摘要:
The present inventors have discovered that 5-Aminolevulinate synthase is essential for fungal pathogenicity. Specifically, the inhibition of 5-Aminolevulinate synthase gene expression in fungi results in no signs of successful infection or lesions. Thus, 5-Aminolevulinate synthase can be used as a target for the identification of antibiotics, preferably antifungals. Accordingly, the present invention provides methods for the identification of compounds that inhibit 5-Aminolevulinate synthase expression or activity. The methods of the invention are useful for the identification of antibiotics, preferably antifungals.
摘要:
The present inventors have discovered that &agr;-Aminoadipate Reductase is essential for fungal pathogenicity. Specifically, the inhibition of &agr;-Aminoadipate Reductase gene expression in fungi results in no signs of successful infection or lesions. Thus, &agr;-Aminoadipate Reductase can be used as a target for the identification of antibiotics, preferably antifungals. Accordingly, the present invention provides methods for the identification of compounds that inhibit &agr;-Aminoadipate Reductase expression or activity. The methods of the invention are useful for the identification of antibiotics, preferably antifungals.
摘要:
The present inventors have discovered that homocitrate synthase is essential for fungal pathogenicity. Specifically, the inhibition of homocitrate synthase gene expression in fungi results in no signs of successful infection or lesions. Thus, homocitrate synthase can be used as a target for the identification of antibiotics, preferably antifungals. Accordingly, the present invention provides methods for the identification of compounds that inhibit homocitrate synthase expression or activity. The methods of the invention are useful for the identification of antibiotics, preferably antifungals.
摘要:
Provided are ligands which bind to and regulate the function of CLEC-2. Nucleic acid CLEC-2 ligands described herein are able to inhibit CLEC-2 mediated platelet aggregation and may also provide use in regulating CLEC-2-mediated processes such as thrombus formation, tumor metastasis, lymphangiogenesis, HIV dissemination, inflammatory response, cytokine production and phagocytosis. Also disclosed herein are modulator molecules which can reverse the activity of the CLEC-2 ligand both in vitro and in vivo and ex vivo.