Evidence map›Paper›PMID 29248972›Full record

ArticleMolecular and cellular biochemistry2018

Pharmacological targeting of HSP90 with 17-AAG induces apoptosis of myogenic cells through activation of the intrinsic pathway.

Akira Wagatsuma, Yuzo Takayama, Takayuki Hoshino, Masataka Shiozuka, Shigeru Yamada, Ryoichi Matsuda, Kunihiko Mabuchi

Abstract read
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In one paragraph

Article in Molecular and cellular biochemistry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 24% 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

7 citing papers in PubMed, 1 synthesis or guideline pooled it, 14 citations in OpenAlex.

  1. Pooled it
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  3. Review
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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

7 authors at 4 institutions in 1 country.

Akira WagatsumaDepartment of Information Physics and Computing, Graduate School of Information Science and Technology, The University of Tokyo, Tokyo, Japan. wagatsuma1969@gmail.com.
Yuzo TakayamaDepartment of Information Physics and Computing, Graduate School of Information Science and Technology, The University of Tokyo, Tokyo, Japan.
Takayuki HoshinoDepartment of Information Physics and Computing, Graduate School of Information Science and Technology, The University of Tokyo, Tokyo, Japan.
Masataka ShiozukaCenter for Clinical and Translational Research, Kyushu University, Fukuoka, Japan.
Shigeru YamadaDepartment of Food and Health Science, Faculty of Human Life Sciences, Jissen Women's University, Tokyo, Japan.
Ryoichi MatsudaDepartment of Life Sciences, Graduate School of Arts and Sciences, The University of Tokyo, Tokyo, Japan.
Kunihiko MabuchiDepartment of Information Physics and Computing, Graduate School of Information Science and Technology, The University of Tokyo, Tokyo, Japan.
Tokyo University of Information Sciences · JPThe University of Tokyo · JPJissen Women's University · JPKyushu University · JP

Funding

Grant in Aid for Scientific Research (C) 25350882
6 · The paper itself

Abstract

We have shown that pharmacological inhibition of HSP90 ATPase activity induces apoptosis of myoblasts during their differentiation. However, the signaling pathways remain not fully characterized. We report that pharmacological targeting of HSP90 with 17-AAG activates the intrinsic pathway including caspase-dependent and caspase-independent pathways. 17-AAG induces the typical apoptotic phenotypes including PARP cleavage, chromatin condensation, and nuclear fragmentation with mitochondrial release of cytochrome c, Smac/DIABLO, procaspase-9 processing, and caspase-3 activation. AIF and EndoG redistribute from the mitochondria into the cytosol and are partially translocated to the nucleus in 17-AAG-treated cells. These results suggest that caspase-dependent and caspase-independent pathways should be considered in apoptosis of myogenic cells induced by inhibition of HSP90 ATPase activity.

Indexed as

Adenosine TriphosphatasesAnimalsApoptosisApoptosis Inducing FactorApoptosis Regulatory ProteinsBenzoquinonesBlotting, WesternCaspase 3Caspase 9Cell NucleusChromatinCytochromes cEndodeoxyribonucleasesEnzyme ActivationHSP70 Heat-Shock ProteinsHSP90 Heat-Shock ProteinsAdenosine TriphosphatasesAIFM1 protein, humanApoptosis Inducing FactorApoptosis Regulatory ProteinsBenzoquinonesCASP9 protein, humanCaspase 3Caspase 9ChromatinCytochromes cDIABLO protein, humanEndodeoxyribonucleasesendonuclease GHSP70 Heat-Shock ProteinsHSP90 Heat-Shock ProteinsIntracellular Signaling Peptides and ProteinsLactams, MacrocyclicMitochondrial ProteinsPoly(ADP-ribose) PolymerasesProto-Oncogene Proteins c-akttanespimycinXIAP protein, humanX-Linked Inhibitor of Apoptosis ProteinApoptosisHSP90MitochondriaMyogenic cell

Identifiers

PMID29248972
OpenAlexW2772866339

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.