Evidence map›Paper›PMID 27498846›Full record

ReviewTrends in cell biology2016

Physiological and Pharmacological Control of BAK, BAX, and Beyond.

Mark P A Luna-Vargas, Jerry Edward Chipuk

Open access · greenAbstract readReview
In one paragraph

Review in Trends in cell biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
10.1field-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

67 citing papers in PubMed, 143 citations in OpenAlex.

  1. Programmed cell death of keratinocytes: an active driver in psoriasis.Apoptosis : an international journal on programmed cell death · 2026
    Review
  2. Melittin inhibits MPPThe Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025
    Article
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7 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

2 authors at 2 institutions in 1 country.

Mark P A Luna-VargasDepartment of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, 10029, USA; The Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York, NY, 10029, USA.
Jerry Edward ChipukDepartment of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, 10029, USA; The Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York, NY, 10029, USA; The Diabetes, Obesity, and Metabolism Institute, Icahn School of Medicine at Mount Sinai, New York, NY, 10029, USA; Department of Dermatology, Icahn School of Medicine at Mount Sinai, New York, NY, 10029, USA; The Graduate School of Biomedical Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, 10029, USA. Electronic address: jerry.chipuk@mssm.edu.
Icahn School of Medicine at Mount Sinai · USThe Graduate Center, CUNY · US

Funding

Translational Research CoreP30DK020541 · NIDDK · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI STREAMSON C CHUA · 2015 to 2026
$27.7M
(PQ5) Role of Mitochondrial Division in Cancer BiologyR01CA206005 · NCI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI CHIPUK, JERRY EDWARD · 2016 to 2020
$1.7M
Function and regulation of the BCL-2 familyR01CA157740 · NCI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI CHIPUK, JERRY EDWARD · 2011 to 2015
$1.7M
NCI NIH HHS R01 CA157740NCI NIH HHS R01 CA206005NIDDK NIH HHS P30 DK020541
6 · The paper itself

Abstract

Cellular commitment to the mitochondrial pathway of apoptosis is accomplished when proapoptotic B cell chronic lymphocytic leukemia/lymphoma (BCL)-2 proteins compromise mitochondrial integrity through the process of mitochondrial outer membrane permeabilization (MOMP). For nearly three decades, intensive efforts focused on the identification and interactions of two key proapoptotic BCL-2 proteins: BCL-2 antagonist killer (BAK) and BCL-2-associated X (BAX). Indeed, we now have critical insights into which BCL-2 proteins interact with BAK/BAX to either preserve survival or initiate MOMP. In contrast, while mitochondria are targeted by BAK/BAX, a molecular understanding of how these organelles govern BAK/BAX function remains less clear. Here, we integrate recent mechanistic insights of proapoptotic BCL-2 protein function in the context of mitochondrial environment, and discuss current and potential pharmacological opportunities to control MOMP in disease.

Indexed as

Amino Acid SequenceAnimalsApoptosisbcl-2-Associated X Proteinbcl-2 Homologous Antagonist-Killer ProteinHumansMembrane Potential, MitochondrialMitochondriaModels, Biologicalbcl-2-Associated X Proteinbcl-2 Homologous Antagonist-Killer ProteinapoptosisBCL-2 familyBH3 mimeticsmitochondriamitochondrial outer membrane permeabilization

Identifiers

PMID27498846
PMCPMC5118054
OpenAlexW2495523499

What OpenQuestion holds

Textmetadata
LicenceTDM
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.