Evidence map›Paper›PMID 18418664›Full record

ArticleCerebellum (London, England)2008

The roles of testicular orphan nuclear receptor 4 (TR4) in cerebellar development.

Yei-Tsung Chen, Loretta L Collins, Shu-Shi Chang, Chawnshang Chang

Abstract read
PubMed Publisher
In one paragraph

Article in Cerebellum (London, England), 2008. 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
0.7field-weighted citation impact, top 37% 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, 22 citations in OpenAlex.

  1. Review
  2. Article
  3. Adult functions for the Drosophila DHR78 nuclear receptor.Developmental dynamics : an official publication of the American Association of Anatomists · 2018
    Article
  4. An Atoh1-S193A Phospho-Mutant Allele Causes Hearing Deficits and Motor Impairment.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Recent advances in the study of testicular nuclear receptor 4.Journal of Zhejiang University. Science. B · 2013
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. 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.

Yei-Tsung ChenGeorge Whipple Laboratory for Cancer Research, Departments of Pathology, Urology, Radiation Oncology, The Cancer Center, Rochester, NY 14642, USA.
Loretta L Collins
Shu-Shi Chang
Chawnshang Chang
University of Rochester · USChina Medical University · TW

Funding

Single and Double Knockout of TR2 and TR4 ReceptorsR01DK063212 · NIDDK · UNIVERSITY OF ROCHESTER · PI CHANG, CHAWNSHANG · 2003 to 2006
$1.5M
TR4 ORPHAN RECEPTOR IN TESTISR01DK056984 · NIDDK · UNIVERSITY OF ROCHESTER · PI CHANG, CHAWNSHANG · 2001 to 2004
$1.1M
NIDDK NIH HHS DK 56984NIDDK NIH HHS DK 63212
6 · The paper itself

Abstract

Since Testicular Receptor 4 (TR4) was cloned, efforts have been made to elucidate its physiological function. To examine the putative functions of TR4, the conventional TR4 knockout (TR4(-/-)) mouse model was generated. Throughout postnatal and adult stages, TR4(-/-) mice exhibited behavioral deficits in motor coordination, suggesting impaired cerebellar function. Histological examination of the postnatal and adult TR4(-/-) cerebellum revealed gross abnormalities in foliation. Further analyses demonstrated changes in the lamination of the TR4(-/-) cerebellar cortex, including reduction in the thickness of both the molecular layer (ML) and the internal granule layer (IGL). Analyses of the developing TR4(-/-) cerebellum indicate that the lamination irregularities observed may result from disrupted granule cell proliferation within the external granule cell layer (EGL), delayed inward migration of post-mitotic granule cells, and increased apoptosis during cerebellar development. In addition, abnormal development of Purkinje cells was observed in the postnatal TR4(-/-) cerebellum, as indicated by aberrant dendritic arborization. In postnatal, neuronal-specific TR4 knockout mice, architectural changes in the cerebellum were similar to those seen in TR4(-/-) animals, suggesting that TR4 function in neuronal lineages might be important for cerebellar morphogenesis, and that the effect on Purkinje cell development is likely mediated by changes elsewhere, such as in granule cells, or is highly dependent on developmental stage. Together, our findings from various TR4 knockout mouse models suggest that TR4 is required for normal cerebellar development and that failure to establish proper cytoarchitecture results in dysfunction of the cerebellum and leads to abnormal behavior.

Indexed as

AnimalsBehavior, AnimalCerebellar CortexCloning, MolecularDeathgamma-Aminobutyric AcidMental DisordersMiceMice, KnockoutPurkinje CellsReceptors, SteroidReceptors, Thyroid Hormonegamma-Aminobutyric AcidNr2c2 protein, mouseReceptors, SteroidReceptors, Thyroid Hormone

Identifiers

PMID18418664
OpenAlexW1995751109

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.