Evidence map›Paper›PMID 26301083›Full record

ArticleCell & bioscience2015

The role of alpha-actinin-4 in human kidney disease.

Di Feng, Clark DuMontier, Martin R Pollak

Open access · goldAbstract read
In one paragraph

Article in Cell & bioscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
3.7field-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

41 citing papers in PubMed, 63 citations in OpenAlex.

  1. Article
  2. Alpha-Actinin-3 Deficiency Links Genetic Susceptibility to Renal Fibrosis: Evidence From Hemodialysis Patients and Murine Models.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Protein tyrosine phosphatase 1B is a regulator of alpha-actinin4 in the glomerular podocyte.Biochimica et biophysica acta. Molecular cell research · 2024
    Article
  11. Article
  12. Article
  13. Modeling ofKidney international reports · 2023
    Article
  14. Article
  15. Article
  16. Cytoskeletal protein degradation in brain death donor kidneys associates with adverse posttransplant outcomes.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2022
    Article
  17. Case report and literature review: AFrontiers in pediatrics · 2022
    Article
  18. Article
  19. Renal cell markers: lighthouses for managing renal diseases.American journal of physiology. Renal physiology · 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

3 authors at 2 institutions in 1 country.

Di FengDivision of Nephrology, Department of Medicine, Beth Israel Deaconess Medical Center, Boston, MA 02215 USA.
Clark DuMontierDepartment of Medicine, Boston University School of Medicine, Boston, MA 02118 USA.
Martin R PollakDivision of Nephrology, Department of Medicine, Beth Israel Deaconess Medical Center, Boston, MA 02215 USA.
Beth Israel Deaconess Medical Center · USBoston University · US

Funding

RESEARCH TRAINING IN NEPHROLOGYT32DK007199 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI POLLAK, MARTIN R. · 1986 to 2022
$6.0M
Biological Mechanism of FSGS-1R37DK059588 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI POLLAK, MARTIN R. · 2011 to 2020
$4.0M
Biological mechanism of familial focal segmental glomerulosclerosis-1R01DK059588 · NIDDK · BRIGHAM AND WOMEN'S HOSPITAL · PI POLLAK, MARTIN R. · 2001 to 2010
$3.5M
NIDDK NIH HHS R01 DK059588NIDDK NIH HHS R37 DK059588NIDDK NIH HHS T32 DK007199
6 · The paper itself

Abstract

Mutations in the Alpha-actinin-4 gene (ACTN4) cause a rare form of familial focal segmental glomerulosclerosis in humans. Individuals with kidney disease-associated ACTN4 mutations tend to have mild to moderate proteinuria, with many developing decreased kidney function progressing to end stage kidney disease. All of the disease-causing ACTN4 mutations identified to date are located within the actin-binding domain of the encoded protein, increasing its binding affinity to F-actin and leading to abnormal actin rich cellular aggregates. The identification of ACTN4 mutations as a cause of human kidney disease demonstrates a key cellular pathway by which alterations in cytoskeletal behavior can mediate kidney disease. Here we review the studies relevant to ACTN4 and its role in mediating kidney disease.

Indexed as

Alpha-actinin-4Cytoskeleton proteinFocal segmental glomerulosclerosisKidneyPodocytes

Identifiers

PMID26301083
PMCPMC4545552
OpenAlexW1867761851

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.