RapamycinFungusV1, Main, Exploration, bibRecord, 001591

Signaling cascades as drug targets in model and pathogenic fungi.

Identifieur interne : 001591 ( Main/Exploration ); précédent : 001590; suivant : 001592

Signaling cascades as drug targets in model and pathogenic fungi.

Auteurs : Robert J. Bastidas [États-Unis] ; Jennifer L. Reedy ; Helena Morales-Johansson ; Joseph Heitman ; Maria E. Cardenas

Source :

Current opinion in investigational drugs (London, England : 2000) [ 1472-4472 ] ; 2008.

RBID : pubmed:18666033

Descripteurs français

KwdFr :
- Antifongiques (pharmacologie), Calcineurine (métabolisme), Humains (MeSH), Inhibiteurs de la calcineurine (MeSH), Mycoses (microbiologie), Mycoses (traitement médicamenteux), Protein-Serine-Threonine Kinases (effets des médicaments et des substances chimiques), Protein-Serine-Threonine Kinases (métabolisme), Protéines de Saccharomyces cerevisiae (effets des médicaments et des substances chimiques), Protéines de Saccharomyces cerevisiae (métabolisme), Protéines du choc thermique HSP90 (effets des médicaments et des substances chimiques), Protéines du choc thermique HSP90 (métabolisme), Systèmes de délivrance de médicaments (MeSH), Transduction du signal (effets des médicaments et des substances chimiques).
MESH :
- effets des médicaments et des substances chimiques : Protein-Serine-Threonine Kinases, Protéines de Saccharomyces cerevisiae, Protéines du choc thermique HSP90, Transduction du signal.
- microbiologie : Mycoses.
- métabolisme : Calcineurine, Protein-Serine-Threonine Kinases, Protéines de Saccharomyces cerevisiae, Protéines du choc thermique HSP90.
- pharmacologie : Antifongiques.
- traitement médicamenteux : Mycoses.
- Humains, Inhibiteurs de la calcineurine, Systèmes de délivrance de médicaments.

English descriptors

KwdEn :
- Antifungal Agents (pharmacology), Calcineurin (metabolism), Calcineurin Inhibitors (MeSH), Drug Delivery Systems (MeSH), HSP90 Heat-Shock Proteins (drug effects), HSP90 Heat-Shock Proteins (metabolism), Humans (MeSH), Mycoses (drug therapy), Mycoses (microbiology), Protein-Serine-Threonine Kinases (drug effects), Protein-Serine-Threonine Kinases (metabolism), Saccharomyces cerevisiae Proteins (drug effects), Saccharomyces cerevisiae Proteins (metabolism), Signal Transduction (drug effects).
MESH :
- chemical , drug effects : HSP90 Heat-Shock Proteins, Protein-Serine-Threonine Kinases, Saccharomyces cerevisiae Proteins.
- chemical , metabolism : Calcineurin, HSP90 Heat-Shock Proteins, Protein-Serine-Threonine Kinases, Saccharomyces cerevisiae Proteins.
- chemical , pharmacology : Antifungal Agents.
- chemical : Calcineurin Inhibitors.
- drug effects : Signal Transduction.
- drug therapy : Mycoses.
- microbiology : Mycoses.
- Drug Delivery Systems, Humans.

Abstract

Microbes evolved to produce natural products that inhibit growth of competing soil microorganisms. In many cases these compounds act on fungi, which are eukaryotes with conserved gene sequences closely related to metazoans, including humans. The calcineurin inhibitors cyclosporin A and FK-506, the Tor inhibitor rapamycin, and the Hsp90 inhibitor geldanamycin, all act via targets conserved from yeast to humans. This allows the use of genetically tractable fungi as models to elucidate how these drugs and their targets function in yeast and human cells. These inhibitors also enable studies aimed at harnessing their intrinsic antimicrobial activities to develop novel antifungal therapies. Extensive studies have revealed a globally conserved role for the Tor protein in regulating growth and proliferation in response to nutrients, and targeting its essential functions results in robust antifungal action. Similarly, a conserved and essential role for calcineurin in fungal virulence has been established and could be targeted by inhibitors for therapeutic uses in a variety of clinical settings. Finally, the discovery that inhibitors of calcineurin or Hsp90 result in dramatic synergism with either azoles or glucan synthase inhibitors (candins) provides another therapeutic vantage point. Taken together, these fungal targets and their inhibitors provide a robust platform from which to develop novel antimicrobial therapies.

PubMed: 18666033
PubMed Central: PMC2715221

Affiliations:

Links toward previous steps (curation, corpus...)

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Le document en format XML

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<term>Protéines du choc thermique HSP90 (métabolisme)</term>
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<front><div type="abstract" xml:lang="en">Microbes evolved to produce natural products that inhibit growth of competing soil microorganisms. In many cases these compounds act on fungi, which are eukaryotes with conserved gene sequences closely related to metazoans, including humans. The calcineurin inhibitors cyclosporin A and FK-506, the Tor inhibitor rapamycin, and the Hsp90 inhibitor geldanamycin, all act via targets conserved from yeast to humans. This allows the use of genetically tractable fungi as models to elucidate how these drugs and their targets function in yeast and human cells. These inhibitors also enable studies aimed at harnessing their intrinsic antimicrobial activities to develop novel antifungal therapies. Extensive studies have revealed a globally conserved role for the Tor protein in regulating growth and proliferation in response to nutrients, and targeting its essential functions results in robust antifungal action. Similarly, a conserved and essential role for calcineurin in fungal virulence has been established and could be targeted by inhibitors for therapeutic uses in a variety of clinical settings. Finally, the discovery that inhibitors of calcineurin or Hsp90 result in dramatic synergism with either azoles or glucan synthase inhibitors (candins) provides another therapeutic vantage point. Taken together, these fungal targets and their inhibitors provide a robust platform from which to develop novel antimicrobial therapies.</div>
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Signaling cascades as drug targets in model and pathogenic fungi.

Signaling cascades as drug targets in model and pathogenic fungi.

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