We developed a Tet-inducible system to express deltaNp63alpha isoform under the control of keratin 5 promoter. Transgenic mice, which were Bigenic (BG) developed a severe skin phenotype with abnormal keratinocyte differentiation and defects in hair follicle development and cycling. Skin samples from transgenic animals and wild type animals were analyzed for global transcriptome changes.
Abnormal hair follicle development and altered cell fate of follicular keratinocytes in transgenic mice expressing DeltaNp63alpha.
Specimen part
View SamplesAnalysis of gene expression changes during mouse salivary gland development using RNA-Seq Overall design: RNA was collected and analyzed for at least two biological replicates each from six developmental timepoints (E14.5, E16.5, E18.5, P5, 4 weeks, 12 weeks)
RNA-seq based transcriptomic map reveals new insights into mouse salivary gland development and maturation.
Age, Specimen part, Cell line, Subject
View SamplesAnalysis of gene-probe expression data (FPKM) for HNSCC cell-lines using single-end RNA-Seq Overall design: RNA was collected and analyzed from 6 HNSCC cell-lines ( SCC15, SCC4, SCC71, UMSCC103, UMSCC29, SCC351)
A global analysis of the complex landscape of isoforms and regulatory networks of p63 in human cells and tissues.
No sample metadata fields
View SamplesAnalysis of protein tyrosine phosphatase 1B (PTP1B) deficient mammary glands from nulliparous mice at estrous and pregnancy day 3, 7, 10 and 15. We used a genetically ablated PTP1B mouse model to gain a deeper knowledge of the role PTP1B plays in mammary gland development and to define the mechanism regulated by this phosphatase.
Protein tyrosine phosphatase 1B restrains mammary alveologenesis and secretory differentiation.
Specimen part
View SamplesTranscriptomics analyses in these Zn-deficient rats revealed the molecular basis of ESCC abrogation by miR-31 knockout: Egln3, a negative regulator of NF-FB, was shown to be a direct miR-31 target; miR-31 inhibition/deletion resulted in suppression of miR-31-associated-EGLN3-NF-KB controlled inflammatory pathways.
Abrogation of esophageal carcinoma development in miR-31 knockout rats.
Treatment
View SamplesAnalysis of hepatic gene expression in mice transiently overexpressing Bcl2 Overall design: 3 control GFP mice and 5 GFP-Bcl2 mice, 8 mouse liver samples total
Bcl2 is a critical regulator of bile acid homeostasis by dictating Shp and lncRNA H19 function.
No sample metadata fields
View SamplesAutophagy is a homeostatic cellular process involved in the degradation of long-lived/damaged cellular components. The role of autophagy in adipogenesis is well recognized, but its role in mature adipocyte function is largely unknown. We show that the autophagy proteins Atg3 and Atg16L1 are required for proper mitochondrial function in mature adipocytes. In contrast to previous studies, we found that post-developmental ablation of autophagy causes peripheral insulin resistance independently of diet or adiposity. Finally, lack of adipocyte autophagy reveals a - cross talk between fat and liver mediated by lipid peroxide-induced Nrf2 signaling. Our data reveal a - role for autophagy in preventing lipid peroxide formation and their transfer in insulin-sensitive peripheral tissues Overall design: Epididymal adipose tissue from 4 WT and 4 Adiponectin-Cre Atg3f/f male mice fed chow diet
Autophagy Ablation in Adipocytes Induces Insulin Resistance and Reveals Roles for Lipid Peroxide and Nrf2 Signaling in Adipose-Liver Crosstalk.
Specimen part, Cell line, Subject
View SamplesWe developed conditional knockout mice where the transcription factor Elf5 (also called ESE-2) is deleted in the mammary glands. Loss of Elf5 results in block in alveologenesis and epithelial differentiation defects. Mammary gland samples from Elf5 knockout and wild type animals were analyzed for global transcriptome changes.
Elf5 inhibits the epithelial-mesenchymal transition in mammary gland development and breast cancer metastasis by transcriptionally repressing Snail2.
Specimen part
View SamplesThe role of estrogen and testosterone in the regulation of gene expression in the proximal reproductive tract is not completely understood. To address this question, mice were treated with testosterone or estradiol and RNA from the efferent ducts and caput epididymis was processed and hybridized to Affymetrix MOE 430 2.0 microarrays. Analysis of array output identified probe sets in each tissue with altered levels in hormone treated versus control animals. Hormone treatment efficacy was confirmed by determination of serum hormone levels pre- and post-treatment and observed changes in transcript levels of previously reported hormone-responsive genes. Tissue-specific hormone sensitivity was observed with 2867 and 3197 probe sets changing significantly in the efferent ducts after estrogen and testosterone treatment, respectively. In the caput epididymis, 117 and 268 probe sets changed after estrogen and testosterone treatment, respectively, demonstrating a greater response to hormone in the efferent ducts than the caput epididymis. Transcripts sharing similar profiles in the intact and hormone-treated animals compared with castrated controls were also identified. Ontological analysis of probe sets revealed a significant number of hormone-regulated transcripts encode proteins associated with lipid metabolism, transcription and steroid metabolism in both tissues. Real-time RT-PCR was employed to confirm array data and investigate other potential hormone-responsive regulators of proximal reproductive tract function. The results of this work reveal previously unknown responses to estrogen in the caput epididymis and to testosterone in the efferent ducts as well as tissue specific hormone sensitivity in the proximal reproductive tract.
Regulation of gene expression by estrogen and testosterone in the proximal mouse reproductive tract.
Sex, Specimen part, Treatment
View SamplesA microarray study of sex- and gonad-biased gene expression was conducted to determine whether zebrafish demonstrate male-specific patterns consistent with those observed in other animals. We identified a large number of genes (5899) demonstrating statistical differences in transcript abundance between male and female Danio rerio. All sex-biases in gene expression were due to differences between testis and ovary, although differences between male and female body likely went undetected due to constraints imposed by study design and statistical criteria. Male-enriched genes were more abundant than female-enriched genes, and the magnitude of expression bias for male-enriched genes was greater than that for female-enriched genes. We also identified a large number of candidate reproductive genes based on elevated transcript abundance in testes and ovaries, relative to male body and female body, respectively. Gene expression patterns in adult zebrafish from this study are consistent with the male-biased patterns typical of most animal taxa studied to date. Recent zebrafish studies designed to address more specific questions have not reported the same findings, but major methodological and analytical differences across these studies could explain discrepancies.
A microarray analysis of sex- and gonad-biased gene expression in the zebrafish: evidence for masculinization of the transcriptome.
Sex
View Samples