Evidence map›Paper›PMID 26395559›Full record

ReviewMedicinal research reviews2016

Direct Activation of Bax Protein for Cancer Therapy.

Zhiqing Liu, Ye Ding, Na Ye, Christopher Wild, Haiying Chen, Jia Zhou

Abstract readReview
In one paragraph

Review in Medicinal research reviews, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 136 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
136citing papers in PubMed, 2 pooled it
5.3field-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

136 citing papers in PubMed, 2 syntheses or guidelines pooled it, 249 citations in OpenAlex.

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76 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

6 authors at 1 institution in 1 country.

Zhiqing LiuChemical Biology Program, Department of Pharmacology and Toxicology, University of Texas Medical Branch, Galveston, TX, 77555.
Ye DingChemical Biology Program, Department of Pharmacology and Toxicology, University of Texas Medical Branch, Galveston, TX, 77555.
Na YeChemical Biology Program, Department of Pharmacology and Toxicology, University of Texas Medical Branch, Galveston, TX, 77555.
Christopher WildChemical Biology Program, Department of Pharmacology and Toxicology, University of Texas Medical Branch, Galveston, TX, 77555.
Haiying ChenChemical Biology Program, Department of Pharmacology and Toxicology, University of Texas Medical Branch, Galveston, TX, 77555.
Jia ZhouChemical Biology Program, Department of Pharmacology and Toxicology, University of Texas Medical Branch, Galveston, TX, 77555.
The University of Texas Medical Branch at Galveston · US

Funding

5-HT2 Receptor Allosterism in Cocaine Use DisorderR01DA038446 · NIDA · UNIVERSITY OF TEXAS MED BR GALVESTON · PI Kathryn A. Cunningham, Jia Zhou · 2015 to 2026
$5.3M
Translational Explorations in Substance Use DisordersT32DA007287 · NIDA · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI Kathryn A. Cunningham, Jonathan Dean Hommel · 1994 to 2026
$4.7M
Core Center for Translational Addiction SciencesP30DA028821 · NIDA · UNIVERSITY OF TEXAS MED BR GALVESTON · PI CUNNINGHAM, KATHRYN A. · 2009 to 2010
$1.5M
Training in Pharmacological SciencesT32GM089657 · NIGMS · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI HANCOCK, JOHN F · 2010 to 2014
$728k
Developing 5-HT2C Receptor Allosteric Modulators to Treat Cocaine Use DisorderF31DA038922 · NIDA · UNIVERSITY OF TEXAS MED BR GALVESTON · PI WILD, CHRISTOPHER TIMOTHY · 2016 to 2017
$63k
NIDA NIH HHS F31 DA038922NIDA NIH HHS P30 DA028821NIDA NIH HHS R01 DA038446NIDA NIH HHS T32 DA007287NIGMS NIH HHS T32 GM089657
6 · The paper itself

Abstract

Bax, a central cell death regulator, is an indispensable gateway to mitochondrial dysfunction and a major proapoptotic member of the B-cell lymphoma 2 (Bcl-2) family proteins that control apoptosis in normal and cancer cells. Dysfunction of apoptosis renders the cancer cell resistant to treatment as well as promotes tumorigenesis. Bax activation induces mitochondrial membrane permeabilization, thereby leading to the release of apoptotic factor cytochrome c and consequently cancer cell death. A number of drugs in clinical use are known to indirectly activate Bax. Intriguingly, recent efforts demonstrate that Bax can serve as a promising direct target for small-molecule drug discovery. Several direct Bax activators have been identified to hold promise for cancer therapy with the advantages of specificity and the potential of overcoming chemo- and radioresistance. Further investigation of this new class of drug candidates will be needed to advance them into the clinic as a novel means to treat cancer.

Indexed as

Amino Acid SequenceAnimalsbcl-2-Associated X ProteinHumansModels, BiologicalMolecular Sequence DataNeoplasmsSignal TransductionSmall Molecule Librariesbcl-2-Associated X ProteinSmall Molecule LibrariesapoptosisBax activatorsBcl-2 family proteinscancer therapydrug discovery

Identifiers

PMID26395559
PMCPMC4752390
OpenAlexW2167807253

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.