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accession-icon GSE63941
Expression data from cultured human esophageal squamous cell carcinoma cell lines and cultured human fibroblasts.
  • organism-icon Homo sapiens
  • sample-icon 26 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Cancer cells express different sets of receptor type tyrosine kinases. These receptor kinases may be activated through autocrine or paracrine mechanisms. Fibroblasts may modify the biologic properties of surrounding cancer cells through paracrine mechansms.

Publication Title

The role of HGF/MET and FGF/FGFR in fibroblast-derived growth stimulation and lapatinib-resistance of esophageal squamous cell carcinoma.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE57429
Expression data from FIT-039 or Flavopiridol compound treated HeLa cells
  • organism-icon Homo sapiens
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

FIT-039 is a novel antiviral compound. Antiviral mechanism of FIT-039 is the inhibition of the viral transcription through suppression of the CTD phosphorylation of RNA polymerase II.

Publication Title

CDK9 inhibitor FIT-039 prevents replication of multiple DNA viruses.

Sample Metadata Fields

Cell line

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accession-icon GSE62947
Expression Data from DMSO or SRPIN803 treated ARPE-19 cells
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

We used microarrays to evaluate the effect of SRPIN803 on gene expression in ARPE-19 cells.

Publication Title

Identification of a Dual Inhibitor of SRPK1 and CK2 That Attenuates Pathological Angiogenesis of Macular Degeneration in Mice.

Sample Metadata Fields

Cell line

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accession-icon GSE58038
Exon Level Expression Profiling: a Novel Unbiased Transcriptome
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [probe set (exon) version (huex10st)

Description

Transcriptome analysis of the effect of RECTAS on fibroblast cells derived from a familial dysautonomia patient.

Publication Title

Rectifier of aberrant mRNA splicing recovers tRNA modification in familial dysautonomia.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE9244
WT vs Klf5 KO ES
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Homozygous disruption of Bteb2/Klf5, a homolog of Drosophila gap gene Krppel, led to increased expression of various differentiation marker genes, such as Fgf5, Cdx2, and Brachyury in mouse ES cells without compromising their ability to differentiate into all three germ layers. Upon removal of LIF, Klf5-deficient ES cells showed faster differentiation kinetics than wild-type ES cells. In contrast, overexpression of Klf5 in ES cells suppressed the transcription of differentiation marker genes, and maintained pluripotency in the absence of LIF. In order to search downstream genes of Klf5, we surveyed genes implicated in ES cell proliferation by microarray analysis

Publication Title

Krüppel-like factor 5 is essential for blastocyst development and the normal self-renewal of mouse ESCs.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE52298
Expression data from Arabidopsis myb3r mutants
  • organism-icon Arabidopsis thaliana
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

Temporal and spatial regulation of cell division is central for generating multicellular organs with predictable sizes and shapes. However, it remains largely unclear how genes with mitotic functions are transcriptionally regulated during organogenesis in plants. Here, we showed that a group of R1R2R3-Myb transcription factors are responsible for developmentally controlled downregulation of variety of mitotic genes in Arabidopsis. Loss of their functions resulted in elevated expression of mitotic genes in quiescent cells including those underwent terminal differentiation. Concomitantly, their mutations enhanced cell division activities in various aspects of plant development, generating organs with increased sizes and irregular architectures. In addition, we showed that this type of R1R2R3-Myb proteins are required for oscillated expression of G2/M-specfiic genes, most likely by inhibiting transcription outside of G2/M in the cell cycle. Our finding uncovered a novel plant-specific mechanism in which scheduled expression of G2/M-specific genes may require their global repression both in the cell cycle and during development.

Publication Title

Transcriptional repression by MYB3R proteins regulates plant organ growth.

Sample Metadata Fields

Specimen part

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accession-icon GSE56026
Gene expression in human endometrial cancer tissues and serous papillary endometrial cancer cell line, SPAC-1L, treated by STAT1-siRNA and/or IFN-gamma
  • organism-icon Homo sapiens
  • sample-icon 71 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Endometrial cancer is one of the most common gynecologic malignancies, and patients with high grade disease, especially serous papillary subtype (SPEC) are often related to the poor outcomes. Recent genome-wide analyses have revealed that SPEC exhibits gene expression profiles that are distinct from the endometrioid histologic subtype; therefore, it is important to identify the SPEC driver genes or pathways responsible for the inherently aggressive phenotypes and to develop SPEC-specific therapies to target these driver genes or pathways.

Publication Title

STAT1 drives tumor progression in serous papillary endometrial cancer.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon SRP186367
Loss of RNA-binding protein Sfpq causes long-gene transcriptopathy in skeletal muscle and severe muscle mass reduction with metabolic myopathy (skeletal muscle, mRNA-seq)
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIon 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

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accession-icon SRP124852
Loss of RNA-binding protein Sfpq causes long-gene transcriptopathy in skeletal muscle and severe muscle mass reduction with metabolic myopathy (Primary culture, rRNA depleted RNA-seq)
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIon 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

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accession-icon SRP058842
PGC reversion to pluripotency involves erasure of DNA methylation from imprinting control centers followed by locus-specific re-methylation
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Primordial germ cells (PGCs) are fate restricted to differentiate into gametes in vivo. However when removed from their embryonic niche PGCs undergo reversion to generate pluripotent embryonic germ cells (EGCs) in vitro. One of the major differences between EGCs and embryonic stem cells (ESCs) involves variable methylation at imprinting control centers (ICCs), a phenomenon that is poorly understood. In the current study we show that reverting PGCs to EGCs involves ICC methylation erasure, which remain stably hypomethylated at Snrpn, Igf2r and Kcnqot1. In contrast, the H19/Igf2 ICC undergoes almost complete de novo remethylation. Using the same approach for PGCs differentiated in vitro from ESCs we show that the Snrpn ICC is erased however the hypomethylated state is highly unstable. We also discovered that when the H19/Igf2 ICC is abnormally hypermethylated in ESCs, ICC methylation is not erased with differentiation into PGCs. This highlights the importance of not only launching germline differentiation with correctly methylated ESC lines but also the need to better stabilize the hypomethylated state in the in vitro derivatives following ICC erasure. Overall design: RNA seq of E9.5 PGCs, iPGCs, PGCLCs and EGCs using small cell numbers from start. N=2 biological replicates in 2 technical sequencing replicates.

Publication Title

PGC Reversion to Pluripotency Involves Erasure of DNA Methylation from Imprinting Control Centers followed by Locus-Specific Re-methylation.

Sample Metadata Fields

No sample metadata fields

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refine.bio is a repository of uniformly processed and normalized, ready-to-use transcriptome data from publicly available sources. refine.bio is a project of the Childhood Cancer Data Lab (CCDL)

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Developed by the Childhood Cancer Data Lab

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Cite refine.bio

Casey S. Greene, Dongbo Hu, Richard W. W. Jones, Stephanie Liu, David S. Mejia, Rob Patro, Stephen R. Piccolo, Ariel Rodriguez Romero, Hirak Sarkar, Candace L. Savonen, Jaclyn N. Taroni, William E. Vauclain, Deepashree Venkatesh Prasad, Kurt G. Wheeler. refine.bio: a resource of uniformly processed publicly available gene expression datasets.
URL: https://www.refine.bio

Note that the contributor list is in alphabetical order as we prepare a manuscript for submission.

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