RNA sequencing of Kv8.2 knockout mouse retina
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE327286 | GEO | 2026/07/02
REPOSITORIES: GEO
Similar Datasets
Project description:NeuroD1 encodes a basic helix-loop-helix transcription factor involved in the development of neural and endocrine structures. NeuroD1 mRNA is highly abundant in the adult mammalian pineal gland and exhibits a developmental expression pattern similar to the retina. This is consistent with the common evolutionary origin of pinealocytes and retinal photoreceptors. Pinealocytes and retinal photoreceptors express a shared set of phototransduction genes and submammalian pinealocytes are photosensitive. In contrast to the retina, the pineal gland is a relatively homogeneous structure, composed 95% of pinealocytes. This makes the pineal gland a particularly useful model for understanding photoreceptor cell biology. The loss of NeuroD1 in the retina results in progressive photoreceptor degeneration and the molecular mechanisms underlying this retinal degeneration phenotype remain unknown. Similarly, the role that NeuroD1 plays in the pineal gland is unknown. To determine the function of NeuroD1 in the pineal gland and retina, a Cre/loxP recombination strategy was used to selectively target a NeuroD1 floxed allele and generate NeuroD1 conditional knockout (cKO) mice. Tissue specificity was conferred using Cre recombinase expressed under the control of the promoter of Crx, a transcription factor selectively expressed in the pineal gland and retina. Pineal and retinal tissues from two-month-old NeuroD1 cKO and control animals were used in microarray studies to identify candidate genes responsible for the photoreceptor degeneration phenotype. The Cre/loxP recombination strategy was used to target a NeuroD1 floxed allele and generate NeuroD1 conditional knockout mice (NeuroD1floxed::Crx-Cre+/-). NeuroD1 floxed mice (NeuroD1floxed::Crx-Cre-/-) served as the controls. Pineal glands and retinas from two-month-old control and conditional knockout mice were collected at ZT6 and ZT20. 3 pools of 6 pineal glands per genotype and respective time of day were collected for each sample. Similarly, 3 pools of 6 retinas each were also collected. RNA from each pool was extracted and hybridized on the Affymetrix Mouse 430 2.0 array.
2012-07-25 | E-GEOD-35396 | biostudies-arrayexpress
Project description:IGF-I exert multiple effects in different retinal cell populations in both physiological and pathological conditions. Transgenic mice overexpressing IGF-I in the retina showed impaired electroretinographic responses at 6-7 months of age that worsen with age. This retinal neuronal dysfunction was correlated with the loss of rod photoreceptors, bipolar, ganglion and amacrines cells. Neuronal alterations were preceded by the overexpression of retinal stress markers, acute phase proteins and gliosis-related genes. IGF-I overexpression leads to chronic gliosis and microgliosis in TgIGF-I retinas, with mild oxidative stress, impaired recycling of glutamate and defective potassium buffering. These impaired supportive functions can contribute to neurodegeneration in TgIGF-I retinas, together with the increased production of pro-inflammatory cytokines, potential mediators of neuronal death.
2013-08-01 | E-MEXP-3786 | biostudies-arrayexpress
Project description:Transcription profiling by array of mouse male retinas to investigate IGF-I-induced chronic gliosis and retinal stress IGF-I exert multiple effects in different retinal cell populations in both physiological and pathological conditions. Transgenic mice overexpressing IGF-I in the retina showed impaired electroretinographic responses at 6-7 months of age that worsen with age. This retinal neuronal dysfunction was correlated with the loss of rod photoreceptors, bipolar, ganglion and amacrines cells. Neuronal alterations were preceded by the overexpression of retinal stress markers, acute phase proteins and gliosis-related genes. IGF-I overexpression leads to chronic gliosis and microgliosis in TgIGF-I retinas, with mild oxidative stress, impaired recycling of glutamate and defective potassium buffering. These impaired supportive functions can contribute to neurodegeneration in TgIGF-I retinas, together with the increased production of pro-inflammatory cytokines, potential mediators of neuronal death. 3 transgenic and 3 wild type biological replicates examined.
2013-04-30 | E-GEOD-46246 | biostudies-arrayexpress
Project description:Transcription profiling by array of mouse male retinas to investigate IGF-I-induced chronic gliosis and retinal stress IGF-I exert multiple effects in different retinal cell populations in both physiological and pathological conditions. Transgenic mice overexpressing IGF-I in the retina showed impaired electroretinographic responses at 6-7 months of age that worsen with age. This retinal neuronal dysfunction was correlated with the loss of rod photoreceptors, bipolar, ganglion and amacrines cells. Neuronal alterations were preceded by the overexpression of retinal stress markers, acute phase proteins and gliosis-related genes. IGF-I overexpression leads to chronic gliosis and microgliosis in TgIGF-I retinas, with mild oxidative stress, impaired recycling of glutamate and defective potassium buffering. These impaired supportive functions can contribute to neurodegeneration in TgIGF-I retinas, together with the increased production of pro-inflammatory cytokines, potential mediators of neuronal death.
2013-04-30 | GSE46246 | GEO
Project description:To assess DNA accessbility in adult Gabra3 knockout mouse retinas, especially at the Gabra1 promoter, we ultilized the Assay for Transposase Accessible Chromatin (ATAC-Seq; Buenrostro et al., 2013) on whole retinas from Gabra3 knockout mice and littermate controls. We observed no significant differences between WT and KO retinas with respect to DNA accessibility.
2022-07-15 | GSE180163 | GEO
Project description:Transcriptomics and phosphoproteomics were carried out in B6.Cg-Mapttm1(EGFP)Klt (mapt knockout: tau-KO) and wild-type (WT) 12-month-old mice to learn about the effects of tau ablation.
2024-02-27 | PXD040416 | JPOST Repository
Project description:Mouse rod photoreceptors isolated from retinas of Prkaa2 rod photoreceptor specific knockout mice were processed for phosphoproteomics to elucidate downstream kinase targets. Prkaa2 is an isoform of the catalytic subunit of AMP-activated protein kinase (AMPK), an essential nutrient-sensing enzyme responsible for maintaining many metabolic processes.
2024-06-16 | PXD045669 | Pride
Project description:Whole body knockout mice lacking IQ-motif containing GTPase-activating protein 2 (IQGAP2) develop spontaneous hepatocellular carcinoma (HCC) at the age of 12 months and older (Schmidt et al., 2008). Hepatic transcript expression profiles were obtained for IQGAP2 knockout and wild-type control mice of two age groups, 6- and 24-month-old. Liver samples from 24-month-old IQGAP2 knockout mice were HCC tumors, livers from all other groups were tumor-free. Results provide insights into the potential role of IQGAP2 as a liver-specific tumor suppressor. Transcript profiles of four groups of mouse livers (N = 3 in each group) were compared using Affymetrix GeneChip® Mouse Genome 430 2.0 Array. The groups included livers from 6- and 24-month-old wild-type (WT) mice and 6- and 24-month-old (KO) Iqgap2-/- mice.
2013-12-13 | E-GEOD-46646 | biostudies-arrayexpress
Project description:The TMT-based quantitative proteomic raw data of 6-month-old WT, 5×FAD, 5×FAD:Usp25 KO mouse cerebral cortex including hippcampus.
2020-09-22 | PXD021637 |