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Alix T. Coste

Researcher at University of Lausanne

Publications -  83
Citations -  4803

Alix T. Coste is an academic researcher from University of Lausanne. The author has contributed to research in topics: Candida albicans & Gene. The author has an hindex of 30, co-authored 73 publications receiving 3928 citations. Previous affiliations of Alix T. Coste include University Hospital of Lausanne & Institut national de la recherche agronomique.

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Antifungal resistance and new strategies to control fungal infections.

TL;DR: It appears that major mechanisms of resistance are essential due to the deregulation of antifungal resistance effector genes, which is a consequence of point mutations occurring in transcriptional regulators of theseEffector genes.
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TAC1, transcriptional activator of CDR genes, is a new transcription factor involved in the regulation of Candida albicans ABC transporters CDR1 and CDR2.

TL;DR: TAC1 appears to be the first C. albicans transcription factor involved in the control of genes mediating antifungal resistance, and is relevant for azole resistance, since a TAC1 allele recovered from an azole-resistant strain could trigger constitutive upregulation of CDR1 and CDR2 in an azolesceptible laboratory strain.
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Flagellin stimulation of intestinal epithelial cells triggers CCL20-mediated migration of dendritic cells

TL;DR: The data show that crosstalk between bacterial flagellin and epithelial cells is essential for the recruitment of DCs, a mechanism that could be instrumental to initiate adaptive immune responses in the gut.
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A Mutation in Tac1p, a Transcription Factor Regulating CDR1 and CDR2, Is Coupled With Loss of Heterozygosity at Chromosome 5 to Mediate Antifungal Resistance in Candida albicans

TL;DR: The mechanisms by which hyperactive alleles become homozygous was addressed by comparative genome hybridization and single nucleotide polymorphism arrays and indicated that loss of TAC1 heterozygosity can occur by recombination between portions of chromosome 5 or by chromosome 5 duplication.
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Genotypic Evolution of Azole Resistance Mechanisms in Sequential Candida albicans Isolates

TL;DR: This work shows that azole resistance was due not only to the presence of specific mutations in azoles resistance genes but also to their increase in copy number by LOH and to the addition of extra Chr 5 copies.