ライフサイエンスコーパス: donovani

1 tivity against the axenic form of Leishmania donovani .

2 and kinetic analysis of ASNA from Leishmania donovani.

3 ctivity against T. brucei rhodesiense and L. donovani.

4 atalyses beta-oxidation of fatty acids in L. donovani.

5 1) and its conjugation pathway in Leishmania donovani.

6 nucleobases and nucleosides as wild type L. donovani.

7 nt importance of AAH to purine salvage by L. donovani.

8 tion by macrophages infected with Leishmania donovani.

9 throponotic transmission cycle of Leishmania donovani.

10 eral leishmaniasis (VL) caused by Leishmania donovani.

11 ne protease activity expressed by Leishmania donovani.

12 eral leishmaniasis (VL) caused by Leishmania donovani.

13 e replacement within a virulent strain of L. donovani.

14 g this large (> 358 kDa) motor protein in L. donovani.

15 nst T. b. rhodesiense, P. falciparum, and L. donovani.

16 restrict the replication of intracellular L. donovani.

17 s involved in mediating susceptibility to L. donovani.

18 Trypanosoma cruzi, T. brucei, and Leishmania donovani.

19 st the intact parasites P. falciparum and L. donovani.

20 genes in human macrophages infected with L. donovani.

21 gainst the kinetoplastid parasite Leishmania donovani.

22 gene from the protozoan parasite Leishmania donovani.

23 olyamine auxotrophy in the Delta adometdc L. donovani.

24 plastida a gene encoding for centrin from L. donovani.

25 g of L. tropica and to a lesser extent of L. donovani.

26 elenocysteinyl-tRNA synthase from Leishmania donovani.

27 ceral leishmaniasis(VL) caused by Leishmania donovani.

28 caused by the protozoan parasite Leishmania donovani.

29 aniasis in children infected with Leishmania donovani.

30 cted against Trypanosoma cruzi or Leishmania donovani.

31 d 3) lower miltefosine-induced killing of L. donovani.

32 intracellular amastigotes form of Leishmania donovani.

33 on of the intracellular protozoan Leishmania donovani.

34 visceral leishmaniasis caused by Leishmania donovani.

35 and increased the early dissemination of L. donovani.

36 eted or nonsecreted chimeric protein with L. donovani 3' nucleotidase (NT-OVA).

37 caused by the protozoan parasite Leishmania donovani, a causative agent of visceral leishmaniasis (V

38 ion of a K39 kinesin homologue in Leishmania donovani, a medically important parasite of humans.

39 Leishmania donovani, a protozoan parasite, causes visceral disease

40 Leishmania donovani AAH is 38 and 23% identical to Saccharomyces ce

41 2.6 microM against cultured T. brucei and L. donovani amastigote-like forms, surpassing the activity

42 tor of ODC, inhibited growth of wild-type L. donovani amastigotes and effectively cured macrophages o

43 asma significantly enhanced the growth of L. donovani amastigotes in human macrophages.

44 highly active with IC(50) values against L. donovani amastigotes of 0.5 +/- 0.2 and 2.3 +/- 0.8 micr

45 dies, these data support a model in which L. donovani amastigotes readily salvage ornithine and have

46 erize chemokine action in the response to L. donovani and also reemphasize that (i) recruited mononuc

47 rine salvage by both life cycle stages of L. donovani and authenticate ASL as a potential drug target

48 iense, Plasmodium falciparum, and Leishmania donovani and cytotoxicities for mammalian cells were inf

49 iense, Plasmodium falciparum, and Leishmania donovani and cytotoxicity against mammalian cells were i

50 STAT1(-/-) mice were highly resistant to L. donovani and developed less immunopathology, whereas T-b

51 es, we generated Deltaarg null mutants in L. donovani and evaluated their ability to proliferate in v

52 determined the structures of the Leishmania donovani and human ribosomes at 2.9 A and 3.6 A, respect

53 caused by infection of C57BL/6 mice with L. donovani and identified an early suppressive role for IL

54 en synthesized and tested against Leishmania donovani and L. amazonensis intracellular amastigotes.

55 l leishmaniasis (VL) is caused by Leishmania donovani and Leishmania infantum chagasi.

56 In cultured L. donovani and T. brucei, treatment with 5 and 0.5 microM

57 e cytochrome c oxidase complex in Leishmania donovani and that upon deletion of its gene the parasite

58 iense, Plasmodium falciparum, and Leishmania donovani and their cytotoxicity for mammalian cells.

59 -) mice to control primary infection with L. donovani and to respond to chemotherapy.

60 rhodesiense , Trypanosoma cruzi , Leishmania donovani , and P. falciparum (K1 isolate).

61 odesiense, Trypanosoma cruzi, and Leishmania donovani), and several showed promising activity.

62 odesiense, Trypanosoma cruzi, and Leishmania donovani), and two compounds (14 and 21) showed good act

63 iense, Plasmodium falciparum, and Leishmania donovani, and for cytotoxicity against mammalian cells.

64 iense, Plasmodium falciparum, and Leishmania donovani, and for cytotoxicity against mammalian cells.

65 oned from Leishmania amazonensis, Leishmania donovani, and Leishmania major, which encoded 60-kDa pro

66 oma brucei rhodesiense, T. cruzi, Leishmania donovani, and Plasmodium falciparum, the causative agent

67 nneled to hypoxanthine and/or xanthine by L. donovani, and that the purine sources within the macroph

68 l components of purine salvage in Leishmania donovani, and therefore Deltaadss and Deltaasl null muta

69 Expression of Leishmania donovani APRT in transgenic T. gondii parasites yielded

70 Selenoproteins of L. donovani are not required for the growth of the promasti

71 species responsible for visceral disease (L. donovani), as well as species associated with persistent

72 iense, Plasmodium falciparum, and Leishmania donovani, as well as cytotoxicity against mammalian cell

73 sion in Escherichia coli implied that the L. donovani ASL could also recognize 5-aminoimidazole-(N-su

74 unds 14, 15, and 25 selectively inhibited L. donovani at nanomolar concentrations and showed much low

75 rgeted gene replacement within a virulent L. donovani background.

76 /day) was further studied against Leishmania donovani/BALB/c mice via the intraperitoneal route for 5

77 culosis, is a potent inhibitor of Leishmania donovani both in vitro and in vivo.

78 mponents of the purine salvage pathway of L. donovani, both ASL and ADSS are cytosolic enzymes.

79 granulomas may thus explain the increased L. donovani burden in the liver and spleen.

80 mycin selectively inhibits the eukaryotic L. donovani, but not human, ribosome.

81 in mice and humans infected with Leishmania donovani, but their contribution to host resistance agai

82 sand flies favor the transmissibility of L. donovani by infected hosts, owing to a systemic effect t

83 f IL-17A rendering susceptibility against L. donovani by regulating the IFN-gamma response and promot

84 hibit sterol biosynthesis in T. cruzi and L. donovani by the inhibition of the enzyme sterol 24-methy

85 ana infection, suggesting that attenuated L. donovani can provide protection against heterologous L.

86 mation such as chronic infection (Leishmania donovani), cancer (melanoma and colorectal carcinoma), a

87 Leishmania donovani cannot synthesize purines de novo and express a

88 Leishmania donovani cannot synthesize purines de novo and obligator

89 lipid, in successful survival of Leishmania donovani, causative agent of the fatal visceral leishman

90 he pathogenic protozoan parasite, Leishmania donovani, causative agent of the tropical infectious dis

91 Vector-transmitted L. infantum and L. donovani caused >/=5-fold increase in spleen weight comp

92 Leishmania donovani causes visceral leishmaniasis (VL), the second

93 w that in muMT mice infected with Leishmania donovani, CD8 T cells displayed a greater cytotoxic pote

94 e C57BL/6 (B6) mice infected with Leishmania donovani, CD8(+) T cell mechanisms are required for gran

95 and subsepecies of such protozoa, Leishmania donovani chagasi causes visceral leishmaniasis.

96 ave implications for human S. mansoni and L. donovani co-infections and also demonstrate that granulo

97 nst T. b. rhodesiense, P. falciparum, and L. donovani combined with high antitrypanosomal efficacy in

98 T. brucei rhodesiense, P. falciparum, and L. donovani compared to pentamidine.

99 able to control hepatic growth of Leishmania donovani compared with wild-type mice.

100 us in aggregate; the Leishmania (Leishmania) donovani complex in aggregate; the species L (L) tropica

101 rypanosomatid pathogen of humans, Leishmania donovani, constitutively expresses a unique externally o

102 lly, four compounds were found to inhibit L. donovani cysteine protease.

103 ial cysteine proteases as well as Leishmania donovani cysteine protease.

104 ral IFN response genes in L. major versus L. donovani DC infections.

105 NT1.1 nucleoside transporter from Leishmania donovani defined two amino acid residues in predicted tr

106 Unlike wild type L. donovani, Deltaadss and Deltaasl parasites in culture ex

107 agent of visceral leishmaniasis, Leishmania donovani, does not prime human DC for IL-12 production.

108 ification of the gene encoding this novel L. donovani enzyme.

109 Our results suggest that, although L. donovani evades host immune response, at least in part t

110 Our results reveal the complexity of L. donovani evolution in the ISC in response to drug treatm

111 Collectively our results showed that L. donovani exploited the macrophage anti-apoptotic protein

112 Leishmania donovani express two members of the equilibrative nucleo

113 mice intravenously infected with Leishmania donovani form heterogeneous skin parasite patches that g

114 The transmission of L. donovani from sick hamsters to flies was surprisingly lo

115 o track the evolution and epidemiology of L. donovani from the ISC.

116 Metalloprotease gp63 (Leishmania donovani gp63 (Ldgp63)) is a critical virulence factor s

117 egg granuloma, consistent with a lack of L. donovani granuloma assembly in this tissue microenvironm

118 ing liver immunopathology and controlling L. donovani growth in TCCR-/- mice.

119 hed S. mansoni infections fail to control L. donovani growth in the liver and spleen.

120 Hs-SAHH > Tc-SAHH > Ld-SAHH (from Leishmania donovani) > Pf-SAHH (from Plasmodium falciparum), which

121 .69% and 80.93 +/- 10.50% against Leishmania donovani /hamster model.

122 mpounds, 16, 17, and 22, were tested in a L. donovani/hamster model.

123 ishmania (Leishmania mexicana complex and L. donovani) has been established.

124 Studies of Leishmania donovani have shown that both ornithine decarboxylase an

125 e STIB900, T. cruzi Tulahuan, and Leishmania donovani HU3.

126 or the growth of the promastigote form of L. donovani in culture, that all uracil and pyrimidine nucl

127 d to kill approximately 90-95% of Leishmania donovani in livers of mice deficient in mechanisms of ac

128 s role in preventing clearance of Leishmania donovani in murine models of VL.

129 ei brucei, Trypanosoma cruzi, and Leishmania donovani in vitro.Only monoesters 7-9 with a log P value

130 show that HSCs are infected with Leishmania donovani in vivo and in vitro and that this infection le

131 visceral leishmaniasis, caused by Leishmania donovani, in contrast to infection in mice, mimics the p

132 udies with nucleoside transport-deficient L. donovani indicate that this phenomenon is mediated by th

133 asis in both life cycle stages of Leishmania donovani, individual mutant lines deficient in either ca

134 s by which resistant clinical isolates of L. donovani induce intracellular events relevant to drug re

135 Our data revealed that L. major, but not L. donovani, induces expression of IRF2, IRF7, and IFIT5, i

136 Consequently, in L. donovani infected BALB/c mice, IL-13 promotes hepatic gr

137 Significantly, MZMs were preserved in L. donovani-infected B6.TNF-alpha(-/-) mice or mice that re

138 n responses were characterized in Leishmania donovani-infected BALB/c mice in which IL-10 was absent

139 as similar therapeutic potential, Leishmania donovani-infected BALB/c mice were injected with anti-IL

140 In nonvaccinated Leishmania donovani-infected BALB/c mice, HASPB- and KMP11-specific

141 L. donovani-infected hamsters underwent xenodiagnoses with

142 In vitro studies clearly show that L. donovani-infected HSCs induce CD4(+) T cells to become T

143 L. donovani-infected IL-13(-/-) mice also responded poorly

144 etect serum antibodies in 104 asymptomaticL. donovani-infected individuals (qualified as positive for

145 Leishmania donovani-infected interleukin-13-/- BALB/c mice showed i

146 Together, the results for the L. donovani-infected livers of chemokine-deficient mice (CX

147 We show that Leishmania donovani-infected macrophages (MPhis) are capable of sti

148 ption factor was significantly reduced in L. donovani-infected macrophages and required de novo trans

149 Moreover, live microscopy of L. donovani-infected macrophages treated with Wnt5a demonst

150 sphatases, thioredoxin, SOCS, and Egr1 in L. donovani-infected macrophages was found to be unaffected

151 Leishmania donovani-infected macrophages were much more resistant t

152 phagocytosis or on cytokines released by L. donovani-infected macrophages, such as interleukin-1beta

153 cells in the skin-draining lymph nodes of L. donovani-infected malnourished mice.

154 how that the enhanced early resistance in L. donovani-infected mice is entirely due to the activity o

155 cci are rapidly trapped in the spleens of L. donovani-infected mice.

156 1, Arg-1, and MRC-1 genes, compared to WT L. donovani-infected mice.

157 Interestingly, L. donovani-infected TCCR-/- mice controlled the parasite g

158 l role for ceramide in the perspective of L. donovani infection and help formulate an antileishmanial

159 cell-deficient CD1d(-/-) mice to Leishmania donovani infection and Leishmania-induced CD1d-dependent

160 IFN-gamma) controls intracellular Leishmania donovani infection and the efficacy of antimony (Sb) che

161 ecruited into the spleen and liver during L. donovani infection and they are preferential targets for

162 nous IL-10 primarily regulates killing in L. donovani infection by suppressing production of and resp

163 L. donovani infection drastically reduced Lys 63-linked ubi

164 uring C57BL/6 mice, intracellular Leishmania donovani infection enhanced Toll-like receptor 4 (TLR4)

165 w that DCs from mice with chronic Leishmania donovani infection fail to migrate from the marginal zon

166 l zone macrophages resulting from Leishmania donovani infection have increased resistance to Streptoc

167 maniasis (VL) by monitoring the course of L. donovani infection in TCCR-deficient C57BL/6 (TCCR-/-) m

168 uired resistance in intracellular Leishmania donovani infection in the liver, inducing gamma interfer

169 Thus, in experimental L. donovani infection in the liver, TLR4 signaling upregula

170 -6, responses to an intracellular Leishmania donovani infection in the livers of IL-6(-/-) and wild-t

171 ed resistance of p110delta(D910A) mice to L. donovani infection is due in part to impaired expansion

172 We further demonstrate that L. donovani infection leads to expansion of HSCs in a p110d

173 We have recently reported that Leishmania donovani infection results in a remarkably selective los

174 nd developed severe liver pathology after L. donovani infection that eventually resolved.

175 hi) iMOs into the liver and spleen during L. donovani infection using a CCR2 antagonist reduces the f

176 tment of Ly6C(hi) iMOs into organs during L. donovani infection, and adaptive transfer of wild type L

177 an efficient Th1 response during Leishmania donovani infection, but they play distinct roles in dete

178 ng, revamping Wnt5a signaling can inhibit L. donovani infection, irrespective of drug sensitivity or

179 afficking and hepatic inflammation during L. donovani infection, it is not essential for immunity aga

180 sults showed that compared with wild-type L. donovani infection, LdCen(-/-) parasites induce signific

181 luation in a mouse model of acute Leishmania donovani infection, one phenylpyridine derivative (37) s

182 nfirming that Wnt5a signaling antagonizes L. donovani infection.

183 cell responses during the early stages of L. donovani infection.

184 rotective manner to animals with existing L. donovani infection.

185 nflammation and granuloma formation after L. donovani infection.

186 lationship of Wnt5a signaling and Leishmania donovani infection.

187 et for therapeutic inhibition in visceral L. donovani infection.

188 d early visceralization following Leishmania donovani infection.

189 Leishmania donovani infects macrophages, disrupting immune homeosta

190 We show that the protozoan Leishmania donovani inhibits CD1 expression and prevents activation

191 The initial macrophage-Leishmania donovani interaction results in the formation of membran

192 Leishmania donovani is a protozoan parasite.

193 Leishmania donovani is an intracellular parasite that infects profe

194 The pathogenic protozoan parasite Leishmania donovani is capable of both de novo pyrimidine biosynthe

195 r contribution to host resistance against L. donovani is not clear.

196 East Africa, where Leishmania donovani is prevalent, faces the highest burden world-wi

197 he lymph node barrier to dissemination of L. donovani is related to insufficient numbers of lymph nod

198 mice with the protozoan parasite Leishmania donovani, is characterized by focal accumulation of infl

199 cted into a Deltaldnt1/Deltaldnt2 Leishmania donovani knockout.

200 regulation in which the parasite Leishmania donovani (Ld) causes mitochondrial depolarization, reduc

201 s of the dimeric APRT enzyme from Leishmania donovani (LdAPRT) bear many similarities to other member

202 e attenuated centrin gene-deleted Leishmania donovani (LdCen(-/-) ) parasites through induction of Th

203 er a live attenuated centrin gene-deleted L. donovani (LdCen1(-/-)) parasite can persist and be both

204 By screening Leishmania donovani libraries with polyclonal antibodies against pr

205 solution significantly suppressed Leishmania donovani liver parasite burdens (p<0.05) but could not i

206 aken together, these results suggest that L. donovani may exploit SOCS for subverting macrophage apop

207 previously observed in mice infected with L. donovani, may thus account for the selective loss of MZM

208 These results suggest that L. donovani might exploit host A20 to inhibit the TLR2-medi

209 flammation was also observed in a Leishmania donovani model of chronic infection.

210 However, in the Leishmania donovani model of pathogen persistence, Il10(-/-)/hIL10B

211 In this study, we showed that Leishmania donovani modulates the TLR2-mediated pathway in macropha

212 mal cells from mice infected with Leishmania donovani more effectively supported differentiation of t

213 In a Leishmania donovani mouse model, two racemic phenylpyridines (71 an

214 which was classified as ABCC2 or Leishmania donovani multidrug resistance protein 2 (LdMRP2).

215 L. donovani mutants deficient in de novo pyrimidine biosynt

216 These studies validate L. donovani NMT as a potential target for development of ne

217 The open reading frame of L. donovani NMT has been amplified and used to overproduce

218 resulting in novel, highly potent Leishmania donovani NMT inhibitors with good selectivity over the h

219 substrate specificity data identify this L. donovani nucleoside hydrolase as a nonspecific nucleosid

220 ated a computational model of the Leishmania donovani nucleoside transporter 1.1 (LdNT1.1) that captu

221 cted transmembrane domains of the Leishmania donovani nucleoside transporter 1.1, LdNT1.1, which tran

222 tly, we have demonstrated that a Deltaodc L. donovani null mutant lacking ornithine decarboxylase (OD

223 etically modified live-attenuated Leishmania donovani parasite cell lines (LdCen(-/-) and Ldp27(-/-))

224 our PfCENs in a centrin knock-out Leishmania donovani parasite line that exhibited a severe growth de

225 vaccines such as centrin deleted Leishmania donovani parasites (LdCen (-/-)) showed protective immun

226 Leishmania donovani parasites are the cause of visceral leishmanias

227 onstrate the potential of live-attenuated L. donovani parasites as pan-Leishmania species vaccines.

228 Starvation of Leishmania donovani parasites for purines leads to a rapid amplific

229 L donovani parasites were serially passaged in mice expose

230 tes (compared to that with wild-type [WT] L. donovani parasites) induced significantly higher product

231 e shown that genetically modified Leishmania donovani parasites, here described as live attenuated pa

232 Leishmania donovani possess two closely related genes that encode h

233 sary for the viability and growth of both L. donovani promastigotes and amastigotes and intimate that

234 drolase was localized to specific foci in L. donovani promastigotes by immunofluorescent assays.

235 In the first phase, L. donovani promastigotes induce activation of acid sphingo

236 0 artemisinin derivatives against Leishmania donovani promastigotes is described for the first time.

237 In fact, in L. donovani promastigotes, we verified for 7 a decrease of

238 s is an essential nutritional pathway for L. donovani promastigotes.

239 te that it is constitutively expressed in L. donovani promastigotes.

240 Leishmania donovani protozoan parasites, the causative agent of vis

241 g IL-13 or TGF-beta enabled inhibition of L. donovani replication but little parasite killing; anti-I

242 yrian hamster (Mesocricetus auratus) with L. donovani reproduced the clinicopathological features of

243 ive protozoan pathogen of humans, Leishmania donovani, resides and multiplies in highly restricted mi

244 is caused by Leishmania major and Leishmania donovani, respectively.

245 tant of L. donovani that establishes that L. donovani salvages purines primarily through hypoxanthine

246 Infection with antimony-resistant Leishmania donovani (Sb(R)LD) induces aggressive pathology in the m

247 r mechanism of antimony-resistant Leishmania donovani (Sb(R)LD)-driven up-regulation of IL-10 and mul

248 infected with antimony-resistant Leishmania donovani (Sb(R)LD).

249 ompared with ones with antimony-sensitive L. donovani (Sb(S)LD) infection.

250 d/inactive form of the parasite enzyme in L. donovani significantly reduced their release of secretor

251 rts extensive skin infection with Leishmania donovani, spatial analyses at macro-(quantitative PCR) a

252 h Dakota) and infection caused by Leishmania donovani species complex.

253 ted individuals (qualified as positive forL. donovani-specific antibodies by direct agglutination tes

254 Previous efforts to generate an L. donovani strain deficient in both hypoxanthine-guanine p

255 istance in two clinically derived Leishmania donovani strains with different inherent resistance to a

256 bisbenzofurans displayed activity against L. donovani superior to that of pentamidine.

257 pite the development of a functional anti-L. donovani Th1 response that can mediate granuloma formati

258 Five congeners were more active against L. donovani than pentamidine.

259 acellular replication of residual Leishmania donovani that escape chemotherapy evolves to a host mech

260 nal lethal Deltahgprt/Deltaxprt mutant of L. donovani that establishes that L. donovani salvages puri

261 polyamine biosynthetic pathway of Leishmania donovani, the causal agent of visceral leishmaniasis, ar

262 In this study the interactions of Leishmania donovani, the causative agent of visceral Leishmaniasis,

263 ens against the tropical parasite Leishmania donovani, the causative agent of visceral leishmaniasis.

264 Unlike wild type L. donovani, the Deltahgprt/Deltaxprt knock-out cannot grow

265 However, for Leishmania donovani, the DNA-binding activity and the majority of r

266 t, IL-12p40 expression is not elicited by L. donovani, the etiological agent of deadly visceral leish

267 polyamine biosynthetic pathway of Leishmania donovani, the etiological agent of visceral leishmaniasi

268 d a proof-of-concept of SL-seq in Leishmania donovani, the main causative agent of visceral leishmani

269 stigated the interactions between Leishmania donovani, the main etiological agent of visceral leishma

270 strate that during infection with Leishmania donovani, the marginal zone of mice undergoes extensive

271 Here we have engineered Leishmania donovani to express high levels of an active LPG2 Golgi

272 o transmit Leishmania infantum or Leishmania donovani to hamsters.

273 by the intra-macrophage parasite Leishmania donovani to protect their "home" from actinomycin D-indu

274 ans were quantified and the sensitivity of L donovani to sodium stibogluconate assessed at each passa

275 y in Leishmania, has not been analyzed in L. donovani To test ARG function in intact parasites, we ge

276 A crystal structure of an active truncated L.donovani TOP1L/TOP1S heterodimer bound to nicked double-

277 inct protozoan (Leishmania major, Leishmania donovani, Toxoplasma gondii) and helminth (Brugia malayi

278 t relevant to human disease, i.e. Leishmania donovani, Trypanosoma cruzi and Trypanosoma brucei.

279 terized a drug-resistant clonal mutant of L. donovani (TUBA5) that is deficient in LdNT1 transport an

280 involving Schistosoma mansoni and Leishmania donovani, two important human pathogens affecting the li

281 highlights the non-canonical function of L. donovani tyrosyl-tRNA synthetase.

282 e Ufm1-mediated modifications, we made an L. donovani Ufm1 null mutant (Ufm1(-/-)).

283 In this work we demonstrate that L. donovani UMPS (LdUMPS) is an essential enzyme in promast

284 it is not essential for immunity against L. donovani, unlike L. major.

285 Genetic analysis has authenticated L. donovani uracil phosphoribosyltransferase (LdUPRT), an e

286 ease from the parasitic protozoan Leishmania donovani, using ab initio computation.

287 In established Leishmania donovani visceral infection in normal mice, anti-interle

288 e failed to control intracellular Leishmania donovani visceral infection, indicating that acquired re

289 ease (SUB; Clan SB, family S8) of Leishmania donovani was cloned and found to possess a unique cataly

290 ease from the parasitic protozoan Leishmania donovani was modeled using ab initio computation.

291 significant uptake of L. tropica by MCs, L. donovani was not phagocytosed.

292 To test this hypothesis, Leishmania donovani was serially passaged in mice exposed to arseni

293 n mice infected with the parasite Leishmania donovani, we identified a transcriptomic network operati

294 th antimony drug-sensitive and -resistant L. donovani, we noted disruption in the steady-state level

295 LdNT2 nucleoside transporter from Leishmania donovani were mutated and the resultant phenotypes evalu

296 is expressed in both life cycle stages of L. donovani, whereas subcellular fractionation and immunofl

297 he only crystal structure is from Leishmania donovani, which expresses a long form of the enzyme with

298 antileishmanial activity against Leishmania donovani with an IC50 value of 9.22 muM.

299 exhibited potent activity against Leishmania donovani with IC(50) values ranging from 3.75 to 10.37 m

300 rypanosoma brucei rhodesiense and Leishmania donovani with IC50 values of 1.55 and 0.22 muM, respecti