Analysis of expression profiles of human pDC cell line (CAL1) compared to an immature T cell line (MOLT4)
Transcription factor E2-2 is an essential and specific regulator of plasmacytoid dendritic cell development.
No sample metadata fields
View SamplesAnalysis of expression profiles of pDCs from wild type and heterozygous E2-2 mice. Results show the control by E2-2 of the expression of pDC-enriched genes.
Transcription factor E2-2 is an essential and specific regulator of plasmacytoid dendritic cell development.
No sample metadata fields
View SamplesMutations in the gene encoding laminin a2 chain cause congenital muscular dystrophy, MDC1A. In skeletal muscle, laminin a2 chain binds at least two receptor complexes; the dystrophin-glycoprotein complex and integrin a7b1. To gain insight into the molecular mechanisms underlying this disorder, we performed gene expression profiling of laminin a2 chain deficient mouse limb muscle. One of the down-regulated genes encodes a protein called calcium and integrin binding protein 2 (Cib2) whose expression and function is unknown. However, the closely related Cib1 has been reported to bind integrin aIIb and may be involved in outside-in-signaling in platelets. Since Cib2 might be a novel integrin a7b1 binding protein in muscle, we have studied Cib2 expression in the developing and adult mouse. Cib2 mRNA is mainly expressed in the developing central nervous system and in developing and adult skeletal muscle. In skeletal muscle Cib2 colocalizes with integrin a7B subunit at the sarcolemma and at the neuromuscular- and myotendinous junctions. Finally, we demonstrate that Cib2 is a calcium binding protein that interacts with integrin a7Bb1D. Thus, our data suggest a role for Cib2 as a cytoplasmic effector of integrin a7Bb1D signaling in skeletal muscle
Cib2 binds integrin alpha7Bbeta1D and is reduced in laminin alpha2 chain-deficient muscular dystrophy.
No sample metadata fields
View SamplesWe recently identified pathogenic KIF1Bb mutations in sympathetic nervous system malignancies that are defective in developmental apoptosis. Here we deleted KIF1Bb in the mouse sympathetic nervous system based on a cre recombination system driven by the dopamine beta hydroxylase (DBH) promoter. We observed impaired sympathetic nervous function and misexpression of genes required for sympathoadrenal lineage differentiation in KIF1Bb deficient sympathetic ganglia. Overall design: We analyzed superior cervical ganglia from post-natal day 1 mice. We compared ganglia from four wild-type control animals (KIF1Bb fl/fl) with ganglia from four animals with conditional knockout of KIF1Bb (KIF1Bb fl/fl : DBHcre +/-).
Neuroblast differentiation during development and in neuroblastoma requires KIF1Bβ-mediated transport of TRKA.
Specimen part, Cell line, Subject
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Gene copy number aberrations are associated with survival in histologic subgroups of non-small cell lung cancer.
Specimen part
View SamplesHypothesis: Non-small cell lung cancer (NSCLC) is characterized by a multitude of genetic aberrations with unknown clinical impact. In this study, we aimed to identify gene copy number changes that correlate with clinical outcome in NSCLC. To maximize the chance to identify clinically relevant events, we applied a strategy involving two prognostically extreme patient groups.
Gene copy number aberrations are associated with survival in histologic subgroups of non-small cell lung cancer.
Specimen part
View SamplesBackground: The ability of an organism to repair DNA damage is implicated in carcinogenesis and aging. Interestingly expression profiling of Nucleotide Excision Repair (NER) deficient segmental progeroid mice revealed gene expression changes resembling these observed in aged wild type animals. Our previous transcriptional profiling of NER-deficient C. elegans xpa-1 mutant showed overrepresentation of genes involved in lifespan determination and upregulation of several oxidative stress response genes (Fensgard et al. Aging 2010). However, since an independent study performed by Boyd and coworkers (Boyd et al. Mut Res 2010) showed limited number of changes in xpa-1 mutant. Therefore to independently validate that transcriptome modulation does take place in xpa-1 mutants, we performed another global gene expression profiling based on 5 independent biological replicates allowing more stringent statistical analysis. Results: In agreement with what was observed by Boyd and coworkers (Boyd et al. Mut Res 2010) current transcriptomic analysis detected fewer changes in xpa-1 C. elegans mutant with only a few genes regulated more than 4-fold. Nevertheless, Gene Ontology (GO) enrichment analysis performed on statistically significantly regulated unique protein coding genes revealed overrepresentation of aging gene cluster. Moreover, as before, overexpression of several genes involved in oxidative stress responses was detected. Conclusion: More stringent statistical analysis predictably resulted in a smaller number of regulated genes and thus overrepresented GOs comparing to the earlier paper. However, major conclusions of the previous study can be still regarded as valid, as the most important aging GO is still overrepresented.
Active transcriptomic and proteomic reprogramming in the C. elegans nucleotide excision repair mutant xpa-1.
No sample metadata fields
View SamplesBackground: Global gene expression profiling has been widely used in lung cancer research to identify clinically relevant molecular subtypes as well as to predict prognosis and therapy response. So far, the value of these multi-gene signatures in clinical practice is unclear and the biological importance of individual genes is difficult to assess as the published signatures virtually do not overlap.
Biomarker discovery in non-small cell lung cancer: integrating gene expression profiling, meta-analysis, and tissue microarray validation.
Sex, Age
View SamplesNeuronal, endocrine and exocrine cells exhibit regulated exocytosis but there is also a body of evidence for regulated exocytosis from other cell types. Myofibroblasts are a stromal cell type that secretes extracellular matrix proteins, growth factors and cytokines; they are important in wound healing and increasingly are recognised to play a role in modifying the cellular microenvironment in cancer. We have established calcium dependent regulated secretion in a subset of myofibroblasts from gastric cancers, adjacent tissue and from normal tissue. We have used microarrays to look for the expression of genes associated with the regulated secretory phenotype.
The neuroendocrine phenotype of gastric myofibroblasts and its loss with cancer progression.
Specimen part
View SamplesTissue material was collected from all breast cancer patients receiving surgery at Karolinska Hospital from 1994-1996. Material was frozen immediatley on dry ice or in liquid nitrogen and stored in -70C freezers. This series contains expression data for n=159 tumors from which RNA could be collected in sufficient amounts and quality for analysis.
Gene expression profiling spares early breast cancer patients from adjuvant therapy: derived and validated in two population-based cohorts.
No sample metadata fields
View Samples