A Leishmania infantum genetic marker associated with miltefosine treatment failure for visceral leishmaniasis

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Conditional gene deletion with DiCre demonstrates an essential role for CRK3 in Leishmania mexicana cell cycle regulation
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From the same journal

Follicular Helper T Cells are Essential for the Elimination of Plasmodium Infection
Pérez-Mazliah, D., Nguyen, M. P., Hosking, C., McLaughlin, S., Lewis, M. D., Tumwine, I., Levy, P. & Langhorne, J., Oct 2017
Article in EBioMedicine

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Mottram - Carnielli Manuscript - Figures - Appendix (EBioMedicine)
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Published copy (DOI)

10.1016/j.ebiom.2018.09.029

Author(s)

Jeremy Charles Mottram
Daniel Jeffares
Juliana Brambilla Carnielli Trindade
Kathryn Crouch
Sarah Jayne Forrester
Vladimir Costa Silva
Silvio F.G. Carvalho
Jeziel D Damasceno
Elaine Brown
Nicholas J Dickens
Dorcas L. Costa
Carlos H.N. Costa
Reynaldo Dietze

Department/unit(s)

Publication details

Journal	EBioMedicine
Date	Accepted/In press - 17 Sep 2018
Date	E-pub ahead of print - 27 Sep 2018
Date	Published (current) - 27 Sep 2018
Volume	36
Number of pages	9
Early online date	27/09/18
Original language	English

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By the same authors

Evaluation of Clan CD C11 peptidase PNT1 and other Leishmania mexicana cysteine peptidases as potential drug targets

Natural Resistance of Leishmania infantum to Miltefosine Contributes to the Low Efficacy in the Treatment of Visceral Leishmaniasis in Brazil

Tissue and host species-specific transcriptional changes in models of experimental visceral leishmaniasis [version 2; referees: 4 approved]

PNT1 is a C11 Cysteine Peptidase Essential for Replication of the Trypanosome Kinetoplast.

Conditional gene deletion with DiCre demonstrates an essential role for CRK3 in Leishmania mexicana cell cycle regulation

From the same journal

Follicular Helper T Cells are Essential for the Elimination of Plasmodium Infection

A Leishmania infantum genetic marker associated with miltefosine treatment failure for visceral leishmaniasis

Full text download(s)

Published copy (DOI)

Author(s)

Department/unit(s)

Publication details

Bibliographical note

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