Evidence map›Paper›PMID 23630292›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2013

Genetic deletion of Rnd3 results in aqueductal stenosis leading to hydrocephalus through up-regulation of Notch signaling.

Xi Lin, Baohui Liu, Xiangsheng Yang, Xiaojing Yue, Lixia Diao, Jing Wang, Jiang Chang

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

37 citing papers in PubMed, 55 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Genetic and molecular mechanisms of hydrocephalus.Frontiers in molecular neuroscience · 2024
    Review
  8. Article
  9. Review
  10. A neural stem cell paradigm of pediatric hydrocephalus.Cerebral cortex (New York, N.Y. : 1991) · 2023
    Article
  11. Rho Kinases in Embryonic Development and Stem Cell Research.Archivum immunologiae et therapiae experimentalis · 2022
    Review
  12. Article
  13. Article
  14. Maternal RND3/RhoE deficiency impairs placental mitochondrial function in preeclampsia by modulating the PPARγ-UCP2 cascade.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    Article
  15. Article
  16. 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

7 authors at 3 institutions in 2 countries.

Xi LinInstitute of Biosciences and Technology, Texas A&M University Health Science Center, Houston, TX 77030, USA.
Baohui Liu
Xiangsheng Yang
Xiaojing Yue
Lixia Diao
Jing Wang
Jiang Chang
Texas A&M Health Science Center · USThe University of Texas MD Anderson Cancer Center · USWuhan University · CN

Funding

Fibrogenic Role of ROCK delta1 and Mechanism in Cardiac RemodelingR01HL102314 · NHLBI · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI CHANG, JIANG · 2010 to 2014
$1.8M
Mechanism of SRF-N-mediated Cardiac SuppressionK02HL098956 · NHLBI · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI CHANG, JIANG · 2010 to 2014
$471k
Mechanistic Study of Cleaved Serum Response Factor in Cardiac HypertrophyR21HL094844 · NHLBI · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI CHANG, JIANG · 2010 to 2011
$403k
NHLBI NIH HHS K02 HL098956NHLBI NIH HHS R01 HL102314NHLBI NIH HHS R21 HL094844
6 · The paper itself

Abstract

Rho family guanosine triphosphatase (GTPase) 3 (Rnd3), a member of the small Rho GTPase family, is involved in the regulation of cell actin cytoskeleton dynamics, cell migration, and proliferation through the Rho kinase-dependent signaling pathway. We report a role of Rnd3 in the pathogenesis of hydrocephalus disorder. Mice with Rnd3 genetic deletion developed severe obstructive hydrocephalus with enlargement of the lateral and third ventricles, but not of the fourth ventricles. The cerebral aqueducts in Rnd3-null mice were partially or completely blocked by the overgrowth of ependymal epithelia. We examined the molecular mechanism contributing to this Rnd3-deficiency-mediated hydrocephalus and found that Rnd3 is a regulator of Notch signaling. Rnd3 deficiency, through either gene deletion or siRNA knockdown, resulted in a decrease in Notch intracellular domain (NICD) protein degradation. However, there was no correlated change in mRNA change, which in turn led to an increase in NICD protein levels. Immunoprecipitation analysis demonstrated that Rnd3 and NICD physically interacted, and that down-regulation of Rnd3 attenuated NICD protein ubiquitination. This eventually enhanced Notch signaling activity and promoted aberrant growth of aqueduct ependymal cells, resulting in aqueduct stenosis and the development of congenital hydrocephalus. Inhibition of Notch activity rescued the hydrocephalus disorder in the mutant animals.

Indexed as

Gene DeletionAnimalsBrainEpendymaGene Expression Regulation, DevelopmentalHEK293 CellsHumansHydrocephalusMiceMice, KnockoutMutationOligonucleotide Array Sequence AnalysisProtein Processing, Post-TranslationalReceptors, Notchrho GTP-Binding ProteinsRNA, Small InterferingReceptors, Notchrho GTP-Binding ProteinsRNA, Small InterferingRND3 protein, humanRnd3 protein, mousedevelopmental brain defectgenetic mouse modelpost-translational modification

Identifiers

PMID23630292
PMCPMC3657816
OpenAlexW1967829417

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.