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accession-icon GSE20918
GENE EXPRESSION ALTERATIONS IN ADULT UTP14b (jsd) MICE BY CONDITIONAL KNOCKOUT OF ANDROGEN RECEPTOR IN SERTOLI CELLS
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Spermatogenesis is dependent primarily on testosterone action on the Sertoli cells. Although the identification of testosterone-regulated target genes in Sertoli cells has been approached using microarray analysis to compare gene expression in mice with androgen receptor (AR) elimination in the Sertoli cells (SCARKO) and wild type mice, the analysis has been complicated by alteration of germ cell composition of the testis when pubertal or adult mice were used and differences in Sertoli-cell gene expression from those in adult when prepubertal mice were used. Since the testicular cell components of adult jsd (Utp14bjsd ,juvenile spermatogonial depletion) mice and SCARKO-jsd mice are essentially identical, consisting of only type A spermatogonia and somatic cells, comparisons of gene expression profiles between jsd and SCARKO-jsd testes would identify AR regulated genes in adult Sertoli cells, with minimum effects of cell number changes. Microarray analysis identified 161 genes as downregulated and 202 genes as upregulated in the SCARKO-jsd mice compared to jsd mice. Some of the genes identified in the previous studies, including Rhox5, Drd4, and Fhod3, were also AR-regulated in the jsd testes but others, such as proteases and components of junctional complexes, were not androgen regulated in our model. Surprisingly, a set of germ-cell-specific genes preferentially expressed in differentiated spermatogonia and meiotic cells, including Meig1, Sycp3, and Ddx4, were all upregulated about 2-fold in SCARKO-jsd testes, demonstrating that, although there was no significant differentiation to spermatocytes in SCARKO-jsd mice, AR-regulated genes in Sertoli cells are involved in the regulation of spermatogonial differentiation. Further gene ontogeny analysis revealed possible sets of genes whose expression changes may be involved in the disruption of Sertoli cell organization in SCARKO-jsd testes.

Publication Title

Gene expression alterations by conditional knockout of androgen receptor in adult sertoli cells of Utp14b(jsd/jsd) (jsd) mice.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE15243
Hormone effects on gene expression in somatic cells of rat testes (Rattus norvegicus)
  • organism-icon Rattus norvegicus
  • sample-icon 35 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

Analysis of hormone effects on irradiated LBNF1 rat testes, which contain only somatic cells except for a few type A spermatgogonia. Rats were treated for 2 weeks with either sham treatment (group X), hormonal ablation (GnRH antagonist and the androgen receptor antagonist flutamide, group XAF), testosterone supplementation (GnRH antagonist and testosterone, group XAT), and FSH supplementation ((GnRH antagonist, androgen receptor antagonist, and FSH, group XAFF). Results provide insight into identifying genes in the somatic testis cells regulated by testosterone, LH, or FSH.

Publication Title

Changes in gene expression in somatic cells of rat testes resulting from hormonal modulation and radiation-induced germ cell depletion.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE15223
Radiation effects on gene expression in rat testes (Rattus norvegicus)
  • organism-icon Rattus norvegicus
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

Analysis of LBNF1 rat testes from controls, containing both somatic and all germ cell types and from irradiated rats in which all cells germ cells except type A spermatgogonia are eliminated. Results provide insight into distinguishing germ and somatic cell genes and identification of somatic cell genes that are upregulated after irradiation.

Publication Title

Changes in gene expression in somatic cells of rat testes resulting from hormonal modulation and radiation-induced germ cell depletion.

Sample Metadata Fields

Specimen part

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accession-icon GSE24672
Estrogen regulated genes in rat testes and their relationship to recovery of spermatogenesis after irradiation
  • organism-icon Rattus norvegicus
  • sample-icon 31 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

Despite numerous observations of effects of estrogens on spermatogenesis, identification of estrogen-regulated genes in the testis is limited. We previously showed in rats, in which irradiation had completely blocked spermatogonial differentiation, that testosterone (T) suppression with GnRH-antagonist and antiandrogen stimulated spermatogenic recovery and addition of estradiol (E2) to this regimen accelerated this recovery. We report here the global changes in testicular cell gene expression induced by the E2 treatment. By minimizing the changes in other hormones and also having concurrent data on the regulation of the genes by those hormones, we were able to dissect the effects of estrogen on gene expression, independent of gonadotropin or T changes. Expression of 20 genes, largely in somatic cells, was up- or down-regulated between 2- and 5-fold by E2. There were also early germ cell genes whose expression increased but this was a result of a small increase in spermatogonial numbers. The striking enrichment of transcripts not corresponding to known genes among the E2-downregulated probes led to the identification of one as micro-RNA miR-34a. We propose that genes whose expression levels are altered in one direction by irradiation and in the opposite direction by both T suppression and E2 treatment are candidates for controlling the block in differentiation. Several genes, including insulin-like 3 (Insl3), satisfied those criteria. If they are indeed involved in the inhibition of spermatogonial differentiation, they may be candidate targets for clinical treatments to enhance recovery of spermatogenesis following gonadotoxic exposures, such as those resulting from cancer therapy.

Publication Title

Estrogen-regulated genes in rat testes and their relationship to recovery of spermatogenesis after irradiation.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon SRP026382
A miR-155-ruled microRNA hierarchy in dendritic cell maturation and macrophage activation
  • organism-icon Mus musculus
  • sample-icon 20 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 1000

Description

MicroRNAs (miRNAs) are small RNAs that play important regulatory roles in many cellular pathways. MiRNAs associate with members of the Argonaute (Ago) protein family and bind to partially complementary sequences on mRNAs and induce translational repression or mRNA decay. MiRNA expression can be controlled by transcription factors and can therefore be cell type- or tissue-specific. Here we have analyzed miRNA expression profiles in murine monocyte-derived dendritic cells (DCs) and macrophages upon stimulation with LPS, LDL, eLDL and oxLDL to identify not only stimuli-specific miRNA, but also to identify a hierarchical miRNA system involving miR-155. For this, miR-155 knockout dendritic cells and macrophages were also sequenced using the same stimuli. Overall design: Sequencing of murine monocyte-derived dendritic cells and macrophages (each wild type and miR-155 knock out cells) matured and stimulated, respectively, by LPS, oxLDL, eLDL or LDL.

Publication Title

A miR-155-dependent microRNA hierarchy in dendritic cell maturation and macrophage activation.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE37714
Mammalian TRIM71 as repressor of mRNAs that inhibits translation and affects mRNA stability
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

The mammalian TRIM-NHL protein TRIM71/LIN-41 is a repressor of mRNA function.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE37713
Expression data from HEK293 Flp-In cells constitutivly expressing FLAG-HA-tagged TRIM71 and that of the parental cell line
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

We identify mammalian TRIM71 as repressor of mRNAs that inhibits translation and affects mRNA stability.

Publication Title

The mammalian TRIM-NHL protein TRIM71/LIN-41 is a repressor of mRNA function.

Sample Metadata Fields

Cell line

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accession-icon SRP019990
miRNAs associated with the different human Argonaute proteins
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer IIx

Description

microRNAs (miRNAs) are small non-coding RNAs that function in literally all cellular processes. miRNAs interact with Argonaute (Ago) proteins and guide them to specific target sites located in the 3’ untranslated region (UTR) of target mRNAs leading to translational repression and deadenylation-induced mRNA degradation. Most miRNAs are processed from hairpin-structured precursors by the consecutive action of the RNase III enzymes Drosha and Dicer. However, processing of miR-451 is Dicer-independent and cleavage is mediated by the endonuclease Ago2. Here we have characterized miR-451 sequence and structure requirements for processing as well as sorting of miRNAs into different Ago proteins. Pre-miR-451 appears to be optimized for Ago2 cleavage and changes result in reduced processing. In addition, we show that the mature miR-451 only associates with Ago2 suggesting that mature miRNAs are not exchanged between different members of the Ago protein family. Based on cloning and deep sequencing of endogenous miRNAs associated with Ago1-3, we do not find evidence for miRNA sorting in human cells. However, Ago identity appears to influence the length of some miRNAs, while others remain unaffected. Overall design: Examination of miRNAs associated with endogenous human Ago1-4 in HeLa cells

Publication Title

microRNAs associated with the different human Argonaute proteins.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE37712
Expression data from mouse embryonic stem cells upon TRIM71 KD and parental ctrl cells
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

We identify mammalian TRIM71 as repressor of mRNAs that inhibits translation and affects mRNA stability. In this data set we compare the expression profile of mouse ES upon Trim71 KD versus that of the parental cells.

Publication Title

The mammalian TRIM-NHL protein TRIM71/LIN-41 is a repressor of mRNA function.

Sample Metadata Fields

Specimen part

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accession-icon GSE57674
siPools: highly complex but accurately defined siRNA pools eliminate Off-target effects
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.0 ST Array (hugene20st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

siPools: highly complex but accurately defined siRNA pools eliminate off-target effects.

Sample Metadata Fields

Cell line

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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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