Evidence map›Paper›PMID 33115448›Full record

ArticleBMC biology2020

TRIM25 promotes Capicua degradation independently of ERK in the absence of ATXN1L.

Derek Wong, Lisa Sogerer, Samantha S Lee, Victor Wong, Amy Lum, Adrian B Levine, Marco A Marra, Stephen Yip

Open access · goldAbstract read
In one paragraph

Article in BMC biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.5field-weighted citation impact, top 36% 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

11 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. TRIM25: A central factor in breast cancer.World journal of clinical oncology · 2021
    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

8 authors at 5 institutions in 2 countries.

Derek WongPathology and Laboratory Medicine, University of British Columbia, Vancouver, Canada.
Lisa SogererDepartment of Electrical and Computer Engineering, Technical University of Munich, Munich, Germany.
Samantha S LeeDepartment of Biological and Chemical Engineering, University of British Columbia, Vancouver, Canada.
Victor WongMolecular Biology and Biochemistry, Simon Fraser University, Burnaby, Canada.
Amy LumMolecular Oncology, BC Cancer Agency, Vancouver, Canada.
Adrian B LevinePathology and Laboratory Medicine, University of British Columbia, Vancouver, Canada.
Marco A MarraCanada's Michael Smith Genome Sciences Centre, BC Cancer, Vancouver, Canada.
Stephen YipPathology and Laboratory Medicine, University of British Columbia, Vancouver, Canada. Stephen.Yip@vch.ca.ORCID 0000-0002-8514-9861
BC Cancer Agency · CAUniversity of British Columbia · CACanada's Michael Smith Genome Sciences Centre · CASimon Fraser University · CATechnical University of Munich · DE

Funding

Canadian Institutes for Health Research
6 · The paper itself

Abstract

backgroundAberrations in Capicua (CIC) have recently been implicated as a negative prognostic factor in a multitude of cancer types through the derepression of targets downstream of the mitogen-activated protein kinase (MAPK) signaling cascade, such as oncogenic E26 transformation-specific (ETS) transcription factors. The Ataxin-family protein ATXN1L has previously been reported to interact with CIC in both developmental and disease contexts to facilitate the repression of CIC target genes and promote the post-translational stability of CIC. However, little is known about the mechanisms at the base of ATXN1L-mediated CIC post-translational stability.

resultsFunctional in vitro studies utilizing ATXN1L

conclusionsThe post-translational regulation of CIC through ATXN1L and TRIM25 independent of ERK activity suggests that the regulation of CIC stability and function is more intricate than previously appreciated and involves several independent pathways. As CIC status has become a prognostic factor in several cancer types, further knowledge into the mechanisms which govern CIC stability and function may prove useful for future therapeutic approaches.

Indexed as

MAP Kinase Signaling SystemCell LineHumansProteolysisRepressor ProteinsTranscription FactorsTripartite Motif ProteinsUbiquitin-Protein LigasesATXN1L protein, humanCIC protein, humanRepressor ProteinsTranscription FactorsTRIM25 protein, humanTripartite Motif ProteinsUbiquitin-Protein LigasesATXN1LBreast carcinomaCapicuaCICGlioblastomaMAPKProteasomal degradationTRIM25Ubiquitin

Identifiers

PMID33115448
PMCPMC7594423
OpenAlexW3097226470

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.