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Chemical Compound Review

Indoleamine     1H-indol-3-amine

Synonyms: SureCN37668, AG-K-88384, CHEBI:28626, NSC-24933, WTI-11954, ...
 
 
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Disease relevance of C01819

 

Psychiatry related information on C01819

  • CONCLUSIONS: While the prevailing view was that the activation of 5-HT(2) receptors is solely responsible for hallucinogenic drug effects, these results support a role for 5-HT(1A) receptors in the effects of the indoleamine hallucinogen 5-MeO-DMT on locomotor activity and PPI in rats [6].
  • The effects of psychological stress on catecholamine and indoleamine metabolism were examined in various brain regions of rats [7].
  • As such, monitoring tryptophan metabolism in chronic immunopathology provides a better understanding of the association between immune activation and IDO and its role in the development of immunodeficiency, anemia and mood disorders [8].
  • To further characterize the effects of this indoleamine on the macrostructure of feeding, a computer-automated data acquisition system was used to analyze macronutrient feeding patterns in freely feeding animals maintained on the pure diets of protein, carbohydrate, and fat [9].
  • The data show that systemic chronic immune activation in patients with Alzheimer's disease and Huntington's disease is associated with significant degradation of tryptophan, which is most likely due to activation of indoleamine (2,3)-dioxygenase by immunologic stimuli [10].
 

High impact information on C01819

 

Chemical compound and disease context of C01819

 

Biological context of C01819

 

Anatomical context of C01819

 

Associations of C01819 with other chemical compounds

 

Gene context of C01819

  • Cells expressing CTLA4-KDEL do not up-regulate the indoleamine 2, 3-dioxygenase enzyme, unlike cells treated with soluble CTLA4-immunoglobin (Ig) [35].
  • An antibody to IFN-gamma, but not IFN-alpha, inhibited the induction of IDO activity by this secreted factor [36].
  • In both cell lines, IFN-gamma induced the expression of indoleamine 2,3-dioxygenase (IDO) activity [37].
  • The IL-1-mediated inhibition of IDO activity and of subsequent antibacterial effect is due to the production of NO [38].
  • The most prominent gamma interferon (IFN-gamma)-induced antimicrobial effector mechanisms are the induction of nitric oxide (NO) synthase (NOS) and of indoleamine 2,3-dioxygenase (IDO) activity [38].
 

Analytical, diagnostic and therapeutic context of C01819

References

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