oxepins and Neuroblastoma

oxepins has been researched along with Neuroblastoma* in 2 studies

Other Studies

2 other study(ies) available for oxepins and Neuroblastoma

ArticleYear
Resilience to social stress coincides with functional DNA methylation of the Crf gene in adult mice.
    Nature neuroscience, 2010, Volume: 13, Issue:11

    DNA methylation regulates gene transcription and has been suggested to encode psychopathologies derived from early life stress. We found that methylation regulated the expression of the Crf (also known as Crh) gene and that chronic social stress in adult mice induced long-term demethylation of this genomic region. Demethylation was observed only in the subset of defeated mice that displayed social avoidance and site-specific knockdown of Crf attenuated the stress-induced social avoidance.

    Topics: Analysis of Variance; Animals; Antidepressive Agents, Tricyclic; Avoidance Learning; Azacitidine; Cell Line, Tumor; Corticotropin-Releasing Hormone; Cyclic AMP; Decitabine; DNA Methylation; Enzyme Inhibitors; Gene Expression Regulation; Genetic Vectors; Green Fluorescent Proteins; Imipramine; Injections, Intraventricular; Male; Mice; Mice, Inbred C57BL; Microdissection; Naphthalenes; Neuroblastoma; Neurons; Oxepins; Paraventricular Hypothalamic Nucleus; RNA Interference; RNA, Messenger; Stress, Psychological

2010
Glyceraldehyde-3-phosphate dehydrogenase, the putative target of the antiapoptotic compounds CGP 3466 and R-(-)-deprenyl.
    The Journal of biological chemistry, 1998, Mar-06, Volume: 273, Issue:10

    R-(-)-Deprenyl (Selegiline) represents one of the drugs currently used for the treatment of Parkinson's disease. This compound was shown to protect neurons or glias from programmed cell death in a variety of models. The mechanism of action of neuroprotection as well as inhibition of apoptosis remains elusive. CGP 3466 is a structurally related analog of R-(-)-deprenyl that exhibits virtually no monoamine oxidase type B inhibiting activity but is neuroprotective in the picomolar concentration range. We showed specific binding of CGP 3466 to glyceraldehyde-3-phosphate dehydrogenase by affinity binding, by affinity labeling, and by means of BIAcore(R) technology. Apoptosis assays based on the human neuroblastoma cell line PAJU established the importance of this interaction for mediating drug-induced inhibition of programmed cell death.

    Topics: Animals; Antiparkinson Agents; Apoptosis; Biosensing Techniques; Brain; Cell Line; Gene Expression Regulation; Glyceraldehyde-3-Phosphate Dehydrogenases; Humans; Microscopy, Fluorescence; Molecular Structure; Muscles; Neuroblastoma; Neuroprotective Agents; Oligonucleotides, Antisense; Oxepins; Parkinson Disease; Photoaffinity Labels; Propylamines; Protein Binding; Rabbits; Rats; Selegiline

1998