Evidence map›Paper›PMID 37693591›Full record

ArticlebioRxiv : the preprint server for biology2023

Generation of isogenic models of Angelman syndrome and Prader-Willi syndrome in CRISPR/Cas9-engineered human embryonic stem cells.

Rachel B Gilmore, Dea Gorka, Christopher E Stoddard, Justin L Cotney, Stormy J Chamberlain

Open access · greenAbstract readPreprint
In one paragraph

Article in bioRxiv : the preprint server for biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed, 2 citations in OpenAlex.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Rachel B GilmoreDepartment of Genetics and Genome Sciences, UConn Health; Farmington, CT, USA.
Dea GorkaDepartment of Genetics and Genome Sciences, UConn Health; Farmington, CT, USA.
Christopher E StoddardDepartment of Genetics and Genome Sciences, UConn Health; Farmington, CT, USA.
Justin L CotneyDepartment of Genetics and Genome Sciences, UConn Health; Farmington, CT, USA.
Stormy J ChamberlainDepartment of Genetics and Genome Sciences, UConn Health; Farmington, CT, USA.
Farmington Community Library · USUniversity of Connecticut · US

Funding

Unraveling mechanisms of genome regulation to understand and improvehuman healthR35GM119465 · NIGMS · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI COTNEY, JUSTIN LEE · 2016 to 2025
$3.9M
Molecular underpinnings of Prader-Willi syndromeR01HD099975 · NICHD · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI CARMICHAEL, GORDON G, COTNEY, JUSTIN LEE · 2019 to 2023
$2.9M
NICHD NIH HHS R01 HD099975NIGMS NIH HHS R35 GM119465Wellcome Trust
6 · The paper itself

Abstract

Angelman Syndrome (AS) and Prader-Willi Syndrome (PWS), two distinct neurodevelopmental disorders, result from loss of expression from imprinted genes in the chromosome 15q11-13 locus most commonly caused by a megabase-scale deletion on either the maternal or paternal allele, respectively. Each occurs at an approximate incidence of 1/15,000 to 1/30,000 live births and has a range of debilitating phenotypes. Patient-derived induced pluripotent stem cells (iPSCs) have been valuable tools to understand human-relevant gene regulation at this locus and have contributed to the development of therapeutic approaches for AS. Nonetheless, gaps remain in our understanding of how these deletions contribute to dysregulation and phenotypes of AS and PWS. Variability across cell lines due to donor differences, reprogramming methods, and genetic background make it challenging to fill these gaps in knowledge without substantially increasing the number of cell lines used in the analyses. Isogenic cell lines that differ only by the genetic mutation causing the disease can ease this burden without requiring such a large number of cell lines. Here, we describe the development of isogenic human embryonic stem cell (hESC) lines modeling the most common genetic subtypes of AS and PWS. These lines allow for a facile interrogation of allele-specific gene regulation at the chromosome 15q11-q13 locus. Additionally, these lines are an important resource to identify and test targeted therapeutic approaches for patients with AS and PWS.

Identifiers

PMID37693591
PMCPMC10491257
OpenAlexW4386330352

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.