Evidence map›Paper›PMID 26483415›Full record

ArticleMolecular and cellular biology2016

Identification of Novel Death-Associated Protein Kinase 2 Interaction Partners by Proteomic Screening Coupled with Bimolecular Fluorescence Complementation.

Barbara Geering, Zina Zokouri, Samuel Hürlemann, Bertran Gerrits, David Ausländer, Adrian Britschgi, Mario P Tschan, Hans-Uwe Simon, Martin Fussenegger

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.5field-weighted citation impact, top 34% 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

6 citing papers in PubMed, 9 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

9 authors at 3 institutions in 1 country.

Barbara GeeringDepartment of Biosystems Science and Engineering, ETH Zurich, Basel, Switzerland barbara.geering@bsse.ethz.ch.ORCID http://orcid.org/0000-0001-7207-5819
Zina ZokouriDepartment of Biosystems Science and Engineering, ETH Zurich, Basel, Switzerland.
Samuel HürlemannDepartment of Biosystems Science and Engineering, ETH Zurich, Basel, Switzerland.
Bertran GerritsFunctional Genomics Center Zurich, ETH Zurich, Zurich, Switzerland.
David AusländerDepartment of Biosystems Science and Engineering, ETH Zurich, Basel, Switzerland.
Adrian BritschgiInstitute of Pathology, University of Bern, Bern, Switzerland.
Mario P TschanInstitute of Pathology, University of Bern, Bern, Switzerland.
Hans-Uwe SimonInstitute of Pharmacology, University of Bern, Bern, Switzerland.
Martin FusseneggerDepartment of Biosystems Science and Engineering, ETH Zurich, Basel, Switzerland Faculty of Science, University of Basel, Basel, Switzerland.
ETH Zurich · CHUniversity of Bern · CHUniversity of Basel · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Death-associated protein kinase 2 (DAPK2) is a Ca(2+)/calmodulin-dependent Ser/Thr kinase that possesses tumor-suppressive functions and regulates programmed cell death, autophagy, oxidative stress, hematopoiesis, and motility. As only few binding partners of DAPK2 have been determined, the molecular mechanisms governing these biological functions are largely unknown. We report the identification of 180 potential DAPK2 interaction partners by affinity purification-coupled mass spectrometry, 12 of which are known DAPK binding proteins. A small subset of established and potential binding proteins detected in this screen was further investigated by bimolecular fluorescence complementation (BiFC) assays, a method to visualize protein interactions in living cells. These experiments revealed that α-actinin-1 and 14-3-3-β are novel DAPK2 binding partners. The interaction of DAPK2 with α-actinin-1 was localized at the plasma membrane, resulting in massive membrane blebbing and reduced cellular motility, whereas the interaction of DAPK2 with 14-3-3-β was localized to the cytoplasm, with no impact on blebbing, motility, or viability. Our results therefore suggest that DAPK2 effector functions are influenced by the protein's subcellular localization and highlight the utility of combining mass spectrometry screening with bimolecular fluorescence complementation to identify and characterize novel protein-protein interactions.

Indexed as

FluorescenceProteomicsApoptosisAutophagyCalcium-Calmodulin-Dependent Protein KinasesCells, CulturedDeath-Associated Protein KinasesHumansProtein BindingCalcium-Calmodulin-Dependent Protein KinasesDAPK2 protein, humanDeath-Associated Protein Kinases

Identifiers

PMID26483415
PMCPMC4702601
OpenAlexW2177433712

What OpenQuestion holds

Textmetadata
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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.