Evidence map›Paper›PMID 23620398›Full record

ArticleJournal of the American Society of Nephrology : JASN2013

Inverted formin 2 regulates actin dynamics by antagonizing Rho/diaphanous-related formin signaling.

Hua Sun, Johannes Schlondorff, Henry N Higgs, Martin R Pollak

Open access · bronzeAbstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

40 citing papers in PubMed, 62 citations in OpenAlex.

  1. Article
  2. Article
  3. ERM Inhibition Confers Ferroptosis Resistance through ROS-Induced NRF2 Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  4. Article
  5. Article
  6. Podocytes in health and glomerular disease.Frontiers in cell and developmental biology · 2025
    Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Role of actin cytoskeleton in podocytes.Pediatric nephrology (Berlin, Germany) · 2021
    Review
  16. Review
  17. Dysregulated Dynein-Mediated Trafficking of Nephrin Causes INF2-related Podocytopathy.Journal of the American Society of Nephrology : JASN · 2021
    Article
  18. Article
  19. The formin INF2 in disease: progress from 10 years of research.Cellular and molecular life sciences : CMLS · 2020
    Review
  20. FSGS-Causing INF2 Mutation Impairs Cleaved INF2 N-Fragment Functions in Podocytes.Journal of the American Society of Nephrology : JASN · 2020
    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

4 authors at 2 institutions in 2 countries.

Hua SunDepartment of Medicine, Beth Israel Deaconess Medical Center, Boston, MA, USA.
Johannes Schlondorff
Henry N Higgs
Martin R Pollak
Beth Israel Deaconess Medical Center · USDartmouth College · US

Funding

INF2 in kidney function and dysfunctionR01DK088826 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI HENRY N HIGGS, MARTIN R. POLLAK · 2010 to 2026
$6.3M
TRPC6 Regulation and its Role in Glomerular PathologyK08DK080947 · NIDDK · BRIGHAM AND WOMEN'S HOSPITAL · PI SCHLONDORFF, JOHANNES S · 2008 to 2012
$822k
NIDDK NIH HHS DK080947NIDDK NIH HHS DK088826NIDDK NIH HHS K08 DK080947NIDDK NIH HHS R01 DK088826
6 · The paper itself

Abstract

Mutations in inverted formin 2 INF2 are a common cause of familial FSGS. INF2 interacts with diaphanous-related formins (mDia) and antagonizes mDia-mediated actin polymerization in response to active Rho signaling, suggesting that dysregulation of these pathways may mediate the development of INF2-related FSGS. However, the precise mechanisms by which INF2 regulates actin-dependent podocyte behavior remain largely unknown. Here, we investigated the possible role of INF2 in both lamellipodia-associated actin dynamics and actin-dependent slit diaphragm (SD) protein trafficking by manipulating the expression of INF2 and the activity of Rho/mDia signaling in cultured podocytes. Activation of mDia in the absence of INF2 led to defective formation of lamellipodia and abnormal SD trafficking. Effects of mutations disrupting the INF2-mDia interaction suggested the specificity of the mDia-antagonizing effect of INF2 in maintaining the lamellipodium. Furthermore, we found that SD trafficking requires INF2 interaction with lipid raft components. In summary, INF2 regulates lamellipodial actin dynamics and the trafficking of slit diaphragm proteins by opposing Rho/mDia-mediated actin polymerization. Thus, in podocytes, INF2 appears to be an important modulator of actin-dependent behaviors that are under the control of Rho/mDia signaling.

Indexed as

ActinsCarrier ProteinsCell Line, TransformedCytosolDimerizationForminsGlomerulosclerosis, Focal SegmentalHumansMembrane MicrodomainsMembrane ProteinsMicrofilament ProteinsPodocytesPoint MutationProtein Structure, QuaternaryProtein TransportPseudopodiaActinsCarrier ProteinsDIAPH2 protein, humanForminsINF2 protein, humanMembrane ProteinsMicrofilament ProteinsnephrinrhoA GTP-Binding ProteinRHOA protein, humanRNA, Small Interfering

Identifiers

PMID23620398
PMCPMC3665394
OpenAlexW2133621860

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.