Evidence map›Paper›PMID 23515530›Full record

ArticleAmerican journal of physiology. Cell physiology2013

Inversin modulates the cortical actin network during mitosis.

Michael E Werner, Heather H Ward, Carrie L Phillips, Caroline Miller, Vincent H Gattone, Robert L Bacallao

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Cell physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

18 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Epithelial Cell Chirality Revealed by Three-Dimensional Spontaneous Rotation.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Planar cell polarity and the kidney.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2014
    Review
  16. Article
  17. Article
  18. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 1 country.

Michael E WernerDepartment of Anatomy and Cell Biology, Indiana University, Indianapolis, IN, USA.
Heather H Ward
Carrie L Phillips
Caroline Miller
Vincent H Gattone
Robert L Bacallao
Indiana University – Purdue University Indianapolis · USRichard L. Roudebush VA Medical Center · USUniversity of New Mexico · US

Funding

PROBE DELIVERY COREP30DK079312 · NIDDK · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI MOLITORIS, BRUCE A · 2007 to 2021
$17.1M
Pathologic Mechanisms of Polycystic Kidney DiseaseR01DK050141 · NIDDK · UNIVERSITY OF NEW MEXICO · PI WANDINGER-NESS, ANGELA · 1995 to 2010
$2.7M
ADPKD Connective Tissue Disorder LinkR21DK067246 · NIDDK · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI BACALLAO, ROBERT L · 2006 to 2007
$299k
NIDDK NIH HHS P30 DK-079312NIDDK NIH HHS P30 DK079312NIDDK NIH HHS R01 DK050141NIDDK NIH HHS R01 DK-50141NIDDK NIH HHS R21 DK-067246NIDDK NIH HHS R21 DK067246
6 · The paper itself

Abstract

Mutations in inversin cause nephronophthisis type II, an autosomal recessive form of polycystic kidney disease associated with situs inversus, dilatation, and kidney cyst formation. Since cyst formation may represent a planar polarity defect, we investigated whether inversin plays a role in cell division. In developing nephrons from inv-/- mouse embryos we observed heterogeneity of nuclear size, increased cell membrane perimeters, cells with double cilia, and increased frequency of binuclear cells. Depletion of inversin by siRNA in cultured mammalian cells leads to an increase in bi- or multinucleated cells. While spindle assembly, contractile ring formation, or furrow ingression appears normal in the absence of inversin, mitotic cell rounding and the underlying rearrangement of the cortical actin cytoskeleton are perturbed. We find that inversin loss causes extensive filopodia formation in both interphase and mitotic cells. These cells also fail to round up in metaphase. The resultant spindle positioning defects lead to asymmetric division plane formation and cell division. In a cell motility assay, fibroblasts isolated from inv-/- mouse embryos migrate at half the speed of wild-type fibroblasts. Together these data suggest that inversin is a regulator of cortical actin required for cell rounding and spindle positioning during mitosis. Furthermore, cell division defects resulting from improper spindle position and perturbed actin organization contribute to altered nephron morphogenesis in the absence of inversin.

Indexed as

ActinsAnimalsCell Migration AssaysHEK293 CellsHeLa CellsHumansKidney CortexMiceMice, KnockoutMicroscopy, ConfocalMitosisTranscription FactorsActinsInvs protein, mouseTranscription Factorsactincytoskeletonmitosismitotic spindlepolycystic kidney disease

Identifiers

PMID23515530
PMCPMC3725518
OpenAlexW2172040201

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.