Background: Cell cycle-specific localization and nuclear function of Phosphatidylinositol-4-phosphate 5-kinase1␣ (PIP5K) is unclear. Results: SUMOylation of PIP5K at Lys-244 and Lys-490 directs its nuclear entry and its interaction with H3K9me3/HP1-␣, respectively. Conclusion: PIP5K functions as a member of the rDNA silencing complex. Significance: Our results indicate a possible novel epigenetic role of PIP5K per se in silencing of rDNA.
Visceral leishmaniasis, a vector-borne tropical disease that is threatening about 350 million people worldwide, is caused by the protozoan parasite Leishmania donovani. Metalloids like arsenic and antimony have been used to treat diseases like leishmaniasis caused by the kinetoplastid parasites. Arsenic (III) at a relatively higher concentration (30 μg/mL) has been shown to have antileishmanial activity, but this concentration is reported to be toxic in several experimental mammalian systems. Nanosized metal (0) particles have been shown to be more effective than their higher oxidation state forms. There is no information so far regarding arsenic nanoparticles (As-NPs) as an antileishmanial agent. We have tested the antileishmanial properties of the As-NPs, developed for the first time in our laboratory. As-NPs inhibited the in vitro growth, oxygen consumption, infectivity, and intramacrophage proliferation of L. donovani parasites at a concentration which is about several fold lower than that of As (III). Moreover, this antileishmanial activity has comparatively less cytotoxic effect on the mouse macrophage cell line. It is evident from our findings that As-NPs have more potential than As (III) to be used as an antileishmanial agent.
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