Evidence map›Paper›PMID 31209350›Full record

ReviewNature chemical biology2019

Targeting BAX to drug death directly.

Loren D Walensky

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature chemical biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
4.5field-weighted citation impact, top 4% 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

50 citing papers in PubMed, 98 citations in OpenAlex.

  1. Article
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  6. Potential of Alkaloids fromCurrent issues in molecular biology · 2025
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  10. Review
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  14. Covalent inhibition of pro-apoptotic BAX.Nature chemical biology · 2024
    Article
  15. Review
  16. Article
  17. Article
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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

1 author at 1 institution in 1 country.

Loren D WalenskyDepartment of Pediatric Oncology, Dana-Farber Cancer Institute, Boston, MA, USA. Loren_Walensky@dfci.harvard.edu.
Dana-Farber Cancer Institute · US

Funding

Dissecting and Targeting Deregulated Mitochondrial Apoptosis in Human CancerR35CA197583 · NCI · DANA-FARBER CANCER INST · PI Loren David Walensky · 2015 to 2026
$12.5M
NCI NIH HHS R35 CA197583
6 · The paper itself

Abstract

BCL-2 family protein interactions regulate apoptosis, a critical process that maintains tissue homeostasis but can cause a host of human diseases when deregulated. Venetoclax is the first FDA-approved drug to reactivate apoptosis in cancer by selectively targeting an anti-apoptotic BCL-2 family member. The drug's activity relies on an 'inhibit the inhibitor' mechanism, whereby blockade of a key surface groove on BCL-2 disables its capacity to neutralize pro-apoptotic effectors, such as BAX, a chief executioner protein of the apoptotic pathway. A series of physiologic and pharmacologic regulatory sites that mediate the activation or inhibition of BAX have recently been identified, providing blueprints for the development of alternative apoptosis modulators to block pathologic cell survival or avert unwanted cell death by drugging BAX directly.

Indexed as

bcl-2-Associated X ProteinCell DeathHumansModels, MolecularMolecular StructureSmall Molecule LibrariesBAX protein, humanbcl-2-Associated X ProteinSmall Molecule Libraries

Identifiers

PMID31209350
OpenAlexW2953358034

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.