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accession-icon GSE30683
ETV5 Mediated Downstream Gene Activation in Spermatogonial Stem Cells
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Insight into mechanisms controlling gene expression in the spermatogonial stem cell (SSC) will improve our understanding of the processes regulating spermatogenesis and aid in treating problems associated with male infertility.

Publication Title

Spermatogonial stem cell self-renewal requires ETV5-mediated downstream activation of Brachyury in mice.

Alternate Accession IDs

E-GEOD-30683

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE15652
GDNF-Regulated Gene Expression in Cultures of Rat Spermatogonial Stem Cells
  • organism-icon Rattus norvegicus
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

Expression of GDNF-regulated genes was studied in cultures of self-renewing rat spermatogonial stem cells established from 8-10 day old rat pups maintained in a defined serum free medium. GDNF is the primary regulator of spermatogonial stem cell self renewal in the rat.

Publication Title

Identification of glial cell line-derived neurotrophic factor-regulated genes important for spermatogonial stem cell self-renewal in the rat.

Alternate Accession IDs

E-GEOD-15652

Sample Metadata Fields

Specimen part

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accession-icon GSE14222
Gene Expression Profiling of the SSC-Enriched Thy1+ and SSC-Depleted Thy1- Fractions of Prepubertal Mouse Testes
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Self-renewal and differentiation of spermatogonial stem cells (SSCs) provides the foundation for testis homeostasis, yet mechanisms that control their functions in mammals are poorly defined. We used microarray transcript profiling to identify specific genes whose expression are augmented in the SSC-enriched Thy1+ germ cell fraction of mouse pup testes. Comparisons of gene expression in the Thy1+ germ cell fraction to the Thy1-depeleted testis cell population identified 202 genes that are expressed 10-fold or higher in Thy1+ cells. This database provided a mining tool to investigate specific characteristics of SSCs and identify novel mechanisms that potentially influence their functions.

Publication Title

Colony stimulating factor 1 is an extrinsic stimulator of mouse spermatogonial stem cell self-renewal.

Alternate Accession IDs

E-GEOD-14222

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP006999
Sequencing of microRNA in spermatogonial stem cell enriched cell populations.
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer II

Description

MicroRNAs (miRs) play a key role in the control of gene expression in a wide array of tissue systems where their functions include the regulation of self-renewal, cellular differentiation, proliferation, and apoptosis. However, the functional importance of individual miRs in controlling spermatogonial stem cell (SSC) homeostasis has not been investigated. Using high-throughout sequencing, we profiled the expression of miRs in the Thy1+ testis cell population, which is highly enriched for SSCs, and the Thy1- cell population, composed primarily of testis somatic cells. In addition, we profiled the global expression of miRs in cultured germ cells, also enriched for SSCs. Our results demonstrate that miR-21, along with miR-34c, -182, -183, -146a, -465a-3p, -465b-3p, -465c-3p, and -465c-5p are preferentially expressed in the Thy1+ SSC-enriched population, as compared to Thy1- somatic cells, and we further observed that Thy1+ SSC-enriched testis cells and SSC-enriched cultured germ cells share remarkably similar miR expression profiles. Overall design: Spermatogonial Stem Cell enriched cell populations (freshly isolated and short-term cultured) and somatic cell populations were isolated from C57B/L6 mouse donors and subjected to small RNA isolation and sequencing.

Publication Title

MicroRNA-21 regulates the self-renewal of mouse spermatogonial stem cells.

Alternate Accession IDs

GSE29613

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE18914
Prepubertal Human Spermatogonia and Mouse Gonocytes Share Conserved Gene Expression of Germline Stem Cell Regulatory
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Full title: Prepubertal Human Spermatogonia and Mouse Gonocytes Share Conserved Gene Expression of Germline Stem Cell Regulatory Molecules

Publication Title

Prepubertal human spermatogonia and mouse gonocytes share conserved gene expression of germline stem cell regulatory molecules.

Alternate Accession IDs

E-GEOD-18914

Sample Metadata Fields

Age

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accession-icon GSE27043
Expression data from aged spermatogonial stem cells
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

In vitro and in vivo aging of mouse spermatogonial stem cells alters stem cell function based on quantitative spermatogonial stem cell transplantation analyses.

Publication Title

In vivo and in vitro aging is detrimental to mouse spermatogonial stem cell function.

Alternate Accession IDs

E-GEOD-27043

Sample Metadata Fields

Specimen part

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accession-icon GSE57061
Expression data for Lck-Cre, Med23flox/flox and Med23flox/flox;Lck-Cre thymocytes +/- 3hr exposure to plate bound anti-CD3 antibody
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)

Description

MED23, a subunit of the Mediator coactivator complex, is important for the expression of a subset of MAPK/ERK pathway-dependent target genes; however, the genes in this subset varies between cell types. MAPK/ERK pathway-dependent processes are essential for T-cell development and function, but whether MED23 has a role in this context is unknown. We generated Med23 conditional knockout mice and induced Med23 deletion in early T cell development using the lineage specific Lck-Cre transgene. While the total cell number and distribution of cell populations in the thymuses of Med23flox/flox;Lck-Cre mice were essentially normal, MED23 null T-cells failed to efficiently populate the peripheral lymphoid organs. MED23 null thymocytes displayed decreased expression of the MAPK/ERK-responsive genes Egr1, Egr2, as well as of the membrane glycoprotein Cd52 (CAMPATH-1). MED23 null CD4 single-positive thymocytes also showed decreased expression of KLF2 (LKLF), a T cell master regulatory transcription factor. Indeed, similarities between the phenotypes of mice lacking MED23 or KLF2 in T-cells suggest that KLF2 deficiency in MED23 null T-cells is one of their key defects. Mechanistic experiments using MED23 null MEFs further suggest that MED23 is required for full activity of the MAPK-responsive transcription factor MEF2, which has previously been shown to mediate Klf2 expression. In summary, our data indicate that MED23 has critical roles in enabling T-cells to populate the peripheral lymphoid organs, possibly by potentiating MEF2-dependent expression of the T-cell transcription factor KLF2.

Publication Title

T-cells null for the MED23 subunit of mediator express decreased levels of KLF2 and inefficiently populate the peripheral lymphoid organs.

Alternate Accession IDs

E-GEOD-57061

Sample Metadata Fields

Sex, Specimen part

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accession-icon SRP069029
PROP1 triggers epithelial-mesenchymal transition-like process in pituitary stem cells [RNA-Seq]
  • organism-icon Mus musculus
  • sample-icon 144 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Mutations in PROP1 are the most common cause of hypopituitarism in humans; therefore, unraveling its mechanism of action is highly relevant from a therapeutic perspective. Our current understanding of the role of PROP1 in the pituitary gland is limited to the regulation of pituitary transcription factors Hesx1 and Pit1. To elucidate the comprehensive PROP1-dependent gene regulatory network, we conducted genome wide analysis of PROP1 DNA binding and effects on gene expression in mutant tissues, isolated stem cells and engineered cell lines. We determined that PROP1 is essential for maintaining proliferation of stem cells and stimulating them to undergo an epithelial to mesenchymal transition-like process necessary for cell migration and differentiation. Genomic profiling reveals that PROP1 binds to and represses claudin 23, characteristic of epithelial cells, and it activates EMT inducer genes: Zeb2, Notch2 and Gli2. Our findings identify PROP1 as a central transcriptional component of pituitary stem cell differentiation. Overall design: Pituitary Colony forming cells mRNA of 13-day old wild type (Prop1 +/+), Prop1 mutants (Prop1df/df), wild type (Pit1+/+) and Pit1 mutants (Pit1 dw/dw) mice were generated by deep sequencing, in triplicates.

Publication Title

PROP1 triggers epithelial-mesenchymal transition-like process in pituitary stem cells.

Alternate Accession IDs

GSE77357

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE10422
Traf2 and Traf3 B cell knockout mice and Baff tg mice - gene expression in lymph node B cells
  • organism-icon Mus musculus
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Tumor necrosis factor-associated factors 2 and 3 (TRAF2 and TRAF3) were shown to function in a co-operative and non-redundant manner to suppress nuclear factor-B2 (NF-B2) activation, gene expression and survival in mature B cells. In the absence of this suppressive activity, B cells developed independently of the obligatory B cell survival factor, BAFF (B cell activating factor of the tumor necrosis factor family). This constitutive, lineage-specific suppression of B cell survival by TRAF2 and TRAF3 determines the requirement for BAFF to sustain B cell development in vivo. We wished to investigate the effect on gene expression in B cells which lacked the negative regulators TRAF2 and TRAF3, and hence had hyperactive NF-kB2 signalling. As Baff-tg mice display a similar phenotype, and have a genetic modification which acts in the same pathway, yet further up, than TRAF2 and TRAF3, we wished to compare and contrast Baff-tg B cells with TRAF2 and TRAF3 deficient B cells. This analysis should identify genes that are important in B cell survival.

Publication Title

TRAF2 and TRAF3 signal adapters act cooperatively to control the maturation and survival signals delivered to B cells by the BAFF receptor.

Alternate Accession IDs

E-GEOD-10422

Sample Metadata Fields

Sex, Age

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accession-icon E-MEXP-215
Transcription profiling of mesenchymal stem cells (MSC) maintained in FCS or autologous serum over time analysed at passage 4 and 10
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

The purpose of this study was to determine whether the serum condition affected the gene expression in mesenchymal stem cells (MSCs)over time. To that end, we compared gene expression in MSCs maintained in regular growth medium supplemented with fetal calf serum (FCS) for 10 passages with gene expression of MSCs cultured in the same conditions for 4 passages for 2 different donors (i.e. donor3 and donor4). Likewise, we compared gene expression in MSCs maintained in regular growth medium supplemented with autologous serum(AS) for 10 passages with gene expression of MSCs cultured in the same conditions for 4 passages for the same 2 donors (i.e. donor3 and donor4). MSCs were cultured in FCS- or AS-supplemented medium and were analyzed at passage 4 and at passage 10.

Publication Title

In vitro expansion of human mesenchymal stem cells: choice of serum is a determinant of cell proliferation, differentiation, gene expression, and transcriptome stability.

Alternate Accession IDs

None

Sample Metadata Fields

Sex, Specimen part, Subject

View Samples
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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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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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