Most FDA approved drugs are not equally effective in all patients, suggesting that identification of biomarkers to predict responders to a chemoprevention agent will be needed to stratify patients and achieve maximum benefit. The goal of this study was to investigate both patient specific and cell-context specific heterogeneity of metformin response, using cancer cell lines fibroblast cell lines and induced pluripotent stem cells differentiated into lung epithelial lineages.
Patient- and Cell Type-Specific Heterogeneity of Metformin Response.
Specimen part, Cell line
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c-Myc regulates self-renewal in bronchoalveolar stem cells.
Specimen part
View SamplesWe performed miRNA and mRNA profiling in BASC cells and c-Myc depleted BASC cells. We built potential miRNA-mRNA interaction networks specific to c-Myc regulation in BASCs
c-Myc regulates self-renewal in bronchoalveolar stem cells.
Specimen part
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MicroRNA networks in mouse lung organogenesis.
Sex
View SamplesWe performed miRNA and mRNA profiling over a 7-point time course, encompassing all recognized stages of lung development and explore dynamically regulated miRNAs and potential miRNA-mRNA interaction networks specific to mouse lung development
MicroRNA networks in mouse lung organogenesis.
Sex
View SamplesMost human tumors have abnormal numbers of chromosomes, a condition known as aneuploidy. The mitotic checkpoint is an important mechanism that prevents aneuploidy through restraining the activity of the anaphase-promoting complex (APC). USP44 was identified as a key regulator of APC activation that maintains the association of MAD2 with the APC co-activator Cdc20. However, the physiological importance of USP44 and its impact on cancer biology are unknown. Here, we show that USP44 is required to prevent tumors in mice and is frequently down-regulated in human lung cancer. USP44 inhibits chromosome segregation errors independently of its role in the mitotic checkpoint by regulating proper centrosome separation, positioning, and mitotic spindle geometry, functions that require direct binding to the centriole protein, centrin. These data reveal a new role for the ubiquitin system in mitotic spindle regulation and underscore the importance of USP44 in the pathogenesis of human cancer.
USP44 regulates centrosome positioning to prevent aneuploidy and suppress tumorigenesis.
Sex, Disease, Disease stage
View SamplesRecurrent Copy Number Variations (CNVs) of human 16p11.2 have been associated with a variety of developmental/neurocognitive syndromes. In particular, deletion of 16p11.2 is found in patients with autism, developmental delay, and obesity. Patients with deletions or duplications have a wide range of clinical features, and siblings carrying the same deletion often have diverse symptoms. To study the consequence of 16p11.2 CNVs in a systematic manner, we used chromosome engineering to generate mice harboring deletion of the chromosomal region corresponding to 16p11.2, as well as mice harboring the reciprocal duplication. These 16p11.2 CNV models have dosage-dependent changes in gene expression, viability, brain architecture, and behavior. For each phenotype, the consequence of the deletion is more severe than that of the duplication. Of particular note is that half of the 16p11.2 deletion mice die postnatally; those that survive to adulthood are healthy and fertile, but have alterations in the hypothalamus and exhibit a behavior trap phenotypea specific behavior characteristic of rodents with lateral hypothalamic and nigrostriatal lesions. Our findings indicate that 16p11.2 CNVs cause both brain and behavioral anomalies, providing new insight into human neurodevelopmental disorders.
Dosage-dependent phenotypes in models of 16p11.2 lesions found in autism.
Sex
View SamplesThis SuperSeries is composed of the SubSeries listed below.
MicroRNA-mRNA interactions in a murine model of hyperoxia-induced bronchopulmonary dysplasia.
Specimen part, Disease, Disease stage, Treatment
View SamplesUnderstanding how lung progenitor cells balance
Integrated proteomic and transcriptomic profiling of mouse lung development and Nmyc target genes.
No sample metadata fields
View Samplescomparison of expression of wildtype lungs and lungs with hypomorphic expression of nmyc. the lungs were pooled from several biological samples. The hypomorphoic mutant was orignally published in Moens CB et al [PMID: 1577267]. this is part of a larger collection of data comparing nmyc misexpression in the lung (gain of fucntion) and protein expression in the hypomorphic lungs.
Integrated proteomic and transcriptomic profiling of mouse lung development and Nmyc target genes.
No sample metadata fields
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