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141.
ABSTRACTMacroautophagy/autophagy deregulation has been observed in perpetuated inflammation and the proliferation of tumor cells. However, the mechanisms underlying these changes have yet to be well-identified. UVRAG is one of the key players of autophagy, but its role in vivo remained puzzling. Our recent study utilized a mouse model with inducible expression of a cancer-derived frameshift (FS) mutation in UVRAG that dominant-negatively inhibits wild-type UVRAG, resulting in impaired stimulus-induced autophagy. The systemically compromised autophagy, particularly mitophagy, notably increases inflammation and associated pathologies. Furthermore, our discovery indicates that time-dependent autophagy suppression and ensuing CTNNB1/β-catenin activation may serve as one tumor-promoting mechanism underpinning age-related cancer susceptibility. 相似文献
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In mice receiving i.v. low doses of 3H-LSD the accumulation of radioactivity in brain appears to reflect a selective binding to high affinity sites as indicated by the heterogenous regional distribution (paralleling that observed in in vitro binding studies) and by the saturable character of the process (ED50 around 30μg.kg?1 in cerebral cortex).The identity of the binding sites was assessed in various regions by administration of agonists or antagonists of different neurotransmitters. In cortex specific accumulation of 3H-LSD was easily prevented by administration of serotonin antagonists (cyproheptadine, methysergide, methiothepin) or by tryptamine derivatives (psilocin, psilocybin, dimethyltryptamine) and 5-hydroxytryptophan + pargyline. Among neuroleptics some prevented 3H-LSD binding (spiperone, haloperidol) whereas 1mg.kg?1 pimozide was ineffective. In addition a large variety of agents (adrenergic, cholinergic, morphine) were ineffective. These data suggest a selective binding to cortical serotonin receptors. 相似文献
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The growth of two strains of Myxococcus virescens exhibiting dispersed growth was followed in casamino acids (N III-C) media and casitone media. The changes in optical density, pH, pigmentation as well as the secretion of bacteriolytic and proteolytic enzymes, DNA and polysaccharides during growth were recorded. In both media the bacteria grew exponentially with a generation time of 4 (casitone) and 20 hours (N III-C) respectively. The maximal cell mass was about 4 times higher in casitone than in casamino acids media. The amounts of bacteriolytic enzymes produced by the two strains in N III-C medium were different but in casitone medium they were about equal and considerably higher. The maximal values of proteolytic enzymes were about the same in both media and always occurred later than the bacteriolytic maxima. Both activity peaks appeared before the phase of decline. The polysaccharide production reached a maximum during the stationary growth phase in both media. A higher value was reached during growth in casitone medium than in N III-C medium. During the phase of decline a second increase of polysaccharide in the medium appeared. No DNA could be detected in the cell-free solutions until the beginning of the phase of decline. 相似文献
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Rohan H. C. Palmer Emma C. Johnson Hyejung Won Renato Polimanti Manav Kapoor Apurva Chitre Molly A. Bogue Chelsie E. Benca-Bachman Clarissa C. Parker Anurag Verma Timothy Reynolds Jason Ernst Michael Bray Soo Bin Kwon Dongbing Lai Bryan C. Quach Nathan C. Gaddis Laura Saba Hao Chen Michael Hawrylycz Shan Zhang Yuan Zhou Spencer Mahaffey Christian Fischer Sandra Sanchez-Roige Anita Bandrowski Qing Lu Li Shen Vivek Philip Joel Gelernter Laura J. Bierut Dana B. Hancock Howard J. Edenberg Eric O. Johnson Eric J. Nestler Peter B. Barr Pjotr Prins Desmond J. Smith Schahram Akbarian Thorgeir Thorgeirsson Dave Walton Erich Baker Daniel Jacobson Abraham A. Palmer Michael Miles Elissa J. Chesler Jake Emerson Arpana Agrawal Maryann Martone Robert W. Williams 《Genes, Brain & Behavior》2021,20(6):e12738
The National Institute on Drug Abuse and Joint Institute for Biological Sciences at the Oak Ridge National Laboratory hosted a meeting attended by a diverse group of scientists with expertise in substance use disorders (SUDs), computational biology, and FAIR (Findability, Accessibility, Interoperability, and Reusability) data sharing. The meeting's objective was to discuss and evaluate better strategies to integrate genetic, epigenetic, and 'omics data across human and model organisms to achieve deeper mechanistic insight into SUDs. Specific topics were to (a) evaluate the current state of substance use genetics and genomics research and fundamental gaps, (b) identify opportunities and challenges of integration and sharing across species and data types, (c) identify current tools and resources for integration of genetic, epigenetic, and phenotypic data, (d) discuss steps and impediment related to data integration, and (e) outline future steps to support more effective collaboration—particularly between animal model research communities and human genetics and clinical research teams. This review summarizes key facets of this catalytic discussion with a focus on new opportunities and gaps in resources and knowledge on SUDs. 相似文献
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