Evidence map›Paper›PMID 23530055›Full record

ArticleMolecular and cellular biology2013

Integration of apoptosis signal-regulating kinase 1-mediated stress signaling with the Akt/protein kinase B-IκB kinase cascade.

Mary C Puckett, Erinn H Goldman, Lisa M Cockrell, Bei Huang, Andrea L Kasinski, Yuhong Du, Cun-Yu Wang, Anning Lin, Hidenori Ichijo, Fadlo Khuri and 1 more

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

13 citing papers in PubMed, 28 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 4 institutions in 2 countries.

Mary C PuckettDepartment of Pharmacology, Emory University School of Medicine, Atlanta, GA, USA.
Erinn H Goldman
Lisa M Cockrell
Bei Huang
Andrea L Kasinski
Yuhong Du
Cun-Yu Wang
Anning Lin
Hidenori Ichijo
Fadlo Khuri
Haian Fu
Emory University · USThe University of Tokyo · JPUniversity of California, Los Angeles · USUniversity of Chicago · US

Funding

Targeting Microtubules and HDAC6 in NSCLCP01CA116676 · NCI · EMORY UNIVERSITY · PI KHURI, FADLO RAJA · 2006 to 2012
$8.0M
Graduate Training in the Pharmacological StudiesT32GM008602 · NIGMS · EMORY UNIVERSITY · PI HALL, RANDY A. · 1996 to 2021
$5.1M
PS-341-induced Apoptosis in Squamous Cell CarcinomaR37DE013848 · NIDCR · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI WANG, CUN-YU · 2006 to 2015
$3.5M
NF-kB Signaling in Osteoclastogenesis and Osteolytic Bone MetastasisR01CA132134 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI WANG, CUN-YU · 2009 to 2013
$1.6M
Mechanism of IKK Signaling NetworkR01GM103868 · NIGMS · UNIVERSITY OF CHICAGO · PI LIN, ANNING · 2013 to 2016
$1.2M
Regulation of TNFa signalingR01GM095313 · NIGMS · UNIVERSITY OF CHICAGO · PI LIN, ANNING · 2011 to 2014
$1.1M
NCI NIH HHS P01 CA116676NCI NIH HHS R01 CA132134NIDCR NIH HHS R37 DE013848NIGMS NIH HHS R01 GM095313NIGMS NIH HHS R01 GM103868NIGMS NIH HHS T32 GM008602
6 · The paper itself

Abstract

Cellular processes are tightly controlled through well-coordinated signaling networks that respond to conflicting cues, such as reactive oxygen species (ROS), endoplasmic reticulum (ER) stress signals, and survival factors to ensure proper cell function. We report here a direct interaction between inhibitor of κB kinase (IKK) and apoptosis signal-regulating kinase 1 (ASK1), unveiling a critical node at the junction of survival, inflammation, and stress signaling networks. IKK can be activated by growth factor stimulation or tumor necrosis factor alpha engagement. IKK forms a complex with and phosphorylates ASK1 at a sensor site, Ser967, leading to the recruitment of 14-3-3, counteracts stress signal-triggered ASK1 activation, and suppresses ASK1-mediated functions. An inhibitory role of IKK in JNK signaling has been previously reported to depend on NF-κB-mediated gene expression. Our data suggest that IKK has a dual role: a transcription-dependent and a transcription-independent action in controlling the ASK1-JNK axis, coupling IKK to ROS and ER stress response. Direct phosphorylation of ASK1 by IKK also defines a novel IKK phosphorylation motif. Because of the intimate involvement of ASK1 in diverse diseases, the IKK/ASK1 interface offers a promising target for therapeutic development.

Indexed as

AnimalsApoptosisChlorocebus aethiopsChromonesCOS CellsHydrogen PeroxideI-kappa B KinaseMAP Kinase Kinase Kinase 5MiceMorpholinesNeuritesPC12 CellsPhosphorylationProto-Oncogene Proteins c-aktRatsSerine2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-oneChromonesHydrogen PeroxideI-kappa B KinaseMAP Kinase Kinase Kinase 5MorpholinesProto-Oncogene Proteins c-aktSerine

Identifiers

PMID23530055
PMCPMC3648060
OpenAlexW2130891925

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.