Evidence map›Paper›PMID 22253195›Full record

ArticleHuman mutation2012

Transcriptional hallmarks of Noonan syndrome and Noonan-like syndrome with loose anagen hair.

Giovanni Battista Ferrero, Gabriele Picco, Giuseppina Baldassarre, Elisabetta Flex, Claudio Isella, Daniela Cantarella, Davide Corà, Nicoletta Chiesa, Nicoletta Crescenzio, Fabio Timeus and 7 more

Open access · bronzeAbstract read
In one paragraph

Article in Human mutation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.4field-weighted citation impact, top 37% 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

8 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Elucidation ofJCI insight · 2017
    Article
  7. Article
  8. The function of Shoc2: A scaffold and beyond.Communicative & integrative biology
    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

17 authors at 7 institutions in 1 country.

Giovanni Battista FerreroDepartment of Pediatrics, University of Torino Medical School, Torino, Italy.
Gabriele Picco
Giuseppina Baldassarre
Elisabetta Flex
Claudio Isella
Daniela Cantarella
Davide Corà
Nicoletta Chiesa
Nicoletta Crescenzio
Fabio Timeus
Giuseppe Merla
Laura Mazzanti
Giuseppe Zampino
Cesare Rossi
Margherita Silengo
Marco Tartaglia
Enzo Medico
University of Turin · ITCandiolo Cancer Institute · ITIstituto Superiore di Sanità · ITCasa Sollievo della Sofferenza · ITIRCCS Azienda Ospedliero-Universitaria di Bologna Policlinico di Sant'Orsola · ITUniversità Cattolica del Sacro Cuore · ITUniversity of Bologna · IT

Funding

Telethon GGP10020
6 · The paper itself

Abstract

Noonan syndrome (NS) is among the most common nonchromosomal disorders affecting development and growth. NS is genetically heterogeneous, being caused by germline mutations affecting various genes implicated in the RAS signaling network. This network transduces extracellular signals into intracellular biochemical and transcriptional responses controlling cell proliferation, differentiation, metabolism, and senescence. To explore the transcriptional consequences of NS-causing mutations, we performed global mRNA expression profiling on peripheral blood mononuclear cells obtained from 23 NS patients carrying heterozygous mutations in PTPN11 or SOS1. Gene expression profiling was also resolved in five subjects with Noonan-like syndrome with loose anagen hair (NS/LAH), a condition clinically related to NS and caused by an invariant mutation in SHOC2. Robust transcriptional signatures were found to specifically discriminate each of the three mutation groups from 21 age- and sex-matched controls. Despite the only partial overlap in terms of gene composition, the three signatures showed a notable concordance in terms of biological processes and regulatory circuits affected. These data establish expression profiling of peripheral blood mononuclear cells as a powerful tool to appreciate differential perturbations driven by germline mutations of transducers involved in RAS signaling and to dissect molecular mechanisms underlying NS and other RASopathies.

Indexed as

Case-Control StudiesFemaleGene Expression ProfilingGranuloma, Giant CellHumansIntracellular Signaling Peptides and ProteinsLeukocytes, MononuclearMaleMutationNoonan SyndromeProtein Tyrosine Phosphatase, Non-Receptor Type 11ras ProteinsSignal TransductionSOS1 ProteinTranscription, GeneticIntracellular Signaling Peptides and ProteinsProtein Tyrosine Phosphatase, Non-Receptor Type 11PTPN11 protein, humanras ProteinsSHOC2 protein, humanSOS1 Protein

Identifiers

PMID22253195
PMCPMC3332054
OpenAlexW2155594030

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.