DCD is a gene amplified and overexpressed in a subset of breast tumors acting as a growth and survival factor. Patients with DCD-positive breast cancer have worse prognostic features. To investigate the role of DCD in breast tumorigenesis, we analyzed the consequences of its downregulation in human breast cancer cell lines using three specific shRNA lentivirus vectors. Genes up- and down-regulated by DCD were identified using Affymetrix microarray and analyzed by MetaCore Platform. We found that loss of DCD expression led to reduced cell proliferation, resistance to apoptosis, and suppressed tumorigenesis in immunodeficient mice. Network analysis of gene expression data revealed perturbed ERBB signaling following DCD shRNA expression including changes in the expression of ERBB receptors and their ligands. These findings imply that DCD promotes breast tumorigenesis via modulating the activity of the ERBB signaling pathways. As ERBB signaling is also important for neural survival, HER2+ breast tumors may highjack DCDs neural survival-promoting functions to promote tumorigenesis.
Dermcidin exerts its oncogenic effects in breast cancer via modulation of ERBB signaling.
Cell line
View SamplesThe molecular events at the basis of prion diseases are characterized by the involvement of several genes which are differentially regulated during the onset and the progression of the infection. Gene expression profiling studies are a powerful tool for the development of preclinical diagnostic tests. Most of the studies performed up to date utilized tissues which are not suitable for a future perspective of a rapid analysis of the infected animals and patients.
Whole Blood Gene Expression Profiling in Preclinical and Clinical Cattle Infected with Atypical Bovine Spongiform Encephalopathy.
Sex, Specimen part
View SamplesTotal RNA samples from Vax2 knockout mouse eyes (at least two biological replicates) were profiled by gene expression. As control we used total RNA from wild type eyes. The analysis was carried out at five different developmental stages: E10.5, E12.5, E16.5, P8, and P60.
Vax2 regulates retinoic acid distribution and cone opsin expression in the vertebrate eye.
Specimen part
View SamplesUntreated HIV-1 infection progresses through acute and asymptomatic stages to AIDS. While each of the three stages has well-known clinical, virologic and immunological characteristics, much less is known of the molecular mechanisms underlying each stage. Here we report lymphatic tissue microarray analyses revealing for the first time stage-specific patterns of gene expression during HIV-1 infection. We show that while there is a common set of key genes with altered expression throughout all stages, each stage has a unique gene-expression signature. The acute stage is most notably characterized by increased expression of hundreds of genes involved in immune activation, innate immune defenses (e.g.MDA-5, TLR-7 and -8, PKR, APOBEC3B, 3F, 3G), adaptive immunity, and in the pro-apoptotic Fas-Fas-L pathway. Yet, quite strikingly, the expression of nearly all acute-stage genes return to baseline levels in the asymptomatic stage, accompanying partial control of infection. In the AIDS stage, decreased expression of numerous genes involved in T cell signaling identifies genes contributing to T cell dysfunction. These common and stage-specific, gene-expression signatures provide new insights into the molecular mechanisms underlying the host response and the slow, natural course of HIV-1 infection.
Microarray analysis of lymphatic tissue reveals stage-specific, gene expression signatures in HIV-1 infection.
Sex, Age, Specimen part, Disease, Disease stage, Race, Subject
View SamplesFrequent hemodialysis is associated with improvement in myocardial mechanics and cardiac gene expression profile
Impact of frequent nocturnal hemodialysis on myocardial mechanics and cardiomyocyte gene expression.
Age, Specimen part
View SamplesMinocycline is a potent modulator of retinal microglia Overall design: Global mRNA expression analysis of CD1 mouse retinas in control, light damage and light damage plus minocycline conditions
Minocycline counter-regulates pro-inflammatory microglia responses in the retina and protects from degeneration.
No sample metadata fields
View SamplesWe have demonstrated that the oncogenic activation of B-RAF (using a truncated delta-BRAF-ER version inducible with tamoxifen) in the melan-a melanocyte cell line triggers the activation of Zeb1 and Twist1 at the expanse of Zeb2 and Snail2. Enforced maintenance of Zeb2 or Snail2 expression reduces the B-RAF oncogenic potential while ectopic expression of Zeb1 or Twist1 cooperates with B-RAF in melan-a cell transformation. To get an insight into the properties of these embryonic transcription factors, gene expression profiles of melan-a-derived cell lines either expressing a non-activated B-RAF (- tamoxifen) or an activated BRAF (+ tamoxifen) alone or in combination with Snail2, Zeb2, Twist1 or Zeb1 have been established.
A switch in the expression of embryonic EMT-inducers drives the development of malignant melanoma.
Cell line
View SamplesSamples 1-8: Tissue-specific RNA sequencing (Illumina) using dissected ring glands isolated from TWO different time points of control (phm>w1118) third instar larvae. Time points are: light phase zt0-4 (which corresponde to 2-4 hours from second to third instar larvae molt); and dark phase zt18-22 (which corresponde to 16-20 hours from second to third instar larvae molt) Samples 9-32: Tissue-specific gene expression (RNA seq Illumina) using dissected ring glands isolated from TWO different time points of third instar larvae. Genotypes were Timeless-RNAi (phm>tim-RNAi), Period-RNAi (phm>per-RNAi), UAS-TimcDNA (phm>UAS-Tim) and UAS-TimcDNA;UAS-PercDNA (phm>UAS-TimcDNA;UAS-PercDNA). Goal was to identify circadin pathway dependent gene sets in the ring gland. Time points were 2-4 hours and 18-20 hours after L2-L3 molt. Overall design: This study comprises two parts: First, Next generation sequencing was used to determine transcriptional profiles from Drosophila ring glands at ZT0-4 versus ZT18-22 in control larvae. Encore Complete RNA-Seq IL Multiplex System 1-8 (Nugen Part No. 0312) and Encore Complete RNA-Seq IL Multiplex System 9-16 (Nugen Part No. 0313) was used for barcoding and multiplex sequencing. Library prep was based on total RNA isolated from dissected ring glands at two different time points during the third instar (the last larval stage of Drosophila development). Libraries were sequenced on a High-Seq Illumina platform. The second part examined gene expression changes in ring glands where we altered circadian signaling by genetic means. Encore Complete RNA-Seq IL Multiplex System was used to prep the cDNA library from total RNA isolated from ring glands of controls, ring gland-specific Timeless-RNAi (phm>tim-RNAi), Period-RNAi (phm>per-RNAi), UAS-Tim-cDNA (phm>UAS-Tim) and UAS-Tim-cDNA; UAS-Per-cDNA (phm>UAS-Tim-cDNA;UAS-Per-cDNA) larvae at two different time points in the day (ZT0-4 and ZT18-22) for the first three genotypes and exclusively at ZT18-22 for the last two genotypes. Each condition was measured by using two biological samples.
The Circadian Clock Is a Key Driver of Steroid Hormone Production in Drosophila.
Specimen part, Subject
View Samples10 day old seedlings were treated with 5uM of the cytokinin Benzyladenine(BA)or DMSO at 15min, 45min, 120min, 480min and 1440min
Expression profiling of cytokinin action in Arabidopsis.
Age, Compound, Time
View SamplesTreatments that stimulate neuronal excitability enhance motor performance after stroke.cAMP-response-element binding protein (CREB) is a transcription factor that plays a key rolein neuronal excitability. Increasing the levels of CREB with a viral vector in a small pool ofmotor neurons enhances motor recovery after stroke, while blocking CREB signaling preventsstroke recovery. Silencing CREB-transfected neurons in the peri-infarct region with thehM4di-DREADD blocks motor recovery. Reversing this inhibition allows recovery to continue,demonstrating that it is possible to turn off and on stroke recovery by manipulating theactivity of CREB-transfected neurons. CREB transfection enhances re-mapping of injuredsomatosensory and motor circuits, and induces the formation of new connections withinthese circuits. CREB is a central molecular node in the circuit responses after stroke that leadto recovery from motor deficits.
CREB controls cortical circuit plasticity and functional recovery after stroke.
Specimen part
View Samples