Similar studies for GEO DataSets (Select 1647) - GEO DataSets

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Items: 3

Select item 16471.

RPE65 null mutant model of Leber's congenital amaurosis

Analysis of retinas of RPE65 null mutants at 2, 4 and 6 months of age. RPE65 is highly expressed in retinal pigment epithelial cells. Mutations in REP65 cause 10-15% of Leber's congenital amaurosis (LCA) cases, a severe form of retinal dystrophy. Results provide insight into early LCA progression.

Organism:: Mus musculus

Type:: Expression profiling by array, transformed count, 3 age, 2 genotype/variation sets

Platform:: GPL1261
Series:: GSE3249
18 Samples

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DataSet

Accession:: GDS1647

ID:: 1647

Select item 2000032492.

Analysis of RPE65 loss of function in mouse retina

(Submitter supplied) To characterize gene response in RPE65-/- mouse model of Leber’s congenital amaurosis during progression of the disease, we analyzed differential gene expression in retinae early in the development of the disease, namely before and at the onset of photoreceptor cell death in knock-out mice of 2, 4 and 6 months of age. Keywords: knock out response over time

Organism:: Mus musculus

Type:: Expression profiling by array

Dataset:: GDS1647
Platform:: GPL1261
18 Samples

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Series

Accession:: GSE3249

ID:: 200003249

Select item 2000534113.

Gene profiling studies in postnatal Mfrprd6 mutant eyes reveal differential expression of Prss56, a trypsin-like serine protease, and genes involved in visual and phototransduction pathways.

(Submitter supplied) Mutations in the membrane frizzled-related gene (Mfrp) are linked to posterior microphthalmia, retinitis pigmentosa and nanophthalmia in humans. In homozygous Mfrprd6 mice, a splice site mutation causes a slow photoreceptor degeneration characterized by shortening and disorganization of outer segments with eventual photoreceptor loss. To better understand the function of MFRP in the retina, microarray analysis was carried out in mutant and control mice at postnatal day14 (P14), prior to the loss of photoreceptors. more...