<Objective> To compare gene expression in labial salivary glands (LSG) of IgG4-related disease (IgG4-RD) with Sjgrens syndrome (SS).
DNA microarray analysis of labial salivary glands in IgG4-related disease: comparison with Sjögren's syndrome.
Sex, Specimen part
View SamplesWe reported that NRP-1 expression on CD4+ T cells was probably induced by NRP-1 transfer from macrophages to T cells. In HER2+ BC, NRP-1 expressing TIIs correlated with better clinical outcomes. Overall design: Examination of monocytes and monocyte derived macrophages.
Downregulation of neuropilin-1 on macrophages modulates antibody-mediated tumoricidal activity.
No sample metadata fields
View SamplesHere we uncover antagonistic regulation of transcript levels in the germline of Caenorhabditis elegans hermaphrodites. The histone methyltransferase MES-4 marks genes expressed in the germline with methylated Lys36 on histone H3 (H3K36me) and promotes their transcription; MES-4 also represses genes normally expressed in somatic cells and genes on the X chromosomes. The DRM complex, which includes E2F/DP and Retinoblastoma homologs, affects germline gene expression and prevents excessive repression of X-chromosome genes. Using genome-scale analyses of germline tissue, we show that common germline-expressed genes are activated by MES-4 and repressed by DRM, and that MES-4 and DRM co-bind many germline-expressed genes. Reciprocally, MES-4 represses and DRM activates a set of autosomal soma-expressed genes and overall X-chromosome gene expression. Mutations in mes-4 or the DRM subunit lin-54 oppositely skew target transcript levels and cause sterility; a double mutant restores near wild-type transcript levels and germ cell development. Together, yin-yang regulation by MES-4 and DRM ensures transcript levels appropriate for germ cell function, elicits robust but not excessive dampening of X-chromosome-wide transcription, and may poise genes for future expression changes. Our study reveals that conserved transcriptional regulators implicated in development and cancer counteract each other to fine-tune transcript dosage.
Opposing activities of DRM and MES-4 tune gene expression and X-chromosome repression in Caenorhabditis elegans germ cells.
Sex
View SamplesPoly(A)+ RNAs were fragmented and sequenced. Poly(A)+ RNAs were fragmented and sequenced.
Position-dependent and neuron-specific splicing regulation by the CELF family RNA-binding protein UNC-75 in Caenorhabditis elegans.
No sample metadata fields
View SamplesThe gene expression patterns in the dentate gyrus of wild-type mice during postnatal development were examined using Affymetrix GeneChip arrays.
Transcriptomic immaturity inducible by neural hyperexcitation is shared by multiple neuropsychiatric disorders.
Specimen part
View SamplesTo define the characteristics of human oral mucosa fibroblasts (hOFs), we analyzed the gene expression of hOFs compared with that of human dermal fibroblasts (hDFs), and that of hOF-derived induced pluripotent stem cells (hOF-iPSCs).
Gene Signature of Human Oral Mucosa Fibroblasts: Comparison with Dermal Fibroblasts and Induced Pluripotent Stem Cells.
Sex, Age, Specimen part
View SamplesWe established the differentiation method of a limb bud organoid from mouse embryonic stem cells (mESCs) using SFEBq. mESCs-derived limb bud organoid selectively differentiate into forelimb or hindlimb by adjusting the retinoic acids activity. To evaluate a correlation of gene expression between limb bud organoid and embryonic tissues (limb bud, branchial arch, cardiac, and tail bud), we performed comparative transcriptome analysis using RNA-seq. Overall design: RNA-seq profiling of mouse embryonic limb bud, branchial arch, cardiac, and tail bud and mESCs-derived forelimb and hindlimb bud mesenchyme (Hnad2::GFP positive), in triplicate, using illumina Hi-seq.
Self-organized formation of developing appendages from murine pluripotent stem cells.
Specimen part, Cell line, Subject
View SamplesGrowing evidences are suggesting that extra-long genes in mammals are vulnerable for full-gene length transcription and dysregulation of long genes is a mechanism underlying human genetic disorders. Skeletal muscle expresses Dystrophin which is 2.26 Mbp in length; however, how long-distance transcription is achieved is totally unknown. We had discovered RNA-binding protein SFPQ preferentially binds to long pre-mRNAs and specifically regulates the cluster of neuronal genes > 100 kbp. Here we investigated the roles of SFPQ for long gene expression, target specificities, and also physiological functions in skeletal muscle. Loss of Sfpq selectively downregulated genes >100 kbp including Dystrophin and caused progressive muscle mass reduction and metabolic myopathy characterized by glycogen accumulation and decreased abundance of mitochondrial oxidative phosphorylation complexes. Functional clustering analysis identified metabolic pathway related genes as the targets of SFPQ. These findings indicate target gene specificities and tissue-specific physiological functions of SFPQ in skeletal muscle. Overall design: We analyzed polyA-tailed RNA profiles including transcribing RNAs in gastrocnemius skeletal muscle ( from 3 control and 3 Sfpq-/- P35 male mice) using Ion-proton.
Loss of RNA-Binding Protein Sfpq Causes Long-Gene Transcriptopathy in Skeletal Muscle and Severe Muscle Mass Reduction with Metabolic Myopathy.
Sex, Specimen part, Cell line, Subject
View SamplesGrowing evidences are suggesting that extra-long genes in mammals are vulnerable for full-gene length transcription and dysregulation of long genes is a mechanism underlying human genetic disorders. Skeletal muscle expresses Dystrophin which is 2.26 Mbp in length; however, how long-distance transcription is achieved is totally unknown. We had discovered RNA-binding protein SFPQ preferentially binds to long pre-mRNAs and specifically regulates the cluster of neuronal genes > 100 kbp. Here we investigated the roles of SFPQ for long gene expression, target specificities, and also physiological functions in skeletal muscle. Loss of Sfpq selectively downregulated genes >100 kbp including Dystrophin and caused progressive muscle mass reduction and metabolic myopathy characterized by glycogen accumulation and decreased abundance of mitochondrial oxidative phosphorylation complexes. Functional clustering analysis identified metabolic pathway related genes as the targets of SFPQ. These findings indicate target gene specificities and tissue-specific physiological functions of SFPQ in skeletal muscle. Overall design: We analyzed rRNA-depleted RNA profiles including transcribing RNAs in primary myoblasts obtained from skeletal muscles of 1-month-old SfpqSM-KO (n=1) and control (n=1) mice under differentiated condition using Ion-proton.
Loss of RNA-Binding Protein Sfpq Causes Long-Gene Transcriptopathy in Skeletal Muscle and Severe Muscle Mass Reduction with Metabolic Myopathy.
Subject
View SamplesWe previously found that mice with heterozygous knockout of the alpha-isoform of calcium/calmodulin-dependent protein kinase II (alpha-CaMKII HKO mice) show various dysregulated behaviors, including cyclic variations in locomotor activity (LA), suggesting that alpha-CaMKII HKO mice may serve as an animal model showing infradian oscillation of mood. We performed gene expression microarray analysis of dentate gyrus from alpha-CaMKII HKO mice. Mice were selected for the sampling such that their LA levels varied among the mice.
Circadian Gene Circuitry Predicts Hyperactive Behavior in a Mood Disorder Mouse Model.
Specimen part
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