Evidence map›Paper›PMID 28212730›Full record

ReviewBiochemical and biophysical research communications2017

The integrated stress response and proteotoxicity in cancer therapy.

David J McConkey

Abstract readReview
In one paragraph

Review in Biochemical and biophysical research communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

54 citing papers in PubMed, 89 citations in OpenAlex.

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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.

David J McConkeyJohns Hopkins Greenberg Bladder Cancer Institute, Brady Urological Institute, 600 North Wolfe Street, Baltimore, MD 21287, United States. Electronic address: djmcconkey@jhmi.edu.
Johns Hopkins Hospital · US

Funding

Proteasome Inhibition and ER StressR01CA127494 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI MCCONKEY, DAVID J. · 2009 to 2013
$1.2M
NCI NIH HHS R01 CA127494
6 · The paper itself

Abstract

A variety of different forms of cellular stress can cause protein misfolding and aggregation and proteotoxicity. The cytoprotective response to proteotoxicity is termed the integrated stress response and involves 4 distinct serine/threonine protein kinases that converge on the translation initiation factor eIF2α, resulting in phosphorylation at S51, cell cycle arrest, and a general inhibition of global protein synthesis. Phosphorylation of eIF2α also promotes translation of ATF4 and the expression of ATF4 target genes that ameliorate proteotoxic stress but can also promote apoptosis. This mini review provides a general overview of these mechanisms and discusses how the inter-tumor heterogeneity that involves them affects sensitivity and resistance to proteasome inhibitors, a new class of cancer therapeutics that promotes tumor cell killing via proteotoxic stress.

Indexed as

Activating Transcription Factor 4AnimalsApoptosiseIF-2 KinaseEukaryotic Initiation Factor-2HumansNeoplasmsPhosphorylationProteasome InhibitorsProtein Serine-Threonine KinasesProteostasis DeficienciesStress, PhysiologicalActivating Transcription Factor 4eIF-2 KinaseEukaryotic Initiation Factor-2Proteasome InhibitorsProtein Serine-Threonine KinasesAutophagyER stressHRIPERKProtein aggregatesTranslationUnfolded protein response

Identifiers

PMID28212730
PMCPMC5319732
OpenAlexW2583487304

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.