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accession-icon GSE8702
Longitudinal Analysis of Progression to Androgen Independence
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Following androgen ablation therapy (AAT), the vast majority of prostate cancer patients develop treatment resistance with a median time of 18-24 months to disease progression. To identify molecular targets that aid in prostate cancer cell survival and contribute to the androgen independent phenotype, we evaluated changes in LNCaP cell gene expression during 12 months of androgen deprivation. At time points reflecting critical growth and phenotypic changes, we performed Affymetrix expression array analysis to examine the effects of androgen deprivation during the acute response, during the period of apparent quiescence, and during the emergence of highly proliferative, androgen-independent prostate cancer cells (LNCaP-AI). We discovered alterations in gene expression for a host of molecules associated with promoting prostate cancer cell growth and survival, regulating cell cycle progression, apoptosis and adrenal androgen metabolism, in addition to AR co-regulators and markers of neuroendocrine disease. These findings illustrate the complexity and unpredictable nature of cancer cell biology and contribute greatly to our understanding of how prostate cancer cells likely survive AAT. The value of this longitudinal approach lies in the ability to examine gene expression changes throughout the cellular response to androgen deprivation; it provides a more dynamic illustration of those genes which contribute to disease progression in addition to specific genes which constitute a malignant androgen-independent phenotype. In conclusion, it is of great importance that we employ new approaches, such as the one proposed here, to continue exploring the cellular mechanisms of therapy resistance and identify promising targets to improve cancer therapeutics.

Publication Title

Longitudinal analysis of androgen deprivation of prostate cancer cells identifies pathways to androgen independence.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE40610
Expression data from a Charcot-Marie-Tooth 1B neuropathy mouse model
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

We have generated mouse models of real CMT1B mutations in the gene encoding for myelin protein zero (P0). One of these mutants, P0S63del is retained in the ER where it elicits an unfolded protein response (UPR). Genetic ablation of the UPR factor CHOP restores the motor capacity in S63del mice. We used microarray to decipher the molecular mechanism undelying the P0S63del neuropathy and the rescue in S63del/Chop null nerves.

Publication Title

Resetting translational homeostasis restores myelination in Charcot-Marie-Tooth disease type 1B mice.

Sample Metadata Fields

Age, Specimen part

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accession-icon SRP162549
KMT2B is selectively required for neuronal transdifferentiation [RNAseq]
  • organism-icon Mus musculus
  • sample-icon 457 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Transdifferentiation of fibroblasts into induced Neuronal cells (iNs) by neuronal-specific transcription factors Brn2, Myt1l and Ascl1 is a paradigmatic example of inter-lineage conversion across epigenetically distant cells. Despite tremendous progress on the transcriptional hierarchy underlying transdifferentiation, the enablers of the concomitant epigenome resetting remain to be elucidated. Here we investigated the role of KMT2A and KMT2B, two histone H3 lysine 4 methylases with cardinal roles in development, through individual and combined inactivation. We found that Kmt2b, whose human homologue's mutations cause dystonia, is selectively required for iN conversion through the suppression of the alternative myocyte program and the induction of neuronal maturation genes. Overall design: In order to study the role of KMT2A and KMT2B during transdifferentiation, we employed conditional mouse strains carrying: i) the exon 2 of Kmt2a and/or Kmt2b flanked by LoxP sites; ii) the knock-in of the YFP-coding gene into one Rosa26 allele, downstream of a LoxP-flanked transcription termination cassette (STOP cassette); and iii) the gene coding for the tamoxifen-inducible version of Cre recombinase knocked into the second Rosa26 allele (Glaser et al., 2006; Kranz et al., 2010; Testa et al., 2004). MEFs were derived from Kmt2a (and/or Kmt2b)fl/fl Cre+ YFP+ embryos and from Kmt2a+/+Kmt2b+/+ Cre+ YFP+ or Kmt2afl/+ Cre+ YFP+ for Kmt2a conditional KO (cKO) as controls (Figure 1A), and were subjected to transdifferentiation. After 13 days of BAM treatment, cells were FACS sorted for PSA-NCAM expression, and the transcriptome of positive and negative cells were independently profiled.

Publication Title

KMT2B Is Selectively Required for Neuronal Transdifferentiation, and Its Loss Exposes Dystonia Candidate Genes.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE65754
Expression data from 10 months old sciatic nerves of Sterol regulatory element binding factor 1c (SREBF-1c) KO mice and relative littermates
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

SREBF-1c is a transcription factor regulating fatty acid biosynthesis. We have charaterized the impact of the abcence of SREBF-1c on the development of peripheral neuropathy

Publication Title

Lack of sterol regulatory element binding factor-1c imposes glial Fatty Acid utilization leading to peripheral neuropathy.

Sample Metadata Fields

Age

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accession-icon GSE10389
Identification of Stat5 Target Genes by siRNA-mediated knockdown
  • organism-icon Mus musculus
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)

Description

STAT5A and STAT5B proteins belong to the family of signal transducers and activators of transcription. They are encoded by 2 separate genes with 91% identity in their amino acid sequences. Despite their high degree of conservation, STAT5A and STAT5B exert non-redundant functions, resulting at least in part from differences in target gene activation. To better characterize the differential contribution of STAT5A and STAT5B in gene regulation, we performed single or double knock-down of STAT5A and STAT5B using small interfering RNA. Subsequent gene expression profiling and RT-qPCR analyses of IL-3-stimulated Ba/F3-beta cells led to the identification of putative novel STAT5 target genes. Chromatin immunoprecipitation assays analyzing the corresponding gene loci identified unusual STAT5 binding sites compared to conventional STAT5 responsive elements. Some of the STAT5 targets identified are upregulated in several human cancers, suggesting that they might represent potential oncogenes in STAT5-associated malignancies.

Publication Title

In vivo identification of novel STAT5 target genes.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE76822
Inhibition of Notch pathway arrests PTEN-deficient advanced prostate cancer by triggering p27-driven cellular senescence
  • organism-icon Mus musculus
  • sample-icon 7 Downloadable Samples
  • Technology Badge IconIllumina MouseRef-8 v2.0 expression beadchip

Description

we evaluated the mechanism behind NOTCH activation in prostate cancer

Publication Title

Inhibition of Notch pathway arrests PTEN-deficient advanced prostate cancer by triggering p27-driven cellular senescence.

Sample Metadata Fields

Specimen part

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accession-icon GSE5620
AtGenExpress: Stress Treatments (Control plants)
  • organism-icon Arabidopsis thaliana
  • sample-icon 35 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

AtGenExpress: A multinational coordinated effort to uncover the transcriptome of the multicellular model organism Arabidopsis thaliana

Publication Title

The AtGenExpress global stress expression data set: protocols, evaluation and model data analysis of UV-B light, drought and cold stress responses.

Sample Metadata Fields

Specimen part

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accession-icon GSE5628
AtGenExpress: Stress Treatments (Heat stress)
  • organism-icon Arabidopsis thaliana
  • sample-icon 31 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

AtGenExpress: A multinational coordinated effort to uncover the transcriptome of the multicellular model organism Arabidopsis thaliana.

Publication Title

The AtGenExpress global stress expression data set: protocols, evaluation and model data analysis of UV-B light, drought and cold stress responses.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE5627
AtGenExpress: Stress Treatments (Wounding stress)
  • organism-icon Arabidopsis thaliana
  • sample-icon 25 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

AtGenExpress: A multinational coordinated effort to uncover the transcriptome of the multicellular model organism Arabidopsis thaliana.

Publication Title

The AtGenExpress global stress expression data set: protocols, evaluation and model data analysis of UV-B light, drought and cold stress responses.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE5626
AtGenExpress: Stress Treatments (UV-B stress)
  • organism-icon Arabidopsis thaliana
  • sample-icon 26 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

AtGenExpress: A multinational coordinated effort to uncover the transcriptome of the multicellular model organism Arabidopsis thaliana.

Publication Title

The AtGenExpress global stress expression data set: protocols, evaluation and model data analysis of UV-B light, drought and cold stress responses.

Sample Metadata Fields

Specimen part

View Samples
...

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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