programmed cell death · 2024
    Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Bilayer Forming Phospholipids as Targets for Cancer Therapy.International journal of molecular sciences · 2022
    Review
  14. Review
  15. SENP3 Promotes an Mff-Primed Bcl-xFrontiers in cell and developmental biology · 2021
    Article
  16. Article
  17. Review
  18. Article
  19. Bcl-2-Protein Family as Modulators of IPCold Spring Harbor perspectives in biology · 2020
    Review
  20. Article
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 5 institutions in 1 country.

Judith MichelsINSERM, U848, Institut Gustave Roussy, Pavillon de Recherche 1, 39 Rue Camille Desmoulins, 94805 Villejuif, France ; Université Paris Sud/Paris XI, 94805 Villejuif, France ; Institut Gustave Roussy, 94805 Villejuif, France.
Oliver Kepp
Laura Senovilla
Delphine Lissa
Maria Castedo
Guido Kroemer
Lorenzo Galluzzi
Inserm · FRInstitut Gustave Roussy · FRCentre de Recherche des Cordeliers · FRHôpital Européen Georges-Pompidou · FRUniversité Paris-Saclay · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The BCL-2 homolog BCL-XL, one of the two protein products of BCL2L1, has originally been characterized for its prominent prosurvival functions. Similar to BCL-2, BCL-XL binds to its multidomain proapoptotic counterparts BAX and BAK, hence preventing the formation of lethal pores in the mitochondrial outer membrane, as well as to multiple BH3-only proteins, thus interrupting apical proapoptotic signals. In addition, BCL-XL has been suggested to exert cytoprotective functions by sequestering a cytosolic pool of the pro-apoptotic transcription factor p53 and by binding to the voltage-dependent anion channel 1 (VDAC1), thereby inhibiting the so-called mitochondrial permeability transition (MPT). Thus, BCL-XL appears to play a prominent role in the regulation of multiple distinct types of cell death, including apoptosis and regulated necrosis. More recently, great attention has been given to the cell death-unrelated functions of BCL-2-like proteins. In particular, BCL-XL has been shown to modulate a number of pathophysiological processes, including-but not limited to-mitochondrial ATP synthesis, protein acetylation, autophagy and mitosis. In this short review article, we will discuss the functions of BCL-XL at the interface between cell death and metabolism.

Identifiers

PMID23533418
PMCPMC3603586
OpenAlexW2068701997

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.