Evidence map›Paper›PMID 30007125›Full record

ReviewCurrent opinion in cell biology2018

RAS GTPase-dependent pathways in developmental diseases: old guys, new lads, and current challenges.

Xosé R Bustelo, Piero Crespo, Isabel Fernández-Pisonero, Sonia Rodríguez-Fdez

Abstract readReview
In one paragraph

Review in Current opinion in cell biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 citing papers in PubMed.

  1. Article
  2. Review
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  6. Article
  7. RAS interaction with Sin1 is dispensable for mTORC2 assembly and activity.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
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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.

Xosé R BusteloCentro de Investigación del Cáncer, Consejo Superior de Investigaciones Científicas (CSIC)-University of Salamanca, 37007 Salamanca, Spain; Instituto de Biología Molecular y Celular del Cáncer, Consejo Superior de Investigaciones Científicas (CSIC)-University of Salamanca, 37007 Salamanca, Spain; Centro de Investigación Biomédica en Red de Cáncer (CIBERONC), Consejo Superior de Investigaciones Científicas (CSIC)-University of Salamanca, 37007 Salamanca, Spain. Electronic address: xbustelo@usal.es.
Piero CrespoCIBERONC, CSIC-University of Cantabria, 39011 Santander, Spain; Instituto de Biomedicina y Biotecnología de Cantabria, CSIC-University of Cantabria, 39011 Santander, Spain.
Isabel Fernández-PisoneroCentro de Investigación del Cáncer, Consejo Superior de Investigaciones Científicas (CSIC)-University of Salamanca, 37007 Salamanca, Spain; Instituto de Biología Molecular y Celular del Cáncer, Consejo Superior de Investigaciones Científicas (CSIC)-University of Salamanca, 37007 Salamanca, Spain; Centro de Investigación Biomédica en Red de Cáncer (CIBERONC), Consejo Superior de Investigaciones Científicas (CSIC)-University of Salamanca, 37007 Salamanca, Spain.
Sonia Rodríguez-FdezCentro de Investigación del Cáncer, Consejo Superior de Investigaciones Científicas (CSIC)-University of Salamanca, 37007 Salamanca, Spain; Instituto de Biología Molecular y Celular del Cáncer, Consejo Superior de Investigaciones Científicas (CSIC)-University of Salamanca, 37007 Salamanca, Spain.

Funding

Worldwide Cancer Research 14-1248
6 · The paper itself

Abstract

Deregulated RAS signaling is associated with increasing numbers of congenital diseases usually referred to as RASopathies. The spectrum of genes and mutant alleles causing these diseases has been significantly expanded in recent years. This progress has triggered new challenges, including the origin and subsequent selection of the mutations driving these diseases, the specific pathobiological programs triggered by those mutations, the type of correlations that exist between the genotype and the clinical features of patients, and the ancillary genetic factors that influence the severity of the disease in patients. These issues also directly impinge on the feasibility of using RAS pathway drugs to treat RASopathy patients. Here, we will review the main developments and pending challenges in this research topic.

Indexed as

DiseaseEmbryonic DevelopmentGerm CellsHumansMutationras ProteinsSignal Transductionras Proteins

Identifiers

PMID30007125
PMCPMC7615762

What OpenQuestion holds

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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.