Evidence map›Paper›PMID 26475605›Full record

ReviewMolecular brain2015

The role of the ubiquitin proteasome system in cerebellar development and medulloblastoma.

Jerry Vriend, Saeid Ghavami, Hassan Marzban

Abstract readReview
In one paragraph

Review in Molecular brain, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
–field-weighted citation impact
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

13 citing papers in PubMed.

  1. [Deubiquitinase USP30 alleviates brain injury after intracerebral hemorrhage by regulating MFN2 ubiquitination].Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2026
    Article
  2. Article
  3. Novel Genetic Variant inNeurology. Genetics · 2024
    Article
  4. E3 Ubiquitin LigaseInternational journal of molecular sciences · 2024
    Article
  5. Review
  6. Article
  7. Review
  8. The proteasome regulator PI31 is required for protein homeostasis, synapse maintenance, and neuronal survival in mice.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Zinc and zinc-containing biomolecules in childhood brain tumors.Journal of molecular medicine (Berlin, Germany) · 2016
    Review
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

3 authors.

Jerry VriendDepartment of Human Anatomy and Cell Science, Rm129, BMSB, 745 Bannatyne Avenue, Winnipeg, MB, Canada.
Saeid GhavamiDepartment of Human Anatomy and Cell Science, Rm129, BMSB, 745 Bannatyne Avenue, Winnipeg, MB, Canada.
Hassan MarzbanDepartment of Human Anatomy and Cell Science, Rm129, BMSB, 745 Bannatyne Avenue, Winnipeg, MB, Canada. Hassan.Marzban@umanitoba.ca.

Funding

Canadian Institutes of Health Research
6 · The paper itself

Abstract

Cerebellar granule cells precursors are derived from the upper rhombic lip and migrate tangentially independent of glia along the subpial stream pathway to form the external germinal zone. Postnatally, granule cells migrate from the external germinal zone radially through the Purkinje cell layer, guided by Bergmann glia fibers, to the internal granular cell layer.Medulloblastomas (MBs) are the most common malignant childhood brain tumor. Many of these tumors develop from precursor cells of the embryonic rhombic lips. Four main groups of MB are recognized. The WNT group of MBs arise primarily from the lower rhombic lip and embryonic brainstem. The SHH group of MBs originate from cerebellar granule cell precursors in the external germinal zone of the embryonic cerebellum. The cellular origins of type 3 and type 4 MBs are not clear.Several ubiquitin ligases are revealed to be significant factors in development of the cerebellum as well as in the initiation and maintenance of MBs. Proteasome dysfunction at a critical stage of development may be a major factor in determining whether progenitor cells which are destined to become granule cells differentiate normally or become MB cells. We propose the hypothesis that proteasomal activity is essential to regulate the critical transition between proliferating granule cells and differentiated granule cells and that proteasome dysfunction may lead to MB. Proteasome dysfunction could also account for various mutations in MBs resulting from deficiencies in DNA checkpoint and repair mechanisms prior to development of MBs.Data showing a role for the ubiquitin ligases β-TrCP, FBW7, Huwe1, and SKP2 in MBs suggest the possibility of a classification of MBs based on the expression (over expression or under expression) of specific ubiquitin ligases which function as oncogenes, tumor suppressors or cell cycle regulators.

Indexed as

AnimalsBrain NeoplasmsCerebellumHumansMedulloblastomaModels, BiologicalProteasome Endopeptidase ComplexUbiquitinProteasome Endopeptidase ComplexUbiquitin

Identifiers

PMID26475605
PMCPMC4609148

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.