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DRP000898
Caenorhabditis elegans
2 Downloadable Samples
Illumina Genome Analyzer IIx
Description
Poly(A)+ RNAs were fragmented and sequenced. Poly(A)+ RNAs were fragmented and sequenced.
Publication Title
Position-dependent and neuron-specific splicing regulation by the CELF family RNA-binding protein UNC-75 in Caenorhabditis elegans.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 27 Downloadable Samples
- Illumina HiSeq 1500
Description
We 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.
Publication Title
Self-organized formation of developing appendages from murine pluripotent stem cells.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Mus musculus
- 6 Downloadable Samples
- Ion Torrent Proton
Description
Growing 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.
Publication Title
Loss of RNA-Binding Protein Sfpq Causes Long-Gene Transcriptopathy in Skeletal Muscle and Severe Muscle Mass Reduction with Metabolic Myopathy.
Sample Metadata Fields
Sex, Specimen part, Cell line, Subject
View Samples- Mus musculus
- 2 Downloadable Samples
- Ion Torrent Proton
Description
Growing 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.
Publication Title
Loss of RNA-Binding Protein Sfpq Causes Long-Gene Transcriptopathy in Skeletal Muscle and Severe Muscle Mass Reduction with Metabolic Myopathy.
Sample Metadata Fields
Subject
View Samples GSE19251- Mus musculus
- 2 Downloadable Samples
Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
High dietary fat intake is a major risk factor for the development of obesity, which is frequently associated with diabetes. To identify genes involved in diabetic nephropathy, GeneChip Expression Analysis was employed to survey the glomerular gene expression profile in diabetic KK/Ta mice fed with a high-fat diet (HFD).
Publication Title
Mindin: a novel marker for podocyte injury in diabetic nephropathy.
Sample Metadata Fields
Sex, Age
View Samples- Homo sapiens
- 15 Downloadable Samples
- Illumina HiSeq 1500
Description
Seckel syndrome (SS) is a rare spectrum of congenital severe microcephaly and dwarfism. One SS-causative gene is Ataxia Telangiectasia and Rad3-Related Protein (ATR), and ATR (c.2101 A>G) mutation causes skipping of exon 9, resulting in a hypomorphic ATR defect in patients. Because ATR governs DNA repair response, the mutation has been considered the cause of an impaired response to DNA replication stress in neuronal progenitor cells (NPCs), which is associated with the pathogenesis of microcephaly. However, the precise mechanism through which the mutation causes SS remains unclear. To address this issue, we established induced pluripotent stem cells (iPSCs) from fibroblasts carrying the ATR mutation and an isogenic ATR-corrected counterpart iPSC clone by genome editing. Interestingly, SS-patient-derived iPSCs (SS-iPSCs) exhibited cell type-specific splicing; exon 9 was dominantly skipped in fibroblasts and iPSC-derived NPCs, but it was included in undifferentiated iPSCs and definitive endodermal cells. SS-iPSC-derived NPCs (SS-NPCs) showed distinct expression profiles from ATR non-mutated NPCs. In SS-NPCs, abnormal mitotic spindles were observed more frequently than in gene-corrected counterparts, and the alignment of NPCs in the surface of the neurospheres was perturbed. Finally, we tested several splicing-modifying compounds and found that a CLK1 inhibitor, TG003, could pharmacologically rescue the exon 9 skipping in SS-NPCs. Furthermore, treatment with TG003 restored the function of ATR in SS-NPCs and decreased the frequency of abnormal mitotic events. In conclusion, our iPSC model of SS revealed a novel function of the ATR mutation in NPCs and NPC-specific missplicing, proving its usefulness for dissecting the pathophysiology of ATR-SS. Overall design: RNA-sequencing was conducted to identify the transcriptomic profiling of iPSC-derived cells
Publication Title
Verification and rectification of cell type-specific splicing of a Seckel syndrome-associated ATR mutation using iPS cell model.
Sample Metadata Fields
Specimen part, Subject
View Samples- Homo sapiens
- 13 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
<Objective> To compare gene expression in labial salivary glands (LSG) of IgG4-related disease (IgG4-RD) with Sjgrens syndrome (SS).
Publication Title
DNA microarray analysis of labial salivary glands in IgG4-related disease: comparison with Sjögren's syndrome.
Sample Metadata Fields
Sex, Specimen part
View Samples- Homo sapiens
- 4 Downloadable Samples
- IonTorrentProton
Description
We 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.
Publication Title
Downregulation of neuropilin-1 on macrophages modulates antibody-mediated tumoricidal activity.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 5 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Tp80 is a novel antiviral compound. Antiviral mechanism of Tp80 is the inhibition of the viral genome replication through the recoverly of GPx2 expression downregulated by HCV infection.
Publication Title
Retinoid derivative Tp80 exhibits anti-hepatitis C virus activity through restoration of GI-GPx expression.
Sample Metadata Fields
Specimen part, Cell line, Treatment
View Samples- Mus musculus
- 23 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
To test TWEAK/Fn14 pathway and relative agents in chronic TNBS colitis
Publication Title
TWEAK/Fn14 pathway promotes a T helper 2-type chronic colitis with fibrosis in mice.
Sample Metadata Fields
Specimen part
View Samples