Evidence map›Paper›PMID 35806349›Full record

ArticleInternational journal of molecular sciences2022

Phosphomimicry on STAU1 Serine 20 Impairs STAU1 Posttranscriptional Functions and Induces Apoptosis in Human Transformed Cells.

Yulemi Gonzalez Quesada, Florence Bonnet-Magnaval, Luc DesGroseillers

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.2field-weighted citation impact, top 53% 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

2 citing papers in PubMed, 2 citations in OpenAlex.

  1. Article
  2. 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

3 authors at 1 institution in 1 country.

Yulemi Gonzalez QuesadaDépartement de Biochimie et Médecine Moléculaire, Faculté de Médecine, Université de Montréal, 2900 Édouard Montpetit, Montreal, QC H3T 1J4, Canada.
Florence Bonnet-MagnavalDépartement de Biochimie et Médecine Moléculaire, Faculté de Médecine, Université de Montréal, 2900 Édouard Montpetit, Montreal, QC H3T 1J4, Canada.ORCID 0000-0001-9111-0130
Luc DesGroseillersDépartement de Biochimie et Médecine Moléculaire, Faculté de Médecine, Université de Montréal, 2900 Édouard Montpetit, Montreal, QC H3T 1J4, Canada.
Université de Montréal · CA

Funding

CIHR MOP-229979Natural Sciences and Engineering Research Council RGPIN-2019-05027
6 · The paper itself

Abstract

Staufen 1 (STAU1) is an RNA-binding protein that is essential in untransformed cells. In cancer cells, it is rather STAU1 overexpression that impairs cell proliferation. In this paper, we show that a modest increase in STAU1 expression in cancer cells triggers apoptosis as early as 12 h post-transfection and impairs proliferation in non-apoptotic cells for several days. Interestingly, a mutation that mimics the phosphorylation of STAU1 serine 20 is sufficient to cause these phenotypes, indicating that serine 20 is at the heart of the molecular mechanism leading to apoptosis. Mechanistically, phosphomimicry on serine 20 alters the ability of STAU1 to regulate translation and the decay of STAU1-bound mRNAs, indicating that the posttranscriptional regulation of mRNAs by STAU1 controls the balance between proliferation and apoptosis. Unexpectedly, the expression of RBD2

Indexed as

Cytoskeletal ProteinsRNA-Binding ProteinsSerineApoptosisCell Transformation, NeoplasticHumansRNA, MessengerCytoskeletal ProteinsRNA-Binding ProteinsRNA, MessengerSerineSTAU1 protein, humanapoptosiscell proliferationposttranscriptional regulationStaufen 1

Identifiers

PMID35806349
PMCPMC9266326
OpenAlexW4283801515

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.