Background: The basic helix-loop-helix transcription factor TWIST1 (Twist) is involved in embryonic cell lineage determination and mesodermal differentiation. There is evidence to indicate that Twist expression plays a role in breast tumor formation and metastasis, but the role of Twist in dysregulating pathways that drive the metastatic cascade is unclear. Importantly, the genes and pathways dysregulated by Twist in cell lines and mouse models have not been validated against data obtained from patient samples.
Genomic pathways modulated by Twist in breast cancer.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
LASP-1: a nuclear hub for the UHRF1-DNMT1-G9a-Snail1 complex.
Specimen part, Cell line
View SamplesLeaves and panicles from recurrent parent KMR3 and a high yielding KMR3-O.rufipogon introgression line were used
Os11Gsk gene from a wild rice, Oryza rufipogon improves yield in rice.
Specimen part
View SamplesNuclear LASP-1 has a direct correlation with the overall survival of breast cancer patients. Gene expression analysis of MCF7 human breast cancer cells cultured in 3D-Matrigel was performed.
LASP-1: a nuclear hub for the UHRF1-DNMT1-G9a-Snail1 complex.
Specimen part, Cell line
View SamplesBovine articular chondrocytes were grown in micromass culture and were either untreated or treated with 5 ng TGF-b1/ml for 8 hours to identify genes regulated by TGF-b.
Altered responsiveness to TGF-β results in reduced Papss2 expression and alterations in the biomechanical properties of mouse articular cartilage.
Specimen part, Treatment
View SamplesWe used microarrays to study the effect of Chd1 loss of function in mouse ES cells.
Chd1 regulates open chromatin and pluripotency of embryonic stem cells.
Cell line
View SamplesNod2 has been extensively characterized as a bacterial sensor that induces an antimicrobial and inflammatory gene expression program. Therefore, it is unclear why Nod2 mutations that disrupt bacterial recognition are paradoxically among the highest risk factors for Crohns disease, which involves an exaggerated immune response directed at intestinal bacteria. Previous studies from our lab have shown that mice deficient in Atg16L1, another Crohns disease susceptibility gene, develop abnormalities in Paneth cells, specialized epithelial cells in the small intestine involved in antimicrobial responses.
Bacterial sensor Nod2 prevents inflammation of the small intestine by restricting the expansion of the commensal Bacteroides vulgatus.
Age, Specimen part
View SamplesPreviously we have shown significant differences in lactation performance, mammary gland histology and expression profiles of mammary transcriptome during peak-lactation (lactation day 9; L9) between the ordinary CBA/CaH (CBA) and the superior QSi5 strains of mice. In the present study, we compared mammary gland histology between CBA and QSi5 at mid-pregnancy (pregnancy day 12; P12). We assessed lactation performance during the first 8 days of lactation of the 13th - 14th generation of the Advanced Intercross Line (AIL) (CBA X QSi5) mice.
Identification of gene sets and pathways associated with lactation performance in mice.
Specimen part
View SamplesResponses of the Human Airway Epithelium Transcriptome to In Vivo Injury
Responses of the human airway epithelium transcriptome to in vivo injury.
Sex, Age, Time
View SamplesWhile the genome sequence of many animals is now complete, their transcriptomes are less well characterised. Both genome-scale tiling arrays and massively parallel sequencing now allow transcriptomes to be mapped at unprecedented depth. We used both technologies to map the C. elegans transcriptome across development. This unbiased overview can serve as a framework for assessing transcriptome changes in a mutant animal and we compared the wild-type data with that of animals that have lost the nonsense-mediated decay (NMD) pathway. Results We find that while the great majority of detectable transcripts map to known gene structures, over 5% of transcribed regions are novel, falling outside current gene annotations. We show that at least 40% of these are novel exons. We also used both technologies to assess isoform complexity and estimate that at least 17% of genes change their major isoform across development. Having mapped the wild-type transcriptome, we examined how this is perturbed in animals lacking nonsense -mediated decay (NMD). NMD prevents expression of prematurely truncated proteins by degrading transcripts containing premature termination codons (PTCs). We find that ~20% of all genes produce transcripts that appear to be targets for NMD. While most of these arise from splicing errors, NMD targets are also enriched for transcripts that contain short open reading frames upstream of the predicted translational start (uORFs). We find an intriguing relationship between the strength of Kozak consensus surrounding the true start codon and the degree to which these uORF containing transcripts are targeted by NMD, suggesting that translational efficiency may be coupled to transcript turnover via the NMD pathway for many transcripts. Conclusions We have generated a high-resolution map of the C. elegans transcriptome and have used it to identify transcripts that are endogenous targets of the NMD machinery. We find that these targets arise principally through splicing errors and suggest that splicing and NMD are highly interlinked processes.
High resolution transcriptome maps for wild-type and nonsense-mediated decay-defective Caenorhabditis elegans.
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