Evidence map›Paper›PMID 35188187›Full record

ArticleDisease models & mechanisms2022

RAS and beyond: the many faces of the neurofibromatosis type 1 protein.

Corina Anastasaki, Paola Orozco, David H Gutmann

Open access · goldAbstract read
In one paragraph

Article in Disease models & mechanisms, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
7.8field-weighted citation impact, top 2% 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

57 citing papers in PubMed, 73 citations in OpenAlex.

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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

3 authors at 1 institution in 1 country.

Corina AnastasakiDepartment of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA.ORCID 0000-0002-9928-6488
Paola OrozcoDepartment of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA.
David H GutmannDepartment of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA.ORCID 0000-0002-3127-5045
Washington University in St. Louis · US

Funding

Defining the Mechanistic Basis for Neurofibromatosis-1 Nervous System Disease HeterogeneityR35NS097211 · NINDS · WASHINGTON UNIVERSITY · PI GUTMANN, DAVID H · 2017 to 2024
$5.7M
Developing Human Induced Pluripotent Stem Cell Precision Oncology ModelsR50CA233164 · NCI · WASHINGTON UNIVERSITY · PI Corina Anastasaki · 2018 to 2026
$1.2M
NCI NIH HHS R50 CA233164NINDS NIH HHS R35 NS097211
6 · The paper itself

Abstract

Neurofibromatosis type 1 is a rare neurogenetic syndrome, characterized by pigmentary abnormalities, learning and social deficits, and a predisposition for benign and malignant tumor formation caused by germline mutations in the NF1 gene. With the cloning of the NF1 gene and the recognition that the encoded protein, neurofibromin, largely functions as a negative regulator of RAS activity, attention has mainly focused on RAS and canonical RAS effector pathway signaling relevant to disease pathogenesis and treatment. However, as neurofibromin is a large cytoplasmic protein the RAS regulatory domain of which occupies only 10% of its entire coding sequence, both canonical and non-canonical RAS pathway modulation, as well as the existence of potential non-RAS functions, are becoming apparent. In this Special article, we discuss our current understanding of neurofibromin function.

Indexed as

Neurofibromatosis 1Neurofibromin 1Genes, Neurofibromatosis 1HumansProteinsSignal TransductionNeurofibromin 1ProteinsCyclic AMPNeurofibrominRASTumor suppressor

Identifiers

PMID35188187
PMCPMC8891636
OpenAlexW4213050171

What OpenQuestion holds

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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.