Evidence map›Paper›PMID 24287595›Full record

ArticleNature communications2013

Proteasomal degradation of Nck1 but not Nck2 regulates RhoA activation and actin dynamics.

Lisa Buvall, Priyanka Rashmi, Esther Lopez-Rivera, Svetlana Andreeva, Astrid Weins, Hanna Wallentin, Anna Greka, Peter Mundel

Open access · bronzeAbstract read
In one paragraph

Article in Nature communications, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.3field-weighted citation impact, top 13% 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

36 citing papers in PubMed, 64 citations in OpenAlex.

  1. Article
  2. Article
  3. Mechanism of Bile Acid in Regulating Platelet Function and Thrombotic Diseases.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  4. Article
  5. NCK1 Modulates Neuronal Actin Dynamics and Promotes Dendritic Spine, Synapse, and Memory Formation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Renal cell markers: lighthouses for managing renal diseases.American journal of physiology. Renal physiology · 2021
    Article
  11. Nck adaptors at a glance.Journal of cell science · 2021
    Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Sinner or Saint?: Nck Adaptor Proteins in Vascular Biology.Frontiers in cell and developmental biology · 2021
    Review
  17. Article
  18. Article
  19. Article
  20. Article
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

8 authors at 4 institutions in 1 country.

Lisa Buvall1] Department of Medicine, Harvard Medical School, Massachusetts General Hospital, Boston, Massachusetts 02129, USA [2].
Priyanka Rashmi
Esther Lopez-Rivera
Svetlana Andreeva
Astrid Weins
Hanna Wallentin
Anna Greka
Peter Mundel
Massachusetts General Hospital · USHarvard University · USIcahn School of Medicine at Mount Sinai · USUniversity of California, San Francisco · US

Funding

Role of B7-1 in Podocytes in Pathogenesis of ProteinuriaR01DK062472 · NIDDK · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI SOBERMAN, ROY · 2004 to 2017
$5.3M
Role of TRPC5 channel inhibition in the treatment of glomerular diseaseR01DK099465 · NIDDK · BROAD INSTITUTE, INC. · PI Anna Greka · 2014 to 2026
$5.1M
CELL AND MOLECULAR BIOLOGICAL ANALYSIS OF SYNAPTOPODINR01DK057683 · NIDDK · YESHIVA UNIVERSITY · PI SOBERMAN, ROY · 2001 to 2015
$4.8M
Regulation of podocyte function by hic-5R01DK091218 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI MUNDEL, PETER H · 2012 to 2015
$1.5M
Senescence and Autophagy as Mediators of Glomerular Injury in DiabetesK08DK093783 · NIDDK · BRIGHAM AND WOMEN'S HOSPITAL · PI WEINS, ASTRID · 2012 to 2016
$793k
TRPC channels in proteinuric kidney diseaseK08DK083511 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI GREKA, ANNA · 2010 to 2013
$634k
NIDDK NIH HHS DK057683NIDDK NIH HHS DK062472NIDDK NIH HHS DK083511NIDDK NIH HHS DK091218NIDDK NIH HHS DK093783NIDDK NIH HHS K08 DK083511NIDDK NIH HHS K08 DK093783NIDDK NIH HHS R01 DK057683NIDDK NIH HHS R01 DK062472NIDDK NIH HHS R01 DK091218NIDDK NIH HHS R01 DK099465
6 · The paper itself

Abstract

The ubiquitously expressed adapter proteins Nck1/2 interact with a multitude of effector molecules to regulate diverse cellular functions including cytoskeletal dynamics. Here we show that Nck1, but not Nck2, is a substrate of c-Cbl-mediated ubiquitination. We uncover lysine 178 in Nck1 as the evolutionarily conserved ubiquitin acceptor site. We previously reported that synaptopodin, a proline-rich actin-binding protein, induces stress fibres by blocking the Smurf1-mediated ubiquitination of RhoA. We now find that synaptopodin competes with c-Cbl for binding to Nck1, which prevents the ubiquitination of Nck1 by c-Cbl. Gene silencing of c-Cbl restores Nck1 protein abundance and stress fibres in synaptopodin knockdown cells. Similarly, expression of c-Cbl-resistant Nck1(K178R) or Nck2 containing the SH3 domain 2 of Nck1 restores stress fibres in synaptopodin-depleted podocytes through activation of RhoA signalling. These findings reveal proteasomal regulation as a key factor in the distinct and non-redundant effects of Nck on RhoA-mediated actin dynamics.

Indexed as

ActinsAdaptor Proteins, Signal TransducingCytoskeletonEnzyme ActivationHEK293 CellsHumansOncogene ProteinsProteasome Endopeptidase ComplexProtein BindingProteolysisProto-Oncogene Proteins c-cblrhoA GTP-Binding ProteinUbiquitinationActinsAdaptor Proteins, Signal TransducingCBL protein, humanNCK2 protein, humanNck proteinOncogene ProteinsProteasome Endopeptidase ComplexProto-Oncogene Proteins c-cblrhoA GTP-Binding Protein

Identifiers

PMID24287595
PMCPMC4698162
OpenAlexW2073601280

What OpenQuestion holds

Textmetadata
LicenceTDM
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.