Evidence map›Paper›PMID 23569252›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2013

Intercellular trafficking of the nuclear oncoprotein DEK.

Anjan K Saha, Ferdinand Kappes, Amruta Mundade, Anja Deutzmann, David M Rosmarin, Maureen Legendre, Nicolas Chatain, Zeina Al-Obaidi, Barbara S Adams, Hidde L Ploegh and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

30 citing papers in PubMed, 51 citations in OpenAlex.

  1. Review
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  12. Potential ofMolecular and clinical oncology · 2022
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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

13 authors at 4 institutions in 2 countries.

Anjan K SahaDepartment of Internal Medicine, Division of Infectious Diseases, University of Michigan, Ann Arbor, MI 48109, USA.
Ferdinand Kappes
Amruta Mundade
Anja Deutzmann
David M Rosmarin
Maureen Legendre
Nicolas Chatain
Zeina Al-Obaidi
Barbara S Adams
Hidde L Ploegh
Elisa Ferrando-May
Nirit Mor-Vaknin
David M Markovitz
University of Michigan–Ann Arbor · USRWTH Aachen University · DEUniversity of Konstanz · DEWhitehead Institute for Biomedical Research · US

Funding

MICHIGAN INSTITUTE FOR CLINICAL AND HEALTH RESEARCH (MICHR) (UL1): (BPCA)UL1RR024986 · NCRR · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI SHANLEY, THOMAS P. · 2007 to 2011
$51.2M
Vector CoreP30AR048310 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MACOSKA, JILL A. · 2001 to 2010
$5.9M
CXC Chemokines and HIV PathogenesisR01AI062248 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MARKOVITZ, DAVID MICHAEL · 2005 to 2009
$1.6M
DEK and TNF inhibitors in juvenile arthritisR01AI087128 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MARKOVITZ, DAVID MICHAEL · 2009 to 2012
$1.5M
RESEARCH TRAINING IN TRANSLATIONAL TUMOR IMMUNOLOGYT32CA088784 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CHANG, ALFRED E · 2001 to 2005
$1.3M
The Role of DEK in the Development of ArthritisK01AR055620 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MOR-VAKNIN, NIRIT · 2009 to 2013
$541k
The Role of DEK in the Development of ArthritisR03AR056748 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MOR-VAKNIN, NIRIT · 2009 to 2011
$206k
NCI NIH HHS T32 CA088784NCI NIH HHS T32-CA-88784-03NCRR NIH HHS UL1 RR024986NCRR NIH HHS UL1-RR-024986NIAID NIH HHS R01 AI062248NIAID NIH HHS R01 AI087128NIAMS NIH HHS 5-P30-AR-048310-07NIAMS NIH HHS K01 AR-055620NIAMS NIH HHS K01 AR055620NIAMS NIH HHS P30 AR048310NIAMS NIH HHS R03 AR056748NIAMS NIH HHS R03 AR-056748-01
6 · The paper itself

Abstract

DEK is a biochemically distinct, conserved nonhistone protein that is vital to global heterochromatin integrity. In addition, DEK can be secreted and function as a chemotactic, proinflammatory factor. Here we show that exogenous DEK can penetrate cells, translocate to the nucleus, and there carry out its endogenous nuclear functions. Strikingly, adjacent cells can take up DEK secreted from synovial macrophages. DEK internalization is a heparan sulfate-dependent process, and cellular uptake of DEK into DEK knockdown cells corrects global heterochromatin depletion and DNA repair deficits, the phenotypic aberrations characteristic of these cells. These findings thus unify the extracellular and intracellular activities of DEK, and suggest that this paracrine loop involving DEK plays a role in chromatin biology.

Indexed as

Cell FractionationChromosomal Proteins, Non-HistoneDNA RepairHeLa CellsHeterochromatinHistonesHumansImage Processing, Computer-AssistedImmunoblottingImmunoprecipitationMicroscopy, FluorescenceOncogene ProteinsParacrine CommunicationPoly-ADP-Ribose Binding ProteinsProtein TransportRNA, Small InterferingChromosomal Proteins, Non-HistoneDEK protein, humanHeterochromatinHistonesOncogene ProteinsPoly-ADP-Ribose Binding ProteinsRNA, Small Interfering

Identifiers

PMID23569252
PMCPMC3637753
OpenAlexW2041940308

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.