Evidence map›Paper›PMID 25672900›Full record

ReviewCellular and molecular life sciences : CMLS2015

La FAM fatale: USP9X in development and disease.

Mariyam Murtaza, Lachlan A Jolly, Jozef Gecz, Stephen A Wood

Abstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 113 papers.

0numbers the graph read from it
0cells of the map it votes in
113citing 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

113 citing papers in PubMed.

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53 more citing papers are in PubMed but not listed here.

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.

Mariyam MurtazaThe Eskitis Institute for Drug Discovery, Griffith University, Brisbane, QLD, Australia.
Lachlan A Jolly
Jozef Gecz
Stephen A Wood

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Deubiquitylating enzymes (DUBs), act downstream of ubiquitylation. As such, these post-post-translational modifiers function as the final arbitrators of a protein substrate's ubiquitylation status, thus regulating its fate. In most instances, DUBs moderate the absolute level of a substrate, its locality or activity, rather than being an "all-or-none" phenomenon. Yet, disruption of this quantitative regulation can produce dramatic qualitative differences. The ubiquitin-specific protease 9X (USP9X/FAM) is a substrate-specific DUB, which displays an extraordinarily high level of sequence conservation from Drosophila to mammals. It is primarily the recent revelations of USP9X's pivotal role in human cancers, both as oncogene or tumour suppressor, in developmental disorders including intellectual disability, epilepsy, autism and developmental delay that has led to a subsequent re-examination of its molecular and cellular functions. Results from experimental animal models have implicated USP9X in neurodegeneration, including Parkinson's and Alzheimer's disease, as well as autoimmune diseases. In this review, we describe the current and accumulated knowledge on the molecular, cellular and developmental aspects of USP9X function within the context of the biological consequences during normal development and disease.

Indexed as

AnimalsApoptosisAutoimmune DiseasesCell PolarityDrosophilaEmbryonic DevelopmentGene Expression Regulation, DevelopmentalHumansNeoplasmsNeurodegenerative DiseasesNeurogenesisProtein Processing, Post-TranslationalProtein TransportUbiquitinationUbiquitin-Specific ProteasesUbiquitin ThiolesteraseUbiquitin-Specific ProteasesUbiquitin ThiolesteraseUSP9X protein, human

Identifiers

PMID25672900
PMCPMC4427618

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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.