Evidence map›Paper›PMID 20717760›Full record

ArticleCell stress & chaperones2010

A cell-based screen for inhibitors of protein folding and degradation.

Frank Boschelli, Jennifer M Golas, Roseann Petersen, Vincent Lau, Lei Chen, Diane Tkach, Qiang Zhao, Dave S Fruhling, Hao Liu, Chaneun Nam and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell stress & chaperones, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.5field-weighted citation impact, top 34% 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

2 citing papers in PubMed, 11 citations in OpenAlex.

  1. Review
  2. 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

11 authors at 1 institution in 1 country.

Frank BoschelliDepartment of Oncology, Wyeth Research (now the Center for Integrative Biology and Biotherapeutics, Pfizer R & D), 401 N. Middletown Rd., Pearl River, NY 10965, USA. boschef@wyeth.com
Jennifer M Golas
Roseann Petersen
Vincent Lau
Lei Chen
Diane Tkach
Qiang Zhao
Dave S Fruhling
Hao Liu
Chaneun Nam
Kim T Arndt
Pfizer (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer cells are exposed to external and internal stresses by virtue of their unrestrained growth, hostile microenvironment, and increased mutation rate. These stresses impose a burden on protein folding and degradation pathways and suggest a route for therapeutic intervention in cancer. Proteasome and Hsp90 inhibitors are in clinical trials and a 20S proteasome inhibitor, Velcade, is an approved drug. Other points of intervention in the folding and degradation pathway may therefore be of interest. We describe a simple screen for inhibitors of protein synthesis, folding, and proteasomal degradation pathways in this paper. The molecular chaperone-dependent client v-Src was fused to firefly luciferase and expressed in HCT-116 colorectal tumor cells. Both luciferase and protein tyrosine kinase activity were preserved in cells expressing this fusion construct. Exposing these cells to the Hsp90 inhibitor geldanamycin caused a rapid reduction of luciferase and kinase activities and depletion of detergent-soluble v-Src::luciferase fusion protein. Hsp70 knockdown reduced v-Src::luciferase activity and, when combined with geldanamycin, caused a buildup of v-Src::luciferase and ubiquitinated proteins in a detergent-insoluble fraction. Proteasome inhibitors also decreased luciferase activity and caused a buildup of phosphotyrosine-containing proteins in a detergent-insoluble fraction. Protein synthesis inhibitors also reduced luciferase activity, but had less of an effect on phosphotyrosine levels. In contrast, certain histone deacetylase inhibitors increased luciferase and phosphotyrosine activity. A mass screen led to the identification of Hsp90 inhibitors, ubiquitin pathway inhibitors, inhibitors of Hsp70/Hsp40-mediated refolding, and protein synthesis inhibitors. The largest group of compounds identified in the screen increased luciferase activity, and some of these increase v-Src levels and activity. When used in conjunction with appropriate secondary assays, this screen is a powerful cell-based tool for studying compounds that affect protein synthesis, folding, and degradation.

Indexed as

Proteasome InhibitorsBenzoquinonesCell Line, TumorDrug Evaluation, PreclinicalEnzyme InhibitorsHistone Deacetylase InhibitorsHistone DeacetylasesHSP40 Heat-Shock ProteinsHSP70 Heat-Shock ProteinsHSP90 Heat-Shock ProteinsHumansLactams, MacrocyclicLuciferases, FireflyMolecular ChaperonesOncogene Protein pp60(v-src)Proteasome Endopeptidase ComplexBenzoquinonesEnzyme InhibitorsgeldanamycinHistone Deacetylase InhibitorsHistone DeacetylasesHSP40 Heat-Shock ProteinsHSP70 Heat-Shock ProteinsHSP90 Heat-Shock ProteinsLactams, MacrocyclicLuciferases, FireflyMolecular ChaperonesOncogene Protein pp60(v-src)Proteasome Endopeptidase ComplexProteasome InhibitorsProtein Synthesis InhibitorsRecombinant Fusion ProteinsRNA, Small InterferingUbiquitin

Identifiers

PMID20717760
PMCPMC3024082
OpenAlexW2075409488

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.