Evidence map›Paper›PMID 25783604›Full record

ArticleInvestigative ophthalmology & visual science2015

Ornithine-δ-Aminotransferase Inhibits Neurogenesis During Xenopus Embryonic Development.

Ying Peng, Sandra K Cooper, Yi Li, Jay M Mei, Shuwei Qiu, Gregory L Borchert, Steven P Donald, Hsiang-Fu Kung, James M Phang

Open access · bronzeAbstract read
In one paragraph

Article in Investigative ophthalmology & visual science, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.6field-weighted citation impact, top 27% 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

2 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Review
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

9 authors at 5 institutions in 2 countries.

Ying PengDepartment of Neurology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China.
Sandra K CooperBasic Research Program, Leidos, Inc., National Cancer Institute at Frederick, National Institutes of Health, Frederick, Maryland, United States.
Yi LiDepartment of Neurology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China.
Jay M MeiMetabolism and Cancer Susceptibility Section, Basic Research Laboratory, National Cancer Institute at Frederick, National Institutes of Health, Frederick, Maryland, United States.
Shuwei QiuDepartment of Neurology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China.
Gregory L BorchertBasic Research Program, Leidos, Inc., National Cancer Institute at Frederick, National Institutes of Health, Frederick, Maryland, United States.
Steven P DonaldMetabolism and Cancer Susceptibility Section, Basic Research Laboratory, National Cancer Institute at Frederick, National Institutes of Health, Frederick, Maryland, United States.
Hsiang-Fu KungState Key Laboratory of Oncology in Southern China, and Centre for Emerging Infectious Diseases, the Chinese University of Hong Kong, Shatin, Hong Kong, China.
James M PhangMetabolism and Cancer Susceptibility Section, Basic Research Laboratory, National Cancer Institute at Frederick, National Institutes of Health, Frederick, Maryland, United States.
Sun Yat-sen University · CNLeidos (United States) · USNational Institutes of Health · USChinese University of Hong Kong · CNFrederick National Laboratory for Cancer Research · US

Funding

Intramural NIH HHSPHS HHS HHSN27612080001
6 · The paper itself

Abstract

purposeIn humans, deficiency of ornithine-δ-aminotransferase (OAT) results in progressive degeneration of the neural retina (gyrate atrophy) with blindness in the fourth decade. In this study, we used the Xenopus embryonic developmental model to study functions of the OAT gene on embryonic development.

methodsWe cloned and sequenced full-length OAT cDNA from Xenopus oocytes (X-OAT) and determined X-OAT expression in various developmental stages of Xenopus embryos and in a variety of adult tissues. The phenotype, gene expression of neural developmental markers, and enzymatic activity were detected by gain-of-function and loss-of-function manipulations.

resultsWe showed that X-OAT is essential for Xenopus embryonic development, and overexpression of X-OAT produces a ventralized phenotype characterized by a small head, lack of axial structure, and defective expression of neural developmental markers. Using X-OAT mutants based on mutations identified in humans, we found that substitution of both Arg 180 and Leu 402 abrogated both X-OAT enzymatic activity and ability to modulate the developmental phenotype. Neurogenesis is inhibited by X-OAT during Xenopus embryonic development.

conclusionsNeurogenesis is inhibited by X-OAT during Xenopus embryonic development, but it is essential for Xenopus embryonic development. The Arg 180 and Leu 402 are crucial for these effects of the OAT molecule in development.

Indexed as

Gene Expression Regulation, DevelopmentalAnimalsEmbryonic DevelopmentNeurogenesisOrnithine-Oxo-Acid TransaminaseReverse Transcriptase Polymerase Chain ReactionRNAXenopus laevisOrnithine-Oxo-Acid TransaminaseRNA

Identifiers

PMID25783604
PMCPMC4554259
OpenAlexW2434013435

What OpenQuestion holds

Textmetadata
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.