Evidence map›Paper›PMID 25135476›Full record

ArticleMolecular and cellular biology2014

Regulation of the death-associated protein kinase 1 expression and autophagy via ATF6 requires apoptosis signal-regulating kinase 1.

Padmaja Gade, Srikanta B Manjegowda, Shreeram C Nallar, Uday B Maachani, Alan S Cross, Dhananjaya V Kalvakolanu

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

46 citing papers in PubMed, 69 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

6 authors at 2 institutions in 1 country.

Padmaja GadeDepartment of Microbiology and Immunology, University of Maryland School of Medicine, Greenebaum Cancer Center, Baltimore, Maryland, USA.
Srikanta B ManjegowdaDepartment of Microbiology and Immunology, University of Maryland School of Medicine, Greenebaum Cancer Center, Baltimore, Maryland, USA.
Shreeram C NallarDepartment of Microbiology and Immunology, University of Maryland School of Medicine, Greenebaum Cancer Center, Baltimore, Maryland, USA.
Uday B MaachaniDepartment of Microbiology and Immunology, University of Maryland School of Medicine, Greenebaum Cancer Center, Baltimore, Maryland, USA.
Alan S CrossDepartment of Medicine, University of Maryland School of Medicine, Greenebaum Cancer Center, Baltimore, Maryland, USA.
Dhananjaya V KalvakolanuDepartment of Microbiology and Immunology, University of Maryland School of Medicine, Greenebaum Cancer Center, Baltimore, Maryland, USA dkalvako@umaryland.edu.
University of Maryland, Baltimore · USU-M Rogel Cancer Center

Funding

MODULATION OF IFN ACTION VIA NOVEL REGULATORY FACTORSR01CA078282 · NCI · UNIVERSITY OF MARYLAND BALTIMORE · PI KALVAKOLANU, DHAN V. · 1998 to 2014
$4.4M
NCI NIH HHS CA78282NCI NIH HHS R01 CA078282
6 · The paper itself

Abstract

The death-associated protein kinase 1 (DAPK1) is an important regulator of cell death and autophagy. Recently, we have identified that ATF6, an endoplasmic reticulum-resident transcription factor, in association with the transcription factor CEBP-β, regulates the gamma interferon (IFN-γ)-induced expression of Dapk1 (P. Gade et al., Proc. Natl. Acad. Sci. U. S. A. 109:10316-10321, 2012, doi.org/10.1073/pnas.1119273109). IFN-γ-induced proteolytic processing of ATF6 and phosphorylation of C/EBP-β were essential for the formation of a novel transcriptional complex that regulates DAPK1. Here, we report that IFN-γ activates the ASK1-MKK3/MKK6-p38 mitogen-activated protein kinase (MAPK) pathway for controlling the activity of ATF6. The terminal enzyme in this pathway, p38 MAPK, phosphorylates a critical threonine residue in ATF6 upstream of its DNA binding domain. ATF6 mutants defective for p38 MAPK phosphorylation fail to undergo proteolytic processing in the Golgi apparatus and drive IFN-γ-induced gene expression and autophagy. We also show that mice lacking Ask1 are highly susceptible to lethal bacterial infection owing to defective autophagy. Together, these results identify a novel host defense pathway controlled by IFN-γ signaling.

Indexed as

AutophagyMAP Kinase Signaling SystemActivating Transcription Factor 6AnimalsBacillus anthracisBinding SitesCell LineDeath-Associated Protein KinasesGene Knockdown TechniquesHumansInterferon-gammaLiverMAP Kinase Kinase Kinase 5MiceMutationPhosphorylationActivating Transcription Factor 6Death-Associated Protein KinasesInterferon-gammaMAP Kinase Kinase Kinase 5

Identifiers

PMID25135476
PMCPMC4386459
OpenAlexW2116344946

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.