Evidence map›Paper›PMID 32993133›Full record

ReviewInternational journal of molecular sciences2020

RET Receptor Tyrosine Kinase: Role in Neurodegeneration, Obesity, and Cancer.

Arun Kumar Mahato, Yulia A Sidorova

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 8% 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

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 71 citations in OpenAlex.

  1. Pooled it
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  7. Refining the Sox10Animal models and experimental medicine · 2025
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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

2 authors at 1 institution in 1 country.

Arun Kumar MahatoInstitute of Biotechnology, University of Helsinki, HiLIFE, Viikinkaari 5D, 00014 Helsinki, Finland.
Yulia A SidorovaInstitute of Biotechnology, University of Helsinki, HiLIFE, Viikinkaari 5D, 00014 Helsinki, Finland.ORCID 0000-0001-8230-0530
University of Helsinki · FI

Funding

Academy of Finland 1325555
6 · The paper itself

Abstract

Rearranged during transfection (RET) is the tyrosine kinase receptor that under normal circumstances interacts with ligand at the cell surface and mediates various essential roles in a variety of cellular processes such as proliferation, differentiation, survival, migration, and metabolism. RET plays a pivotal role in the development of both peripheral and central nervous systems. RET is expressed from early stages of embryogenesis and remains expressed throughout all life stages. Mutations either activating or inhibiting RET result in several aggressive diseases, namely cancer and Hirschsprung disease. However, the physiological ligand-dependent activation of RET receptor is important for the survival and maintenance of several neuronal populations, appetite, and weight gain control, thus providing an opportunity for the development of disease-modifying therapeutics against neurodegeneration and obesity. In this review, we describe the structure of RET, its signaling, and its role in both normal conditions as well as in several disorders. We highlight the differences in the signaling and outcomes of constitutive and ligand-induced RET activation. Finally, we review the data on recently developed small molecular weight RET agonists and their potential for the treatment of various diseases.

Indexed as

AnimalsHirschsprung DiseaseHumansMutationNeoplasmsNeurodegenerative DiseasesNeuronsObesityProto-Oncogene Proteins c-retRetinitis PigmentosaProto-Oncogene Proteins c-retRET protein, humancancerglial cell line-derived neurotrophic factor (GDNF) family ligands (GFLs)growth differentiation factor 15 (GDF15)hirschsprung diseaseneurodegenerationneurorestorationobesityrearranged in transfection (RET)RET agonistretinitis pigmentosa

Identifiers

PMID32993133
PMCPMC7583994
OpenAlexW3089012118

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.