GEO DataSets

(Submitter supplied) Df16(A)+/- mice line is a model of human 22q11 microdeletion syndrome. We conducted an unbiased evaluation of the transcriptional difference in the prefrontal cortex and hippocampus areas between mutant and wild type animals at two early developmental stages (embryonic day 17 and postnatal day 6). These mice were generated by chromosomal engineering and carry a microdeltion of ~1.3Mb in the mouse locus syntenic to the human 22q11.1 The reasoning behind this expression profiling is that consistent alterations in transcriptional programs reflect either downstream (immediate or remote) effects of the deficiency or reactive (compensatory) changes, and can thus point to affected biological processes and molecular functions. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL11180

127 Samples

Download data: CEL

(Submitter supplied) This represents an unbiased evaluation of the transcriptional response in the prefrontal cortex and hippocampus areas in the Df(16)A/+ mice, a mouse model of human 22q11 microdeletion syndrome. These mice were generated by chromosomal engineering and carry a microdeltion of ~1.3Mb in the mouse locus syntenic to the human 22q11.1 The reasoning behind this expression profiling is that alterations in transcriptional programs reflect either downstream (immediate or remote) effects of the deficiency or reactive (compensatory) changes, and can thus point to affected biological processes and molecular functions. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Datasets:

GDS3478 GDS3479

Platform:

GPL1261

40 Samples

Download data: CEL, EXP

Analysis of hippocampi of Df(16)A/+ animals. Df(16)A/+ animals carry microdeletions of about 1.3Mb in the locus syntenic to human 22q11.2. Individuals with 22q11.2 microdeletions show behavioral and cognitive deficits and are at high risk of developing schizophrenia.

Organism:

Mus musculus

Type:

Expression profiling by array, transformed count, 2 strain sets

Platform:

GPL1261

Series:

GSE10784

20 Samples

Download data: CEL, EXP

Analysis of prefrontal cortex of Df(16)A/+ animals. Df(16)A/+ animals carry microdeletions of about 1.3Mb in the locus syntenic to human 22q11.2. Individuals with 22q11.2 microdeletions show behavioral and cognitive deficits and are at high risk of developing schizophrenia.

Organism:

Mus musculus

Type:

Expression profiling by array, transformed count, 2 strain sets

Platform:

GPL1261

Series:

GSE10784

20 Samples

Download data: CEL, EXP

(Submitter supplied) Df16(A)+/- mice line is a model of human 22q11 microdeletion syndrome. We conducted an unbiased evaluation of the transcriptional difference in the prefrontal cortex between mutant and wild type animals at exon level. These mice were generated by chromosomal engineering and carry a microdeltion of ~1.3Mb in the mouse locus syntenic to the human 22q11.1 The reasoning behind this expression profiling is that consistent alterations in transcriptional programs reflect either downstream (immediate or remote) effects of the deficiency or reactive (compensatory) changes, and can thus point to affected biological processes and molecular functions. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL11533

24 Samples

Download data: CEL

(Submitter supplied) Among the fundamental unresolved questions in psychiatry is why symptoms of psychosis, such as auditory hallucinations in schizophrenia, fail to appear until early adulthood. Here we report that in mouse models of 22q11.2 deletion syndrome (22q11DS), a leading genetic cause of schizophrenia, synaptic transmission at thalamocortical inputs to the auditory cortex becomes disrupted later in life, thereby recapitulating the adult onset of psychosis. more...

Organism:

Mus musculus

Type:

Non-coding RNA profiling by array

Platform:

GPL17912

56 Samples

Download data: TXT

(Submitter supplied) miR-132 and miR-212 are structurally-related microRNAs that have been found to exert powerful modulatory effects within the central nervous system (CNS). Notably, these microRNAs are tandomly processed from the same non-coding transcript, and share a common seed sequence: thus it has been difficult to assess the distinct contribution of each microRNA to gene expression within the CNS. Here, we employed a combination of conditional knockout and transgenic mouse models to examine the contribution of the miR-132/212 gene locus to learning and memory, and then to assess the distinct effects that each microRNA has on hippocampal gene expression. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL9250

18 Samples

Download data: TXT

(Submitter supplied) Progressive ventricular enlargement is one of the most reproducible and recognizable structural abnormalities in schizophrenia, and is associated with more severe symptoms and poorer clinical outcome. The mechanisms of ventricular enlargement in schizophrenia is unknown. We identified that progressive ventricular enlargement is associated with deceleration of motile cilia beating in ependymal cells lining ventricular walls in murine models of schizophrenia-associated 22q11 deletion syndrome (22q11DS). more...

Organism:

Mus musculus

Type:

Non-coding RNA profiling by array

Platform:

GPL21265

16 Samples

Download data: TXT

(Submitter supplied) We intend to screen altered genes after overexpression of miR-196a in HD transgenic mice. Two transgenic mouse lines were used in this study, including HD transgenic mice and HD transgenic mice overexpressing miR-196a. The mice were all at approximate 12 months of age. At this point, HD transgenic mice showed severve motor dysfunctions, whereas HD transgenic mice overexpressing miR-196a displayed mild motor dysfunctions.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL13692

5 Samples

Download data: GPR

(Submitter supplied) Koolen-de Vries syndrome (KdVS) is a multi-system disorder characterized by intellectual disability, friendly behavior, and congenital malformations. The syndrome is caused either by microdeletions in the 17q21.31 chromosomal region or by variants in the KANSL1 gene. The reciprocal 17q21.31 microduplication syndrome is associated with psychomotor delay, and reduced social interaction. To investigate the pathophysiology of 17q21.31 microdeletion and microduplication syndromes, we generated three mouse models: 1) the deletion (Del/+); or 2) the reciprocal duplication (Dup/+) of the 17q21.31 syntenic region; and 3) a heterozygous Kansl1 (Kans1+/-) model. more...

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL13112

12 Samples

Download data: TXT, XLSX

(Submitter supplied) 22q11-deletion syndrome (22q11DS) is a developmental anomaly caused by a microdeletion on human chromosome 22q11. Although mouse models indicated Tbx1 as the gene responsible of the syndrome, the phenotypic spectrum of del22q11 patients is complex suggesting that gene-gene and gene-environment interactions, probably during embryonic development, are crucial in delineating the pathogenesis of 22q11DS. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL3634

14 Samples

Download data