# _embedded.samples[].characteristics.submission description[].text
Effective anti-viral immunity depends on the ability of infected cells or cells triggered with virus-derived nucleic acids to produce type I interferon (IFN), which activates transcription of numerous antiviral genes. However, disproportionately strong or chronic IFN expression is a common cause of inflammatory and autoimmune diseases. Here we describe an epigenetic mechanism that determines cell-type specific differences in IFN and IFN-stimulated gene expression in response to exogenous signals. We identify di-methylation of histone H3 at lysine 9 (H3K9me2) as a suppressor of IFN and IFN-inducible antiviral gene expression. We show that levels of H3K9me2 at IFN and IFN stimulated genes (ISG) correlate inversely with the scope and amplitude of IFN and ISG expression in fibroblasts and dendritic cells. Accordingly, genetic ablation or pharmacological inactivation of lysine methyltransferase G9a, which is essential for the generation of H3K9me2, resulted in phenotypic conversion of fibroblasts into highly potent IFN-producing cells and rendered these cells resistant to pathogenic RNA viruses. In summary, our studies implicate H3K9me2 and enzymes controlling its abundance as key regulators of innate antiviral immunity. Examination of gene expression in response to PolyI:C in WT and G9a deficient MEFs

# _embedded.samples[].characteristics.submission title[].text
Histone H3 lysine 9 di-methylation as an epigenetic signature of the interferon response (WT and G9a deficient MEFs)

# _embedded.samples[].characteristics.sample title[].text
Uveal melanoma from enucleation 46 [UCSF]

# _embedded.samples[].organization[].Name
Washington University School of Medicine

# _embedded.samples[].characteristics.sample title[].text
Uveal melanoma from enucleation 35 [UCSF]

# _embedded.samples[].organization[].Name
Washington University School of Medicine

# _embedded.samples[].characteristics.description[].text
Epithelial ovarian cancers primary_data_description: Log relative ratio calclulated by Affymetric Genotyping Console

# _embedded.samples[].characteristics.description[].text
Epithelial ovarian cancers primary_data_description: Log relative ratio calclulated by Affymetric Genotyping Console

# _embedded.samples[].characteristics.sample title[].text
Uveal melanoma from enucleation 49 [UCSF]

# _embedded.samples[].organization[].Name
Washington University School of Medicine

# _embedded.samples[].characteristics.description[].text
Epithelial ovarian cancers primary_data_description: Log relative ratio calclulated by Affymetric Genotyping Console

# _embedded.samples[].characteristics.description[].text
This sample is of Antirrhinum majus cv. Maryland True Pink petal tissue harvested seven days after anthesis. It is the third of three biological replicates used in this experiment.

# _embedded.samples[].characteristics.sample source name[].text
Antirrhinum majus cv. Maryland True Pink petal d7

# _embedded.samples[].characteristics.description[].text
Epithelial ovarian cancers primary_data_description: Log relative ratio calclulated by Affymetric Genotyping Console

# _embedded.samples[].characteristics.submission description[].text
Ovarian cancer is characterized by multiple structural aberrations; most are passenger alterations which do not confer tumor growth. Like many cancers, it is a heterogeneous disease and till date, the histotype-specific copy number landscape has been difficult to elucidate. To dissect the heterogeneity of ovarian cancer and understand the pathogenesis of its various histotypes, we developed an in silico hypothesis-driven workflow to identify histotype-specific copy number aberrations across multiple datasets of epithelial ovarian cancer. In concordance with previous studies on global copy number changes, our study showed similar alterations. However, when the landscape was de-convoluted into histotypes, distinct alterations were observed. We report here a comprehensive histotype-specific copy number landscape of ovarian cancer and showed that there is genomic diversity between the histotypes; some involving well known cancer genes and some novel potential driver genes. Besides preferential occurrence of alterations in some histotypes, opposite trends of alteration were observed; such as ERBB2 amplification in mucinous but deletion in serous tumors. The landscape highlights the need for identifying histotype-specific aberrations in ovarian cancer and present potential to tailor management of ovarian cancer based on molecular signature of histotypes. 46 archived frozen tumor samples collected from Department of Obstetrics and Gynecology, Tri-Service General Hospital, Taiwan, containing 9 clear cell, 6 mucinous, and 31 serous. Data was pre-processed and normalized with Hapmap CHB using the Affymetric Genotyping Console.

# _embedded.samples[].characteristics.submission title[].text
The histotype-specific copy-number landscape of ovarian cancer (copy number SNP)

# _embedded.samples[].characteristics.sample title[].text
Uveal melanoma from enucleation 54 [UCSF]

# _embedded.samples[].organization[].Name
Washington University School of Medicine

# _embedded.samples[].characteristics.description[].text
Epithelial ovarian cancers primary_data_description: Log relative ratio calclulated by Affymetric Genotyping Console

# _embedded.samples[].characteristics.submission description[].text
The spinal cord does not spontaneously regenerate after injury and a treatment that ensures functional recovery after spinal cord injury (SCI) is still not available. Recently, fibroblasts have been directly converted into induced neural stem cells (iNSCs) following the forced expression of different combinations of transcription factors. Although directly converted iNSCs have been considered as a potentialcell source for clinical applications, their therapeutic potential has not been investigated yet. Here we show that iNSCs directly converted from mouse fibroblasts enhance the functional recovery after SCI in rats. Mouse embryonic fibroblasts (MEFs) were directly converted into iNSCs using four transcription factors (Brn4, Sox2, Klf4 and c-Myc). iNSCs showed gene expression profiles similar to cNSCs as determined by microarray analysis. MEFs were derived from C3H mouse strain embryos at embryonic day (E)13.5 after removing the head and all internal organs including the gonads and the spinal cord. 5x10^4 fibroblasts were transduced with replication-defective retroviral particles coding for Sox2, Klf4, c-Myc, and Brn4. After 48 h, the transduced fibroblasts were cultured in standard NSC medium. iNSC clusters were observed 4-5 weeks after transduction and expanded. Both MEFs and cNSCs were used as negative and positive control, respectively.

# _embedded.samples[].characteristics.submission title[].text
Therapeutic potential of induced neural stem cells for spinal cord injury

# _embedded.samples[].characteristics.strain[].text
Oregon-R(official name : Oregon-R-modENCODE genotype : wild type )