This SuperSeries is composed of the SubSeries listed below.
Distinct and combinatorial functions of Jmjd2b/Kdm4b and Jmjd2c/Kdm4c in mouse embryonic stem cell identity.
Sex, Specimen part
View SamplesWe used microarray to determine the changes in gene expression profile after KD of Jmjd2b and Jmjd2c compared to Anti-GFP KD from mES cells
Distinct and combinatorial functions of Jmjd2b/Kdm4b and Jmjd2c/Kdm4c in mouse embryonic stem cell identity.
Sex, Specimen part
View SamplesWe established several iPSCs from healthy donors, familial ALS (FALS) patients, and sporadic ALS (SALS) patients. Using our differentiation protocol originally developed, we differentiated these iPSCs toward spinal motor neurons (MNs) and reproduced ALS pathology in a dish.
Modeling sporadic ALS in iPSC-derived motor neurons identifies a potential therapeutic agent.
Specimen part, Disease, Treatment, Subject
View SamplesThe Affymetrix Human Gene 2.0 ST array was used to measure differential expression of RNA isolated from normal and Diamond Blackfan anemia (DBA) erythroid progenitors after ex vivo expansion of circulating, peripheral blood derived hematopoietic stem cells under erythroid growth conditions. The gene-level probe summaries reported in this series were computed using RMA as implemented in the Bioconductor package Oligo v1.36.1.
Molecular convergence in ex vivo models of Diamond-Blackfan anemia.
Specimen part
View SamplesDiamond Blackfan anemia is a congenital bone marrow failure syndrome characterized by hypoproliferative anemia, often with associated physical abnormalities. Perturbations of the ribosome appear critically important to the development of DBA, as alterations in 9 different ribosomal protein genes have been identified in multiple unrelated families, along with rarer abnormalities of additional ribosomal proteins. However, presently only 50-60% of patients have an identifiable genetic lesion by ribosomal protein gene sequencing. Using genome-wide SNP array to evaluate for regions of recurrent copy variation, we identified 2 patients with mosaic loss in the region of the the chromosome 5-deleted region involved in somatically-acquired 5q- myelodysplastic syndrome.
Diminutive somatic deletions in the 5q region lead to a phenotype atypical of classical 5q- syndrome.
Sex, Specimen part, Disease, Disease stage, Treatment
View SamplesWe investigated transcriptional changes in CD4CD8aa and CD4 intraepthelial lymphocytes.
Transcriptional reprogramming of mature CD4⁺ helper T cells generates distinct MHC class II-restricted cytotoxic T lymphocytes.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Deficiency of schnurri-2, an MHC enhancer binding protein, induces mild chronic inflammation in the brain and confers molecular, neuronal, and behavioral phenotypes related to schizophrenia.
Specimen part
View SamplesSchnurri-2 (Shn-2), an NF-kappa B site-binding protein, tightly binds to the enhancers of major histocompatibility complex (MHC) class I genes and inflammatory cytokines, which have been shown to harbor common variant single nucleotide polymorphisms associated with schizophrenia. Shn-2 knockout mice show behavioral abnormalities that strongly resemble those of schizophrenics. We performed gene expression microarray analysis of dentate gyri from Shn-2 knockout and wild-type control mice.
Deficiency of schnurri-2, an MHC enhancer binding protein, induces mild chronic inflammation in the brain and confers molecular, neuronal, and behavioral phenotypes related to schizophrenia.
Specimen part
View SamplesSchnurri-2 (Shn-2), an NF-kappa B site-binding protein, tightly binds to the enhancers of major histocompatibility complex (MHC) class I genes and inflammatory cytokines, which have been shown to harbor common variant single nucleotide polymorphisms associated with schizophrenia. Shn-2 knockout mice show behavioral abnormalities that strongly resemble those of schizophrenics. We performed gene expression microarray analysis of prefrontal cortices from Shn-2 knockout and wild-type control mice.
Deficiency of schnurri-2, an MHC enhancer binding protein, induces mild chronic inflammation in the brain and confers molecular, neuronal, and behavioral phenotypes related to schizophrenia.
Specimen part
View SamplesSchnurri-2 (Shn-2), an NF-kappa B site-binding protein, tightly binds to the enhancers of major histocompatibility complex (MHC) class I genes and inflammatory cytokines, which have been shown to harbor common variant single nucleotide polymorphisms associated with schizophrenia. Shn-2 knockout mice show behavioral abnormalities that strongly resemble those of schizophrenics. We performed gene expression microarray analysis of hippocampi from Shn-2 knockout and wild-type control mice.
Deficiency of schnurri-2, an MHC enhancer binding protein, induces mild chronic inflammation in the brain and confers molecular, neuronal, and behavioral phenotypes related to schizophrenia.
Sex, Specimen part
View Samples