Downregulation of FeSOD-A expression in Leishmania infantum alters trivalent antimony and miltefosine susceptibility.

Ana Maria Murta SantiPaula Alves SilvaIsabella Fernandes Martins SantosSilvane Maria Fonseca Murta

Published in: Parasites & vectors (2021)

The unsuccessful attempts to delete FeSOD-A suggest that this gene is essential in L. infantum. This enzyme plays an important role in the defence against oxidative stress and infectivity in THP-1 macrophages. FeSOD-A-deficient L. infantum parasites deregulate their metabolic pathways related to antimony and miltefosine resistance.

Keyphrases

oxidative stress
poor prognosis
cell proliferation
signaling pathway
genome wide
copy number
long non coding rna
diabetic rats
genome wide identification
heat stress