Evidence map›Paper›PMID 30208054›Full record

ArticlePloS one2018

The Trim family of genes and the retina: Expression and functional characterization.

Rebecca Chowdhury, Lauren A Laboissonniere, Andrea K Wester, Madison Muller, Jeffrey M Trimarchi

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.4field-weighted citation impact, top 39% 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

7 citing papers in PubMed, 14 citations in OpenAlex.

  1. Trim9 regulates the directional differentiation of retinal Müller cells to retinal ganglion cells.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2023
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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

5 authors at 1 institution in 1 country.

Rebecca ChowdhuryDepartment of Genetics, Development and Cell Biology, Iowa State University, Ames, Iowa, United States of America.
Lauren A LaboissonniereDepartment of Genetics, Development and Cell Biology, Iowa State University, Ames, Iowa, United States of America.ORCID 0000-0002-4260-5900
Andrea K WesterDepartment of Genetics, Development and Cell Biology, Iowa State University, Ames, Iowa, United States of America.
Madison MullerDepartment of Genetics, Development and Cell Biology, Iowa State University, Ames, Iowa, United States of America.
Jeffrey M TrimarchiDepartment of Genetics, Development and Cell Biology, Iowa State University, Ames, Iowa, United States of America.ORCID 0000-0001-7923-1538
Iowa State University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To better understand the mechanisms that govern the development of retinal neurons, it is critical to gain additional insight into the specific intrinsic factors that control cell fate decisions and neuronal maturation. In the developing mouse retina, Atoh7, a highly conserved transcription factor, is essential for retinal ganglion cell development. Moreover, Atoh7 expression in the developing retina occurs during a critical time period when progenitor cells are in the process of making cell fate decisions. We performed transcriptome profiling of Atoh7+ individual cells isolated from mouse retina. One of the genes that we found significantly correlated with Atoh7 in our transcriptomic data was the E3 ubiquitin ligase, Trim9. The correlation between Trim9 and Atoh7 coupled with the expression of Trim9 in the early mouse retina led us to hypothesize that this gene may play a role in the process of cell fate determination. To address the role of Trim9 in retinal development, we performed a functional analysis of Trim9 in the mouse and did not detect any morphological changes in the retina in the absence of Trim9. Thus, Trim9 alone does not appear to be involved in cell fate determination or early ganglion cell development in the mouse retina. We further hypothesize that the reason for this lack of phenotype may be compensation by one of the many additional TRIM family members we find expressed in the developing retina.

Indexed as

AnimalsBasic Helix-Loop-Helix ProteinsCarrier ProteinsEmbryo, MammalianFemaleGenotypeIn Situ HybridizationMiceMice, KnockoutNerve Tissue ProteinsPregnancyRetinaRetinal NeuronsTranscriptomeTripartite Motif ProteinsUbiquitin-Protein LigasesAtoh7 protein, mouseBasic Helix-Loop-Helix ProteinsCarrier ProteinsNerve Tissue ProteinsTrim9 protein, mouseTripartite Motif ProteinsUbiquitin-Protein Ligases

Identifiers

PMID30208054
PMCPMC6135365
OpenAlexW2892236630

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.