Tapinella atrotomentosa strain:MSH-12
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ABSTRACT:
PROVIDER: PRJNA346771 | ENA |
REPOSITORIES: ENA
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Project description:Tapinella atrotomentosa MSH-12 Standard Draft genome sequencing
| PRJNA346770 | ENA
Project description:Pseudomonas aeruginosa MSH-10 Genome sequencing and assembly
| PRJNA201849 | ENA
Project description:Alterations in endoplasmic reticulum (ER) homeostasis have been implicated in the pathophysiology of obesity and type-2 diabetes (T2D). Acute ER stress induction in the hypothalamus produces glucose metabolism perturbations. However, the neurobiological basis linking hypothalamic ER stress with abnormal glucose metabolism remains unknown. Here we report that genetic and induced models of hypothalamic ER stress are associated with alterations in systemic glucose homeostasis due to increased gluconeogenesis (GNG) independent of body weight changes. Defective alpha melanocyte-stimulating hormone (a-MSH) production underlies this metabolic phenotype, as pharmacological strategies aimed at rescuing hypothalamic a-MSH content reversed this phenotype at metabolic and molecular level. Collectively, our results posit defective a-MSH processing as a fundamental mediator of enhanced GNG in the context of hypothalamic ER stress, and establish a-MSH deficiency in proopiomelanocortin (POMC) neurons as a potential contributor to the pathophysiology of T2D.
2015-06-18 | GSE62263 | GEO
Project description:Alterations in endoplasmic reticulum (ER) homeostasis have been implicated in the pathophysiology of obesity and type-2 diabetes (T2D). Acute ER stress induction in the hypothalamus produces glucose metabolism perturbations. However, the neurobiological basis linking hypothalamic ER stress with abnormal glucose metabolism remains unknown. Here we report that genetic and induced models of hypothalamic ER stress are associated with alterations in systemic glucose homeostasis due to increased gluconeogenesis (GNG) independent of body weight changes. Defective alpha melanocyte-stimulating hormone (a-MSH) production underlies this metabolic phenotype, as pharmacological strategies aimed at rescuing hypothalamic a-MSH content reversed this phenotype at metabolic and molecular level. Collectively, our results posit defective a-MSH processing as a fundamental mediator of enhanced GNG in the context of hypothalamic ER stress, and establish a-MSH deficiency in proopiomelanocortin (POMC) neurons as a potential contributor to the pathophysiology of T2D. Total RNA was extracted from whole-liver of 6-week old control (3 biological replicates) and POMCMfn2KO mice (5 biological replicates)
2015-06-18 | E-GEOD-62263 | biostudies-arrayexpress
Project description:Aeromonas phage MSh-2020a isolate:Environment Genome sequencing
| PRJNA641255 | ENA
Project description:Multicenter Study of Hydroxyurea (MSH)
| PRJNA701326 | ENA
Project description:Multicenter Study of Hydroxyurea (MSH)
| PRJNA701327 | ENA
Project description:We determined the gene expression profiles of murine melan-a melanocytes treated with ASP or alpha-MSH over a 4 days time course using genome-wide oligonucleotide microarrays. As expected, the gene expression patterns emphasized the opposing effects of the 2 ligands, and there were significant reductions in expression of numerous melanogenic proteins elicited by ASP, which correlates with its inhibition of pigmentation. However, ASP also unexpectidly modulated the expression of genes involved in various other cellular pathways, including glutathione synthesis and redox metabolism. Many genes up-regulated by ASP are involved in morphogenesis, cell adhesion and ECM-receptor interactions. Treatment with ASP or alpha-MSH was performed for 3 hr, 1 day, 2 days, 3 days and 4 days, in triplicate. Each biological replicate was submitted to a direct hybridization (treated/untreated samples) after coupling with Cy5 or Cy3 and to a reverse dye-swap, leading to 2 replicated hybridization for each biological sample. A total of 6 hybridized arrays was used for each of the 5 time points, for each drug.
2009-02-02 | E-GEOD-14089 | biostudies-arrayexpress
Project description:Neurons in the arcuate nucleus (ARC) sense the fed/fasted state and regulate hunger. ARCAgRP neurons release GABA, NPY and the melanocortin-4 receptor (MC4R) antagonist, AgRP, and are activated by fasting1-4. When stimulated, they rapidly and potently drive hunger5,6. ARCPOMC neurons, in contrast, release the MC4R agonist, α-MSH, and are viewed as the counterpoint to ARCAgRP neurons. They are regulated in an opposite fashion and their activity leads to decreased hunger2,4,7. Together, ARCAgRP and ARCPOMC neurons constitute the ARC feeding center. Against this, however, is the finding that ARCPOMC neurons, unlike ARCAgRP neurons, fail to affect food intake over the timescale of minutes to hours following opto- or chemogenetic stimulation5,8. This suggests a rapidly acting component of the ARC satiety pathway is missing. Here, we show that excitatory ARC neurons identified by expression of vesicular glutamate transporter 2 (VGLUT2) and the oxytocin receptor, unlike ARCPOMC neurons, rapidly cause satiety when chemo- or optogenetically manipulated. These glutamatergic ARC projections synaptically converge with GABAergic ARCAgRP projections on MC4R-expressing neurons in the paraventricular hypothalamus (PVHMC4R neurons), which are known to mediate satiety9. ARCPOMC neurons also send dense projections to the PVH. Importantly, the α-MSH they release post-synaptically potentiates glutamatergic synaptic activity onto PVHMC4R neurons – including that emanating from ARCVglut2 neurons. This suggests a means by which α-MSH can bring about satiety – via postsynaptic potentiation of this novel ARCVglut2 to PVHMC4R satiety circuit. Thus, while fast (GABA and NPY) and slow (AgRP) ARC hunger signals are delivered together by ARCAgRP neurons10,11, the temporally analogous satiety signals from the ARC, glutamate and α-MSH, are delivered separately by two parallel, interacting projections (from ARCVGLUT2 and ARCPOMC neurons). Discovery of this rapidly acting excitatory ARC → PVH satiety circuit, and its regulation by α-MSH, provides new insight into regulation of hunger/satiety.
2016-11-21 | GSE81789 | GEO
Project description:We determined the gene expression profiles of murine melan-a melanocytes treated with ASP or alpha-MSH over a 4 days time course using genome-wide oligonucleotide microarrays. As expected, the gene expression patterns emphasized the opposing effects of the 2 ligands, and there were significant reductions in expression of numerous melanogenic proteins elicited by ASP, which correlates with its inhibition of pigmentation. However, ASP also unexpectidly modulated the expression of genes involved in various other cellular pathways, including glutathione synthesis and redox metabolism. Many genes up-regulated by ASP are involved in morphogenesis, cell adhesion and ECM-receptor interactions.
2009-02-03 | GSE14089 | GEO