Evidence map›Paper›PMID 26484118›Full record

ArticleGenomics data2014

Transcriptional profiling of the postnatal brain of the Ts1Cje mouse model of Down syndrome.

Kai-Leng Tan, King-Hwa Ling, Chelsee A Hewitt, Pike-See Cheah, Ken Simpson, Lavinia Gordon, Melanie A Pritchard, Gordon K Smyth, Tim Thomas, Hamish S Scott

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Genomics data, 2014. 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.

No citing paper in PubMed yet.

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

10 authors.

Kai-Leng TanNeurobiology and Genetics Group, GRMRC-Medical Genetics Laboratory, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia, Selangor, Malaysia ; Department of Human Anatomy, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia, Selangor, Malaysia.
King-Hwa LingNeurobiology and Genetics Group, GRMRC-Medical Genetics Laboratory, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia, Selangor, Malaysia ; Walter and Eliza Hall Institute of Medical Research, Victoria, Australia ; Department of Obstetrics and Gynaecology, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia, Selangor, Malaysia.
Chelsee A HewittWalter and Eliza Hall Institute of Medical Research, Victoria, Australia ; Pathology Department, The Peter MacCallum Cancer Centre, East Melbourne, Victoria, Australia.
Pike-See CheahNeurobiology and Genetics Group, GRMRC-Medical Genetics Laboratory, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia, Selangor, Malaysia ; Department of Human Anatomy, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia, Selangor, Malaysia.
Ken SimpsonWalter and Eliza Hall Institute of Medical Research, Victoria, Australia.
Lavinia GordonWalter and Eliza Hall Institute of Medical Research, Victoria, Australia.
Melanie A PritchardDepartment of Biochemistry and Molecular Biology, Monash University, Melbourne, Victoria, Australia.
Gordon K SmythWalter and Eliza Hall Institute of Medical Research, Victoria, Australia ; Department of Mathematics and Statistics, The University of Melbourne, Parkville, Victoria, Australia.
Tim ThomasWalter and Eliza Hall Institute of Medical Research, Victoria, Australia ; Department of Medical Biology, University of Melbourne, Melbourne, Victoria, Australia.
Hamish S ScottWalter and Eliza Hall Institute of Medical Research, Victoria, Australia ; Centre for Cancer Biology, University of South Australia, Department of Molecular Pathology, SA Pathology, Adelaide, Australia ; School of Molecular and Biomedical Bioscience, University of Adelaide, Adelaide, Australia ; School of Medicine, Faculty of Health Sciences, University of Adelaide, Adelaide, Australia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Ts1Cje mouse model of Down syndrome (DS) has partial trisomy of mouse chromosome 16 (MMU16), which is syntenic to human chromosome 21 (HSA21). It develops various neuropathological features demonstrated by DS patients such as reduced cerebellar volume [1] and altered hippocampus-dependent learning and memory [2,3]. To understand the global gene expression effect of the partially triplicated MMU16 segment on mouse brain development, we performed the spatiotemporal transcriptome analysis of Ts1Cje and disomic control cerebral cortex, cerebellum and hippocampus harvested at four developmental time-points: postnatal day (P)1, P15, P30 and P84. Here, we provide a detailed description of the experimental and analysis procedures of the microarray dataset, which has been deposited in the Gene Expression Omnibus (GSE49050) database.

Indexed as

Down syndromeGene expressionMicroarrayPostnatal brain

Identifiers

PMID26484118
PMCPMC4535870

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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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.