Evidence map›Paper›PMID 32540856›Full record

ArticleJournal of the American Society of Nephrology : JASN2020

Phosphorylation of ACTN4 Leads to Podocyte Vulnerability and Proteinuric Glomerulosclerosis.

Di Feng, Mukesh Kumar, Jan Muntel, Susan B Gurley, Gabriel Birrane, Isaac E Stillman, Lai Ding, Minxian Wang, Saima Ahmed, Johannes Schlondorff and 8 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 9% 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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Mechanisms of podocyte injury in genetic kidney disease.Pediatric nephrology (Berlin, Germany) · 2025
    Review
  5. Review
  6. Article
  7. Article
  8. Terpene extract from the stem ofJournal of pharmaceutical analysis · 2024
    Article
  9. Article
  10. Human organ chips for regenerative pharmacology.Pharmacology research & perspectives · 2024
    Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Cytoskeleton Rearrangements Modulate TRPC6 Channel Activity in Podocytes.International journal of molecular sciences · 2021
    Article
  20. Review
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

18 authors at 7 institutions in 2 countries.

Di FengDivision of Nephrology, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts dfeng@bidmc.harvard.edu mpollak@bidmc.harvard.edu.ORCID 0000-0001-5652-176X
Mukesh KumarDepartment of Pathology, Boston Children's Hospital and Harvard Medical School, Boston, Massachusetts.
Jan MuntelBiognosys AG, Schlieren, Switzerland.
Susan B GurleyDivision of Nephrology and Hypertension, Oregon Health & Science University, Portland, Oregon.
Gabriel BirraneDivision of Experimental Medicine, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts.
Isaac E StillmanDivision of Nephrology, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts.
Lai DingNeuroTechnology Studio, Program for Interdisciplinary Neuroscience, Brigham and Women's Hospital, Boston, Massachusetts.
Minxian WangBroad Institute of Harvard and Massachusetts Institute of Technology, Cambridge, Massachusetts.ORCID 0000-0002-3753-508X
Saima AhmedDepartment of Pathology, Boston Children's Hospital and Harvard Medical School, Boston, Massachusetts.
Johannes SchlondorffDivision of Nephrology, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts.
Seth L AlperDivision of Nephrology, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts.
Tom FerranteWyss Institute for Biologically Inspired Engineering at Harvard University, Boston, Massachusetts.
Susan L MarquezWyss Institute for Biologically Inspired Engineering at Harvard University, Boston, Massachusetts.
Carlos F NgWyss Institute for Biologically Inspired Engineering at Harvard University, Boston, Massachusetts dfeng@bidmc.harvard.edu mpollak@bidmc.harvard.edu.
Richard NovakWyss Institute for Biologically Inspired Engineering at Harvard University, Boston, Massachusetts.
Donald E IngberWyss Institute for Biologically Inspired Engineering at Harvard University, Boston, Massachusetts.
Hanno SteenDepartment of Pathology, Boston Children's Hospital and Harvard Medical School, Boston, Massachusetts.
Martin R PollakDivision of Nephrology, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts dfeng@bidmc.harvard.edu mpollak@bidmc.harvard.edu.
Beth Israel Deaconess Medical Center · USBoston Children's Hospital · USHarvard University · USBroad Institute · USBiognosys (Switzerland) · CHBrigham and Women's Hospital · USOregon Health & Science University · US

Funding

STRUCTURE-FUNCTION RELATIONSHIPS IN THE ALIMENTARY TRACTP30DK034854 · NIDDK · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI LYNN BRY · 1986 to 2026
$32.4M
RESEARCH TRAINING IN NEPHROLOGYT32DK007199 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI POLLAK, MARTIN R. · 1986 to 2022
$6.0M
Renal Genomics CoreP30DK096493 · NIDDK · DUKE UNIVERSITY · PI COFFMAN, THOMAS M · 2012 to 2016
$5.9M
Biological Mechanism of FSGS-1R37DK059588 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI POLLAK, MARTIN R. · 2011 to 2020
$4.0M
The interaction between mechanical forces and cytoskeletal impairments in podocyte mediated kidney diseaseK01DK114329 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI FENG, DI · 2018 to 2022
$744k
NIDDK NIH HHS K01 DK114329NIDDK NIH HHS P30 DK034854NIDDK NIH HHS P30 DK096493NIDDK NIH HHS R37 DK059588NIDDK NIH HHS T32 DK007199
6 · The paper itself

Abstract

backgroundGenetic mutations in

methodsUsing mass spectrometry, we found that ACTN4 is phosphorylated at serine (S) 159 in human podocytes. We used phosphomimetic and nonphosphorylatable ACTN4 to comprehensively study the effects of this phosphorylation

resultsCompared with the wild type ACTN4, phosphomimetic ACTN4 demonstrated increased binding and bundling activity with F-actin

conclusionsThese findings suggest that increased phosphorylation of ACTN4 at S159 leads to biochemical, cellular, and renal pathology that is similar to pathology resulting from human disease-causing mutations in ACTN4. ACTN4 may mediate podocyte injury as a consequence of both genetic mutations and signaling events that modulate phosphorylation.

Indexed as

Protein Processing, Post-TranslationalActininActinsAlbuminuriaAnimalsCells, CulturedFemaleGlomerulosclerosis, Focal SegmentalGlucoseHumansLab-On-A-Chip DevicesMaleMiceNephrectomyPeptidomimeticsPhosphorylationActininActinsACTN4 protein, humanActn4 protein, mouseGlucosePeptidomimeticsSerineTransforming Growth Factor betachronic kidney diseasecytoskeletonfocal segmental glomerulosclerosisglomerular diseasepodocyteproteinuria

Identifiers

PMID32540856
PMCPMC7351002
OpenAlexW3035099720

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.