Expression data from retinas of wildtype and Nhlh2 knockout mice
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE16756 | GEO | 2009/06/25
SECONDARY ACCESSION(S): PRJNA117465
REPOSITORIES: GEO
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Project description:Nhlh2 is a neuronal helix-loop-helix transcription factor. The goal of this study was to determine the pattern of gene expression in wildtype mouse retina and to compare it to that in the retinas of mice in which the nhlh2 gene had been knocked out. RNA was extracted from three pairs of littermates, each comprising one wildtype and one knockout sample. The littermate samples are: retina_wt_rep1 & retina_nhlh2_rep1; retina_wt_rep2 and retina_nhlh2_rep2; retina_wt_rep3 & retina_nhlh2_rep3.
2010-03-03 | E-GEOD-16756 | biostudies-arrayexpress
Project description:As a metabolic disease, diabetes often leads to health complications such as heart failure, nephropathy, neurological disorders, and vision loss. Diabetic retinopathy (DR) affects as many as 100 million people worldwide. The mechanism of DR is complex and known to impact both neural and vascular components in the retina. While recent advances in the field have identified major cellular signaling contributing to DR pathogenesis, little has been reported on the protein post-translational modifications (PTM) -known to define protein localization, function, and activity -in the diabetic retina overall. Protein glycosylation is the enzymatic addition of carbohydrates to proteins, which can influence many protein attributes including folding, stability, function, and subcellular localization. Olinked glycosylation is the addition of sugars to an oxygen atom in amino acids with a free oxygen atom in their side chain (i.e., threonine, serine). To date, more than 100 congenital disorders of glycosylation have been described. However, no studies have identified the retinal O-linked glycoproteome in health or disease. With a critical need to expedite the discovery of PTMomics in diabetic retinas, we identified both global changes in protein levels and the retinal O-glycoproteome of control and diabetic mice. Liquid chromatography/mass spectrometry-based glycoproteomics and high throughput screening identified proteins differentially glycosylated in the retinas of wildtype and diabetic mice. Here, we provide evidence that diabetes shifts O-glycosylation of metabolic and synaptic proteins in the retina.
2023-08-16 | PXD044269 | Pride
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:Genome-wide DNA accessibility in Gabra3a knockout and wildtype control mouse retinas.
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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:As a metabolic disease, diabetes often leads to health complications such as heart failure, nephropathy, neurological disorders, and vision loss. Diabetic retinopathy (DR) affects as many as 100 million people worldwide. The mechanism of DR is complex and known to impact both neural and vascular components in the retina. While recent advances in the field have identified major cellular signaling contributing to DR pathogenesis, little has been reported on the protein post-translational modifications (PTM) -known to define protein localization, function, and activity -in the diabetic retina overall. Protein glycosylation is the enzymatic addition of carbohydrates to proteins, which can influence many protein attributes including folding, stability, function, and subcellular localization. Olinked glycosylation is the addition of sugars to an oxygen atom in amino acids with a free oxygen atom in their side chain (i.e., threonine, serine). To date, more than 100 congenital disorders of glycosylation have been described. However, no studies have identified the retinal O-linked glycoproteome in health or disease. With a critical need to expedite the discovery of PTMomics in diabetic retinas, we identified both global changes in protein levels and the retinal O-glycoproteome of control and diabetic mice. Liquid chromatography/mass spectrometry-based glycoproteomics and high throughput screening identified proteins differentially glycosylated in the retinas of wildtype and diabetic mice. Here, we provide evidence that diabetes shifts O-glycosylation of metabolic and synaptic proteins in the retina.
2023-08-16 | PXD044270 | Pride
Project description:Seven-day-old C57BL/6 mice and IL-19 knockout (KO) mice were subjected to 75% oxygen for 5 days to induce OIR. To explore the mechanism that caused by IL-19 on retinal neovascularization, Gene expressions among retinas of room air control mice, OIR wildtype mice, and OIR IL-19 knockout mice were measured by RNA-sequencing (RNA-seq).
2022-01-24 | GSE194176 | GEO
Project description:This quantitative protepomics study (TMT10 isobaric labeling) of the protein expression in the retina of Msi1/Msi2 double knockout mouse compared to floxed controls. The Msi1 and Msi2 genes were knocked out in photoreceptor cells using tamoxifen inducible Cre (Cre-ERT2) under the control of Pde6g promoter. Tamoxifen was administered by intrapertoneal injection for three consecutive day starting at postnatald day 30, and the retina was collected at postnatal day 51. Retinas from floxed animals lacking the Cre recombinase and treated with tamoxifen were used as controls. Five biological replicates for each knockout (three femailes, two males) and control (two femaes and three males) group were used.
2022-03-10 | PXD030748 | Pride
Project description:In vitro, both 5PP-InsP5 (IP7) and 1,5(PP)2InsP4 (IP8) can pyrophosphorylate peptides and proteins. It is unclear, which inositol pyrophosphate species is responsible for installing endogenous pyrophosphorylation in cells. In order to test this, we used HCT116 cells deficient in IP8 synthesis. Both enzymes that convert IP7 to IP8 are knocked out in this cell line. Importantly, this cell line does overaccumulates IP7, complicating the analysis.
We found no obvious difference in the number of observable pyrophosphorylation sites between the knockout and wildtype, suggesting that either IP7 or both molecules are responsible for creating pyrophosphoproteins in cells.
2024-03-12 | PXD048031 | JPOST Repository
Project description:Background: Adult zebrafish spontaneously regenerate their retinas after damage. Although a number of genes and signaling pathways involved in regeneration have been identified, the extent of mechanisms regulating regeneration is unclear. Small non-coding RNAs, microRNAs (miRNAs), that regulate regeneration of various tissues in lower vertebrates were examined for their potential roles in regulating zebrafish retinal regeneration. Results: To investigate the requirement of miRNAs during zebrafish retinal regeneration, we knocked down the expression of the miRNA-processing enzyme Dicer in retinas prior to light-induced damage. Dicer loss significantly reduced proliferation of Müller glia-derived neuronal progenitor cells during regeneration. To identify individual miRNAs with roles in retina regeneration, we collected retinas at different stages of light damage and performed small RNA high-throughput sequencing. We identified subsets of miRNAs that were differentially expressed during active regeneration but returned to basal levels once regeneration was completed. To validate the roles of differentially expressed miRNAs, we knocked down 6 different miRNAs that were upregulated in expression during regeneration and demonstrated that they have distinct effects on neuronal progenitor cell proliferation and migration during retina regeneration. Conclusions: miRNAs are necessary for retinal regeneration. miRNA expression is dynamic during regeneration. miRNAs function during initiation and progression of retinal regeneration. Identification of miRNAs before, during and after completion of zebrafish retinal regeneration
2014-09-20 | E-GEOD-58702 | biostudies-arrayexpress