Project description:Transcript profiling analysis of AtFBP7 mutant seedlings compared to wild type using Arabidopsis ATH1 GeneChip array. Keywords: 5 day old light grown seedlings, wild type and mutant
Project description:Transcript profiling analysis of vfb (Vier F-Box) mutant seedlings compared to wild type using Arabidopsis ATH1 GeneChip array. Keywords: 10 day old light grown seedlings, wild type and mutant
Project description:Transcript profiling analysis of csn4-1 light grown mutant seedlings compared to wild type using Arabidopsis ATH1 GeneChip array Keywords: 7 day old light grown seedlings, wild type and mutant
Project description:Transcript profiling analysis of Hydraulic conductivity of Root 1 (HCR1) mutant compared to wild type (Col-0) using ARABIDOPSIS GENE1.1ST ARRAY STRIP (901793, Affymetrix, Santa Clara, USA).
Project description:Transcript profiling analysis of csn3-1, csn4-1 and csn5 (csn5a-2 csn5b) light grown and dark grown mutant seedlings compared to light grown and dark grown wild type using Arabidopsis ATH1 GeneChip array Keywords: mutant analysis, growth condition analysis
Project description:Transcription profiling by array of Arabidopsis MKK9DD (constitutively active MKK9 kinase mutant) overexpressing seedlings and Pi-starved wild type seedlings to identify the same regulated genes
Project description:Exploring miRNA-related antisense transcription in Arabidopsis through RNA transcript profiling of smRNA pathway-defective mutants on a custom high-resolution oligonucleotide array.
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.