Similar Datasets
Project description:Reports on common mutations in neuroendocrine tumors (NET) are rare and clonality of NET metastases has not been investigated in this tumor entity yet. We selected a NET and a the corresponding lymph node and liver metastases as well as the derivative cell lines to screen for somatic mutations in the primary NET and to track the fate of genetic changes (by Affymetrix SNP 6.0 micorarray and targeted resequencing by 454 GS FLX) and during metastasis and in vitro progression. using Affymetrix SNP 6.0 Arrays.
2012-07-17 | GSE39371 | GEO
Project description:Gills of teleost fish represent a vital multifunctional organ; however, they are subjected to environmental stressors, causing gill damage. Gill damage is associated with significant losses in the Atlantic salmon aquaculture industry. Gill disorders due to environmental stressors are exacerbated by global environmental changes, especially with open-net pen aquaculture (as farmed fish lack the ability to escape those events). The local and systemic response to gill damage, concurrent with several environmental insults, are not well investigated. We performed field sampling to collect gill and liver tissue after several environmental insults. Using a 44K salmonid microarray platform, we aimed to compare the transcriptomes of pristine and moderately damaged gill tissue. The gill damage-associated biomarker genes and associated qPCR assays arising from this study will be valuable in future research aimed at developing therapeutic diets to improve farmed salmon gill health.
2022-03-24 | GSE186728 | GEO
Project description:Expression profile of human GEP-NET tumors, including 113 fresh frozen biopsies of primary and metastatic tumours originating from pancreas (P-NET, 83 primary and 30 metastasis), 81 from small intestine (SI-NET, 44 primary and 37 metastasis), and 18 from rectum (RE-NET, 3 primary and 15 metastasis).
2018-02-25 | GSE98894 | GEO
Project description:Biological carbon fixation is foundational to the biosphere. Most autotrophs are thought to possess one carbon fixation pathway. The hydrothermal vent tubeworm Riftia pachyptila’s chemoautotrophic symbionts, however, possess two functional pathways: the Calvin Benson-Bassham (CBB) and the reductive tricarboxylic acid (rTCA) cycles. Little is known about how Riftia’s symbionts and related organisms coordinate the functioning of these two pathways. Here we investigated net carbon fixation rates, transcriptional/metabolic responses, and transcriptional co-expression patterns of Riftia pachyptila’s endosymbionts by incubating tubeworms at environmental pressures, temperature, and geochemistry. Results showed that rTCA and CBB transcriptional patterns varied in response to different geochemical regimes and that each pathway is allied to specific metabolic processes, suggesting distinctive yet complementary roles in metabolic function. Net carbon fixation rates were also exemplary, and accordingly we propose that co-activity of CBB and rTCA may be an adaptation for maintaining high carbon fixation rates, conferring a fitness advantage in dynamic vent environments.
2024-03-28 | GSE249345 | GEO
Project description:Background: The goal of this study was to determine the transcriptional consequences of norepinephrine transporter (NET) gene deletion in noradrenergic neuron differentiation. The norepinephrine transporter (NET) is the target of powerful mind-altering substances, such as tricyclic antidepressants and the drug of abuse, cocaine. NET function in adult noradrenergic neurons of the peripheral and central nervous systems is that of a scavenger that internalizes norepinephrine from the synaptic cleft. By contrast, norepinephrine (NE) transport has a different role in embryogenesis. It promotes differentiation of neural crest cells and locus ceruleus progenitors into noradrenergic neurons, whereas NET inhibitors, such as the tricyclic antidepressant desipramine and the drug of abuse, cocaine, inhibit noradrenergic differentiation. While NET structure und regulation of NET function is well described, little is known about downstream targets of NE transport. Results: We have determined by long serial analysis of gene expression (LongSAGE) the gene expression profiles of in vitro differentiating wild type and norepinephrine transporter-deficient (NETKO) neural crest derivatives. Comparison analyses with the wild type library (GSM 105765) have identified a number of important differentially expressed genes, including genes relevant to noradrenergic neuron differentiation and to the phenotype of NETKO mice. Furthermore we have identified novel differentially expressed genes. Conclusions: Loss of NET function during embryonic development deregulates signaling pathways that are critically involved in neural crest formation and noradrenergic neuron differentiation. The library was constructed from total RNA of 60 neural crest culture at culture day 7. The neural tubes were dissected from E9.5 embryos that lack the norepinephrine transporter gene.
2008-06-23 | E-GEOD-11788 | biostudies-arrayexpress
Project description:While strongly implicated in Postural Tachycardia Syndrome (POTS), considerable controversy exists regarding norepinephrine transporter (NET) loss-of-function. POTS is characterized by the clinical symptoms of orthostatic intolerance, light-headedness, tachycardia and syncope or near syncope with upright posture. Abnormal sympathetic nervous system activity is typical, of a type which suggests dysfunction of the NET, with evidence the gene responsible is under tight epigenetic control. Using RNA of isolated chromatin combined with sequencing (RICh-Seq) we show let7i miRNA suppresses NET by MeCP2. Vorinostat restores epigenetic control and NET expression in POTS.
2017-01-07 | GSE93235 | GEO
Project description:Abstract. Objectives: Neutrophil extracellular traps (NETs) are extracellular lattices composed of nucleic material bound to neutrophil granule proteins. NETs may play pathogenic roles in development and severity of autoimmune diseases such as systemic lupus erythematosus (SLE), at least in part, through induction of type I interferon (IFN) responses via externalization of oxidized immunostimulatory DNA. A distinct subset of SLE proinflammatory neutrophils (low density granulocytes; LDGs) displays enhanced ability to form proinflammatory NETs that damage the vasculature. We assessed whether NET-bound RNA can contribute to inflammatory responses in endothelial cells and the pathways that mediate this effect. Methods: Expression of newly-synthesized RNA was quantified if healthy control and lupus NETs. The ability of endothelial cells to take up NET-bound RNA and downstream induction of type I IFN responses was quantified. RNAs present in NETs were sequenced and specific small RNAs were tested for induction of endothelial type I IFN pathways. Results: NETs extruded newly-synthesized RNA that was internalized by endothelial cells and this was enhanced when NET nucleic acids were oxidized, particularly in lupus LDG NETs. Internalization of NET-bound total RNA by endothelial cells was dependent on endosomal TLRs and the actin cytoskeleton and induced type I IFN stimulated genes (ISGs). This ISG induction was dependent on NET-associated miR-let7b, a small RNA expressed at higher levels in LDG NETs, which acted as a TLR7 agonist. Conclusion: These results highlight underappreciated roles for small RNAs externalized in NETs in the induction of proinflammatory responses in vascular cells, with implications to lupus vasculopathy.
2023-07-31 | GSE160143 | GEO