Evidence map›Paper›PMID 35674905›Full record

ArticleMethods in molecular biology (Clifton, N.J.)2022

Functional Studies of Genetic Variants Associated with Human Diseases in Notch Signaling-Related Genes Using Drosophila.

Sheng-An Yang, Jose L Salazar, David Li-Kroeger, Shinya Yamamoto

Open access · greenAbstract read
In one paragraph

Article in Methods in molecular biology (Clifton, N.J.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

3 citing papers in PubMed, 3 citations in OpenAlex.

  1. Review
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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 at 2 institutions in 1 country.

Sheng-An YangDepartment of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX, USA.
Jose L SalazarDepartment of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX, USA.
David Li-KroegerJan and Dan Duncan Neurological Research Institute, Texas Children's Hospital, Houston, TX, USA. likroege@bcm.edu.
Shinya YamamotoDepartment of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX, USA. yamamoto@bcm.edu.
Baylor College of Medicine · USTexas Children's Hospital · US

Funding

PROGRAM IN HUMAN MOLECULAR GENETICST32GM008307 · NIGMS · BAYLOR COLLEGE OF MEDICINE · PI SHAULSKY, GAD · 1990 to 2020
$6.6M
UNDERSTANDING THE ROLE OF TM2D FAMILY GENES IN NOTCH SIGNALING AND ALZHEIMER'S DISEASERF1AG071557 · NIA · BAYLOR COLLEGE OF MEDICINE · PI YAMAMOTO, SHINYA · 2021 to 2021
$1.2M
BRAIN MACROPHAGES AND REPRODUCTIVE AGINGR01AG015457 · NIA · YALE UNIVERSITY · PI NAFTOLIN, FREDERICK · 1999 to 2002
$791k
NIA NIH HHS R01 AG015457NIA NIH HHS RF1 AG071557NIGMS NIH HHS T32 GM008307
6 · The paper itself

Abstract

Rare variants in the many genes related to Notch signaling cause diverse Mendelian diseases that affect myriad organ systems. In addition, genome- and exome-wide association studies have linked common and rare variants in Notch-related genes to common diseases and phenotypic traits. Moreover, somatic mutations in these genes have been observed in many types of cancer, some of which are classified as oncogenic and others as tumor suppressive. While functional characterization of some of these variants has been performed through experimental studies, the number of "variants of unknown significance" identified in patients with diverse conditions keeps increasing as high-throughput sequencing technologies become more commonly used in the clinic. Furthermore, as disease gene discovery efforts identify rare variants in human genes that have yet to be linked to a disease, the demand for functional characterization of variants in these "genes of unknown significance" continues to increase. In this chapter, we describe a workflow to functionally characterize a rare variant in a Notch signaling related gene that was found to be associated with late-onset Alzheimer's disease. This pipeline involves informatic analysis of the variant of interest using diverse human and model organism databases, followed by in vivo experiments in the fruit fly Drosophila melanogaster. The protocol described here can be used to study variants that affect amino acids that are not conserved between human and fly. By "humanizing" the almondex gene in Drosophila with mutant alleles and heterologous genomic rescue constructs, a missense variant in TM2D3 (TM2 Domain Containing 3) was shown to be functionally damaging. This, and similar approaches, greatly facilitate functional interpretations of genetic variants in the human genome and propel personalized medicine.

Indexed as

DrosophilaDrosophila melanogasterAnimalsExomeGenetic Predisposition to DiseaseGenomicsHumansPhenotypealmondexAlzheimer’s diseaseDrosophila melanogasterFunctional genomicsGenome-wide association studies (GWAS)Notch signalingTM2D3Variant of unknown significance (VUS)Whole-exome sequencing (WES)Whole-genome sequencing (WGS)

Identifiers

PMID35674905
PMCPMC9396741
OpenAlexW4286836574

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.