Evidence map›Paper›PMID 19768111›Full record

ArticlePloS one2009

Loss of RhoB expression enhances the myelodysplastic phenotype of mammalian diaphanous-related Formin mDia1 knockout mice.

Aaron D DeWard, Kellie Leali, Richard A West, George C Prendergast, Arthur S Alberts

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

12 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. RhoA/mDia-1/profilin-1 signaling targets microvascular endothelial dysfunction in diabetic retinopathy.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2015
    Review
  6. Review
  7. Rho GTPases in erythroid maturation.Current opinion in hematology · 2014
    Review
  8. Review
  9. Article
  10. Altered apoptotic responses in neurons lacking RhoB GTPase.The European journal of neuroscience · 2011
    Article
  11. The 5q- syndrome: biology and treatment.Current treatment options in oncology · 2011
    Article
  12. 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

5 authors at 2 institutions in 1 country.

Aaron D DeWardLaboratory of Cell Structure and Signal Integration, Van Andel Research Institute, Grand Rapids, Michigan, United States of America.
Kellie Leali
Richard A West
George C Prendergast
Arthur S Alberts
Van Andel Institute · USLankenau Institute for Medical Research · US

Funding

RhoB Signaling in Cancer Suppression and Cell SuicideR01CA100123 · NCI · LANKENAU INSTITUTE FOR MEDICAL RESEARCH · PI PRENDERGAST, GEORGE C · 2003 to 2007
$1.7M
NCI NIH HHS R01 CA100123
6 · The paper itself

Abstract

Myelodysplastic syndrome (MDS) is characterized by ineffective hematopoiesis and hyperplastic bone marrow. Complete loss or interstitial deletions of the long arm of chromosome 5 occur frequently in MDS. One candidate tumor suppressor on 5q is the mammalian Diaphanous (mDia)-related formin mDia1, encoded by DIAPH1 (5q31.3). mDia-family formins act as effectors for Rho-family small GTP-binding proteins including RhoB, which has also been shown to possess tumor suppressor activity. Mice lacking the Drf1 gene that encodes mDia1 develop age-dependent myelodysplastic features. We crossed mDia1 and RhoB knockout mice to test whether the additional loss of RhoB expression would compound the myelodysplastic phenotype. Drf1(-/-)RhoB(-/-) mice are fertile and develop normally. Relative to age-matched Drf1(-/-)RhoB(+/-) mice, the age of myelodysplasia onset was earlier in Drf1(-/-)RhoB(-/-) animals--including abnormally shaped erythrocytes, splenomegaly, and extramedullary hematopoiesis. In addition, we observed a statistically significant increase in the number of activated monocytes/macrophages in both the spleen and bone marrow of Drf1(-/-)RhoB(-/-) mice relative to Drf1(-/-)RhoB(+/-) mice. These data suggest a role for RhoB-regulated mDia1 in the regulation of hematopoietic progenitor cells.

Indexed as

Gene Expression RegulationAnimalsBone Marrow CellsCarrier ProteinsFetal ProteinsForminsHematopoietic Stem CellsMacrophagesMiceMice, KnockoutMicrofilament ProteinsMonocytesMyelodysplastic SyndromesNuclear ProteinsPhenotyperhoB GTP-Binding ProteinCarrier ProteinsDiap1 protein, mouseFetal ProteinsForminsMicrofilament ProteinsNuclear ProteinsrhoB GTP-Binding Protein

Identifiers

PMID19768111
PMCPMC2740832
OpenAlexW2003991896

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.