Protocadherin 12 (Pcdh12) is a transmembrane adhesive protein with homophilic adhesive properties and expressed in endothelial cells, the glycogen trophoblast cells of the placenta, and the mesangial cells of kidney glomeruli. Pcdh12-deficient mice are alive although they show alterations in placenta development.
Protocadherin 12 deficiency alters morphogenesis and transcriptional profile of the placenta.
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Specimen part
View SamplesNeural stem cells were sorted according to their activated or quiescent state by flow cytometry using a set of 3 markers (LeX, CD24 and EGFR)
Distinct Molecular Signatures of Quiescent and Activated Adult Neural Stem Cells Reveal Specific Interactions with Their Microenvironment.
Sex, Specimen part
View SamplesTranscript analysis in the fry1 arabidopsis mutant compared to the pht1;4 (DCJ) control in leaves and roots of the plant. The experiment was duplicated.
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Specimen part
View SamplesMicroarray analysis was performed in order to detail the global changes of gene expression in Fancg -/- embryonic Primordial Germ Cells and decipher molecular pathways underlying defects of primordial germ cell development in KO embryos.
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Sex, Specimen part
View SamplesMicroarray analysis was performed in order to detail the gene expression profiles in murine b-2M-SPa-6+c-kit-undifferentiated and b-2M-SPa-6+c-kit+ differentiating spermatogonia. These data were used to compare human and mouse transcriptomes of undifferentiated spermatogonia.
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Specimen part
View SamplesTotal body irradiation (TBI) of mice using two dose rates, conventional dose rate (CDR) versus flash dose rate (FLASH), induced transient decrease of number of LT-HScs in bone marrow and a total recovery of these cells 15 days after TBI
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Sex, Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Genome-wide nucleosome specificity and function of chromatin remodellers in ES cells.
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View SamplesLarge-scale gene expression profiling of peripheral blood mononuclear cells from Rheumatoid Arthritis (RA) patients could provide a molecular description that reflects the contribution of diverse cellular responses associated with this disease. The aim of our study is to identify peripheral blood gene expression profiles for RA patients, using Illumina technology, to gain insights into RA molecular mechanisms. The Illumina Human-6v2 Expression BeadChips were used for a complete genome-wide transcript profiling of peripheral blood mononuclear cells from 18 RA patients and 15 Controls. Differential analysis per gene was performed with one-way analysis of variance (ANOVA) and P values were adjusted to control the False Discovery Rate (FDR<5%). Genes differentially expressed at significant level between patients and controls were analyzed using Gene Ontology (GO) in the PANTHER database to identify biological processes. A differentially expression of 339 Reference Sequence genes (238 down-regulated and 101 up-regulated) between the two groups was observed. We identified a remarkably elevated expression of a spectrum of genes involved in Immunity and Defense in peripheral blood mononuclear cells of RA patients compared to Controls. This result is confirmed by GO analysis, suggesting that these genes could be activated systemically in RA. No significant down-regulated ontology groups were found. Microarrays data were validated by real time PCR in a set of nine genes showing a high degree of correlation. Our study highlighted several new genes that could contribute in the identification of innovative clinical biomarkers for diagnostic procedures and therapeutic intervention. Further studies on larger scale groups of patients should be performed with the same technology to replicate these results and to allow clinical stratification.
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Sex, Age, Specimen part
View SamplesNeuronal migration disorders such as lissencephaly and subcortical band heterotopia (SBH) are associated with epilepsy and intellectual disability. Doublecortin (DCX), LIS1 and alpha1-tubulin (TUBA1A), are mutated in these disorders, however corresponding mouse mutants do not show heterotopic neurons in the neocortex. On the other hand, the spontaneously arisen HeCo mouse mutant displays this phenotype. The study of this model reveals novel mechanisms of heterotopia formation. While, HeCo neurons migrate at the same speed as WT, abnormally distributed dividing progenitors were found throughout the cortical wall from E13. Through genetic studies we identified Eml1 as the mutant gene in HeCo mice. No full length transcripts of Eml1 were identified due to a retrotransposon insertion in an intron. Re-expression of Eml1, coding for a microtubule-associated protein, rescues the HeCo progenitor phenotype. We further show that EML1 is mutated in giant ribbon-like heterotopia in human. Our data link abnormal spindle orientations, ectopic progenitors and severe heterotopia in mouse and human.
Mutations in Eml1 lead to ectopic progenitors and neuronal heterotopia in mouse and human.
Specimen part
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