Evidence map›Paper›PMID 28647489›Full record

ArticleBiochemical pharmacology2017

A high throughput assay to identify substrate-selective inhibitors of the ERK protein kinases.

Chad J Miller, Yagmur Muftuoglu, Benjamin E Turk

Abstract read
In one paragraph

Article in Biochemical pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
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

4 citing papers in PubMed.

  1. Article
  2. Linear motif specificity in signaling through p38α and ERK2 mitogen-activated protein kinases.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  3. Article
  4. 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

3 authors.

Chad J MillerDepartment of Pharmacology, Yale University School of Medicine, New Haven, CT 06520, United States.
Yagmur MuftuogluDepartment of Pharmacology, Yale University School of Medicine, New Haven, CT 06520, United States.
Benjamin E TurkDepartment of Pharmacology, Yale University School of Medicine, New Haven, CT 06520, United States. Electronic address: ben.turk@yale.edu.

Funding

Yale SPORE in Skin CancerP50CA121974 · NCI · YALE UNIVERSITY · PI RUTH HALABAN · 2006 to 2026
$43.9M
INSTITUTIONAL NATIONAL RESEARCH SERVICE AWARDT32GM007324 · NIGMS · YALE UNIVERSITY · PI BENNETT, ANTON M · 1987 to 2022
$6.2M
NCI NIH HHS P50 CA121974NIGMS NIH HHS T32 GM007324
6 · The paper itself

Abstract

Extracellular signal-regulated kinases 1 and 2 (ERK1/2) phosphorylate a variety of substrates important for survival and proliferation, and their activity is frequently deregulated in tumors. ERK pathway inhibitors have shown clinical efficacy as anti-cancer drugs, but most patients eventually relapse due to reactivation of the pathway. One factor limiting the efficacy of current therapeutics is the difficulty in reaching clinically effective inhibition of the ERK pathway in the absence of on-target toxicities. Here, we describe an assay suitable for high throughput screening to discover substrate selective ERK1/2 inhibitors, which may have a larger therapeutic window than conventional inhibitors. Specifically, we aim to target a substrate-binding pocket within the ERK1/2 catalytic domain outside of the catalytic cleft. The assay uses an AlphaScreen format to detect phosphorylation of a high-efficiency substrate harboring an essential docking site motif. Pilot screening established that the assay is suitably robust for high-throughput screening. Importantly, the assay can be conducted at high ATP concentrations, which we show reduces the discovery of conventional ATP-competitive inhibitors. These studies provide the basis for high-throughput screens to discover new classes of non-conventional ERK1/2 inhibitors.

Indexed as

Binding SitesCatalytic DomainEscherichia coliMAP Kinase Signaling SystemMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Molecular Docking SimulationProtein Kinase InhibitorsRadioligand AssaySubstrate SpecificityTransfectionMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Protein Kinase InhibitorsHigh-throughput screeningKinase inhibitorMitogen-activated protein kinasePhosphorylationProtein kinase

Identifiers

PMID28647489
PMCPMC5678991

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Registered trials

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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.