Evidence map›Paper›PMID 24396733›Full record

ArticleCurrent chemical genomics and translational medicine2013

A High Throughput Assay for Discovery of Small Molecules that Bind AMP-activated Protein Kinase (AMPK).

Sarah E Sinnett, Jonathan Z Sexton, Jay E Brenman

Open access · diamondAbstract read
In one paragraph

Article in Current chemical genomics and translational medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.4field-weighted citation impact, top 35% 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

3 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
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 at 1 institution in 1 country.

Sarah E SinnettNeurobiology Curriculum, University of North Carolina Chapel Hill (UNC);
Jonathan Z SextonBiomanufacturing Research Institute and Technology Enterprise, North Carolina Central University;
Jay E BrenmanUNC Neuroscience Center; ; Department of Cell Biology and Physiology, UNC.
University of North Carolina at Chapel Hill · US

Funding

UNC Neuroscience Center Research Cores: MicroscopyP30NS045892 · NINDS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI ZYLKA, MARK J. · 2003 to 2022
$11.5M
Genetic Elucidation of AMP-Activated Protein Kinase Signaling MechanismsR01NS080108 · NINDS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI BRENMAN, JAY · 2012 to 2016
$1.6M
High-Content Screening for Peroxisome Biogenesis for Type-II Diabetes.R01DK088248 · NIDDK · NORTH CAROLINA CENTRAL UNIVERSITY · PI BRENMAN, JAY, SEXTON, JONATHAN ZACHARY · 2011 to 2013
$980k
NIDDK NIH HHS R01 DK088248NINDS NIH HHS P30 NS045892NINDS NIH HHS R01 NS080108
6 · The paper itself

Abstract

AMPK is a conserved heterotrimeric serine-threonine kinase that regulates anabolic and catabolic pathways in eukaryotes. Its central role in cellular and whole body metabolism makes AMPK a commonly proposed therapeutic target for illnesses characterized by abnormal energy regulation, including cancer and diabetes. Many AMPK modulators, however, produce AMPK-independent effects. To identify drugs that modulate AMPK activity independent of the canonical ATP-binding pocket found throughout the kinome, we designed a robust fluorescence-based high throughput screening assay biased toward the identification of molecules that bind the regulatory region of AMPK through displacement of MANT-ADP, a fluorescent ADP analog. Automated pin tools were used to rapidly transfer small molecules to a low volume assay mixture on 384-well plates. Prior to assay validation, we completed a full assay optimization to maximize the signal-to-background and reduce variability for robust detection of small molecules displacing MANT-ADP. After validation, we screened 13,120 molecules and identified 3 positive hits that dose-dependently inhibited the protein-bound signal of MANT-ADP in the presence of both full-length AMPK and the truncated "regulatory fragment" of AMPK, which is missing the kinase active site. The average Z'-factor for the screen was 0.55 and the compound confirmation rate was 60%. Thus, this fluorescence-based assay may be paired with in vitro kinase assays and cell-based assays to help identify molecules that selectively regulate AMPK with fewer off-target effects on other kinases.

Indexed as

ADPAMPKcanonical ATP-binding siteenvironment-sensitive fluorophorehigh throughput assayregulatory fragment.

Identifiers

PMID24396733
PMCPMC3854666
OpenAlexW1997926777

What OpenQuestion holds

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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.