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1 tivity against the axenic form of Leishmania donovani .
2 elenocysteinyl-tRNA synthase from Leishmania donovani.
3 ceral leishmaniasis(VL) caused by Leishmania donovani.
4  caused by the protozoan parasite Leishmania donovani.
5 aniasis in children infected with Leishmania donovani.
6 cted against Trypanosoma cruzi or Leishmania donovani.
7 d 3) lower miltefosine-induced killing of L. donovani.
8 intracellular amastigotes form of Leishmania donovani.
9 on of the intracellular protozoan Leishmania donovani.
10  visceral leishmaniasis caused by Leishmania donovani.
11  and increased the early dissemination of L. donovani.
12 and kinetic analysis of ASNA from Leishmania donovani.
13 ctivity against T. brucei rhodesiense and L. donovani.
14 atalyses beta-oxidation of fatty acids in L. donovani.
15 1) and its conjugation pathway in Leishmania donovani.
16  nucleobases and nucleosides as wild type L. donovani.
17 nt importance of AAH to purine salvage by L. donovani.
18 tion by macrophages infected with Leishmania donovani.
19 ne protease activity expressed by Leishmania donovani.
20 eral leishmaniasis (VL) caused by Leishmania donovani.
21 e replacement within a virulent strain of L. donovani.
22 g this large (> 358 kDa) motor protein in L. donovani.
23 nst T. b. rhodesiense, P. falciparum, and L. donovani.
24 restrict the replication of intracellular L. donovani.
25 ch are associated with protection against L. donovani.
26 s involved in mediating susceptibility to L. donovani.
27 0) against the protozoan parasite Leishmania donovani.
28  mg/kg) for the treatment of VL caused by L. donovani.
29 onocytes, which mediate susceptibility to L. donovani.
30 throponotic transmission cycle of Leishmania donovani.
31 eral leishmaniasis (VL) caused by Leishmania donovani.
32 g of L. tropica and to a lesser extent of L. donovani.
33  caused by the protozoan parasite Leishmania donovani, a causative agent of visceral leishmaniasis (V
34 ion of a K39 kinesin homologue in Leishmania donovani, a medically important parasite of humans.
35                                   Leishmania donovani AAH is 38 and 23% identical to Saccharomyces ce
36                             Additionally, L. donovani activates IDO/kynurenine/AHR signaling in BMM s
37 tor of ODC, inhibited growth of wild-type L. donovani amastigotes and effectively cured macrophages o
38 asma significantly enhanced the growth of L. donovani amastigotes in human macrophages.
39  highly active with IC(50) values against L. donovani amastigotes of 0.5 +/- 0.2 and 2.3 +/- 0.8 micr
40 dies, these data support a model in which L. donovani amastigotes readily salvage ornithine and have
41 lquinoline derivatives, targeting Leishmania donovani, among which CQFC1 showed the highest efficacy
42 erize chemokine action in the response to L. donovani and also reemphasize that (i) recruited mononuc
43 rine salvage by both life cycle stages of L. donovani and authenticate ASL as a potential drug target
44 iense, Plasmodium falciparum, and Leishmania donovani and cytotoxicities for mammalian cells were inf
45 iense, Plasmodium falciparum, and Leishmania donovani and cytotoxicity against mammalian cells were i
46  STAT1(-/-) mice were highly resistant to L. donovani and developed less immunopathology, whereas T-b
47 es, we generated Deltaarg null mutants in L. donovani and evaluated their ability to proliferate in v
48  determined the structures of the Leishmania donovani and human ribosomes at 2.9 A and 3.6 A, respect
49  caused by infection of C57BL/6 mice with L. donovani and identified an early suppressive role for IL
50 en synthesized and tested against Leishmania donovani and L. amazonensis intracellular amastigotes.
51 ites of the Leishmania donovani complex - L. donovani and L. infantum - cause the fatal disease visce
52 ty against a range of clinically relevant L. donovani and L. infantum isolates.
53 l leishmaniasis (VL) is caused by Leishmania donovani and Leishmania infantum chagasi.
54 caused by the protozoan parasites Leishmania donovani and Leishmania infantum, is one of the major pa
55 caused by the protozoan parasites Leishmania donovani and Leishmania infantum.
56 fective for the treatment of VL caused by L. donovani and mediates its antileishmanial activity by pr
57 rypanosoma brucei rhodesiense and Leishmania donovani and nanomolar potency against Plasmodium falcip
58 e cytochrome c oxidase complex in Leishmania donovani and that upon deletion of its gene the parasite
59 iense, Plasmodium falciparum, and Leishmania donovani and their cytotoxicity for mammalian cells.
60 -) mice to control primary infection with L. donovani and to respond to chemotherapy.
61 plastid species, putative stem-loops from L. donovani and Trypanosoma brucei nucleobase transporter m
62 rhodesiense , Trypanosoma cruzi , Leishmania donovani , and P. falciparum (K1 isolate).
63 odesiense, Trypanosoma cruzi, and Leishmania donovani), and several showed promising activity.
64 odesiense, Trypanosoma cruzi, and Leishmania donovani), and two compounds (14 and 21) showed good act
65    Expression of ISP2 was not detected in L. donovani, and a transgenic line constitutively expressin
66 iense, Plasmodium falciparum, and Leishmania donovani, and for cytotoxicity against mammalian cells.
67 iense, Plasmodium falciparum, and Leishmania donovani, and for cytotoxicity against mammalian cells.
68 oma brucei rhodesiense, T. cruzi, Leishmania donovani, and Plasmodium falciparum, the causative agent
69 reening these compounds against T. cruzi, L. donovani, and S. mansoni.
70 nneled to hypoxanthine and/or xanthine by L. donovani, and that the purine sources within the macroph
71 l components of purine salvage in Leishmania donovani, and therefore Deltaadss and Deltaasl null muta
72                         Selenoproteins of L. donovani are not required for the growth of the promasti
73 iense, Plasmodium falciparum, and Leishmania donovani, as well as cytotoxicity against mammalian cell
74 sion in Escherichia coli implied that the L. donovani ASL could also recognize 5-aminoimidazole-(N-su
75 unds 14, 15, and 25 selectively inhibited L. donovani at nanomolar concentrations and showed much low
76 rgeted gene replacement within a virulent L. donovani background.
77 /day) was further studied against Leishmania donovani/BALB/c mice via the intraperitoneal route for 5
78 culosis, is a potent inhibitor of Leishmania donovani both in vitro and in vivo.
79 mponents of the purine salvage pathway of L. donovani, both ASL and ADSS are cytosolic enzymes.
80 granulomas may thus explain the increased L. donovani burden in the liver and spleen.
81 that miR155 contributes to the control of L. donovani but is not essential for infection resolution.
82 erimental visceral leishmaniasis (Leishmania donovani) but more severe disease in a model of malaria
83 mycin selectively inhibits the eukaryotic L. donovani, but not human, ribosome.
84  in mice and humans infected with Leishmania donovani, but their contribution to host resistance agai
85  sand flies favor the transmissibility of L. donovani by infected hosts, owing to a systemic effect t
86 f IL-17A rendering susceptibility against L. donovani by regulating the IFN-gamma response and promot
87 hibit sterol biosynthesis in T. cruzi and L. donovani by the inhibition of the enzyme sterol 24-methy
88 ana infection, suggesting that attenuated L. donovani can provide protection against heterologous L.
89 mation such as chronic infection (Leishmania donovani), cancer (melanoma and colorectal carcinoma), a
90                                   Leishmania donovani cannot synthesize purines de novo and express a
91                                   Leishmania donovani cannot synthesize purines de novo and obligator
92  lipid, in successful survival of Leishmania donovani, causative agent of the fatal visceral leishman
93 he pathogenic protozoan parasite, Leishmania donovani, causative agent of the tropical infectious dis
94        Vector-transmitted L. infantum and L. donovani caused >/=5-fold increase in spleen weight comp
95                                   Leishmania donovani causes visceral leishmaniasis (VL), the second
96 w that in muMT mice infected with Leishmania donovani, CD8 T cells displayed a greater cytotoxic pote
97 e C57BL/6 (B6) mice infected with Leishmania donovani, CD8(+) T cell mechanisms are required for gran
98 and subsepecies of such protozoa, Leishmania donovani chagasi causes visceral leishmaniasis.
99 ave implications for human S. mansoni and L. donovani co-infections and also demonstrate that granulo
100 nst T. b. rhodesiense, P. falciparum, and L. donovani combined with high antitrypanosomal efficacy in
101 T. brucei rhodesiense, P. falciparum, and L. donovani compared to pentamidine.
102 able to control hepatic growth of Leishmania donovani compared with wild-type mice.
103        Protozoan parasites of the Leishmania donovani complex - L. donovani and L. infantum - cause t
104 us in aggregate; the Leishmania (Leishmania) donovani complex in aggregate; the species L (L) tropica
105 leishmaniasis (VL), caused by the Leishmania donovani complex, is a fatal, neglected tropical disease
106 the evolution and genetics of the Leishmania donovani complex.
107 lly, four compounds were found to inhibit L. donovani cysteine protease.
108 ral IFN response genes in L. major versus L. donovani DC infections.
109                          Unlike wild type L. donovani, Deltaadss and Deltaasl parasites in culture ex
110 were compared on small amounts of Leishmania donovani DNA, testing their ability to preserve specific
111  agent of visceral leishmaniasis, Leishmania donovani, does not prime human DC for IL-12 production.
112        Our results suggest that, although L. donovani evades host immune response, at least in part t
113      Our results reveal the complexity of L. donovani evolution in the ISC in response to drug treatm
114      Collectively our results showed that L. donovani exploited the macrophage anti-apoptotic protein
115 llectively, our findings demonstrate that L. donovani exploits specific histone lysine methyltransfer
116 mmunoprecipitation analysis revealed that L. donovani facilitated H3K36 dimethylation at TNF-alpha pr
117  mice intravenously infected with Leishmania donovani form heterogeneous skin parasite patches that g
118                       The transmission of L. donovani from sick hamsters to flies was surprisingly lo
119 o track the evolution and epidemiology of L. donovani from the ISC.
120             Metalloprotease gp63 (Leishmania donovani gp63 (Ldgp63)) is a critical virulence factor s
121  egg granuloma, consistent with a lack of L. donovani granuloma assembly in this tissue microenvironm
122 ing liver immunopathology and controlling L. donovani growth in TCCR-/- mice.
123 hed S. mansoni infections fail to control L. donovani growth in the liver and spleen.
124 Hs-SAHH > Tc-SAHH > Ld-SAHH (from Leishmania donovani) > Pf-SAHH (from Plasmodium falciparum), which
125 .69% and 80.93 +/- 10.50% against Leishmania donovani /hamster model.
126 mpounds, 16, 17, and 22, were tested in a L. donovani/hamster model.
127                        Studies of Leishmania donovani have shown that both ornithine decarboxylase an
128               Here, we identified Leishmania donovani heat shock protein 78 (LdHSP78), a putative cas
129 stigate the impact of phosphosites in the L. donovani heat shock protein 90.
130 and Kenya, where the disease is caused by L. donovani Here, we report the discovery and characterizat
131                 Heterozygous knockouts of L. donovani HSP78 (LdHSP78+/-) and Leishmania mexicana HSP7
132 or the growth of the promastigote form of L. donovani in culture, that all uracil and pyrimidine nucl
133 d to kill approximately 90-95% of Leishmania donovani in livers of mice deficient in mechanisms of ac
134    We report poor intracellular growth of L. donovani in macrophages from knockout mice for NE (ela(-
135 s role in preventing clearance of Leishmania donovani in murine models of VL.
136  show that HSCs are infected with Leishmania donovani in vivo and in vitro and that this infection le
137 visceral leishmaniasis, caused by Leishmania donovani, in contrast to infection in mice, mimics the p
138 udies with nucleoside transport-deficient L. donovani indicate that this phenomenon is mediated by th
139 asis in both life cycle stages of Leishmania donovani, individual mutant lines deficient in either ca
140 s by which resistant clinical isolates of L. donovani induce intracellular events relevant to drug re
141           In this study, we observed that L. donovani induced the expression of histone lysine methyl
142  Our data revealed that L. major, but not L. donovani, induces expression of IRF2, IRF7, and IFIT5, i
143                          Consequently, in L. donovani infected BALB/c mice, IL-13 promotes hepatic gr
144                  In nonvaccinated Leishmania donovani-infected BALB/c mice, HASPB- and KMP11-specific
145 ng organ parasite burden significantly in L. donovani-infected BALB/c mice.
146                                           L. donovani-infected hamsters underwent xenodiagnoses with
147        In vitro studies clearly show that L. donovani-infected HSCs induce CD4(+) T cells to become T
148                                           L. donovani-infected IL-13(-/-) mice also responded poorly
149 etect serum antibodies in 104 asymptomaticL. donovani-infected individuals (qualified as positive for
150                                   Leishmania donovani-infected interleukin-13-/- BALB/c mice showed i
151             Together, the results for the L. donovani-infected livers of chemokine-deficient mice (CX
152                      We show that Leishmania donovani-infected macrophages (MPhis) are capable of sti
153              Moreover, live microscopy of L. donovani-infected macrophages treated with Wnt5a demonst
154 sphatases, thioredoxin, SOCS, and Egr1 in L. donovani-infected macrophages was found to be unaffected
155                                   Leishmania donovani-infected macrophages were much more resistant t
156 cells in the skin-draining lymph nodes of L. donovani-infected malnourished mice.
157 how that the enhanced early resistance in L. donovani-infected mice is entirely due to the activity o
158 1, Arg-1, and MRC-1 genes, compared to WT L. donovani-infected mice.
159 cci are rapidly trapped in the spleens of L. donovani-infected mice.
160                            Interestingly, L. donovani-infected TCCR-/- mice controlled the parasite g
161 l role for ceramide in the perspective of L. donovani infection and help formulate an antileishmanial
162 IFN-gamma) controls intracellular Leishmania donovani infection and the efficacy of antimony (Sb) che
163 ecruited into the spleen and liver during L. donovani infection and they are preferential targets for
164                                           L. donovani infection drastically reduced Lys 63-linked ubi
165 uring C57BL/6 mice, intracellular Leishmania donovani infection enhanced Toll-like receptor 4 (TLR4)
166 l zone macrophages resulting from Leishmania donovani infection have increased resistance to Streptoc
167 in VL, we monitored the course of Leishmania donovani infection in miR155 knockout (miR155KO) and wil
168 ic mechanisms were involved in control of L. donovani infection in miR155KO mice.
169 maniasis (VL) by monitoring the course of L. donovani infection in TCCR-deficient C57BL/6 (TCCR-/-) m
170 uired resistance in intracellular Leishmania donovani infection in the liver, inducing gamma interfer
171                     Thus, in experimental L. donovani infection in the liver, TLR4 signaling upregula
172 -6, responses to an intracellular Leishmania donovani infection in the livers of IL-6(-/-) and wild-t
173 ed resistance of p110delta(D910A) mice to L. donovani infection is due in part to impaired expansion
174               We further demonstrate that L. donovani infection leads to expansion of HSCs in a p110d
175 nd developed severe liver pathology after L. donovani infection that eventually resolved.
176 hi) iMOs into the liver and spleen during L. donovani infection using a CCR2 antagonist reduces the f
177      Neutrophil elastase promotes Leishmania donovani infection via interferon-beta.
178 tment of Ly6C(hi) iMOs into organs during L. donovani infection, and adaptive transfer of wild type L
179  an efficient Th1 response during Leishmania donovani infection, but they play distinct roles in dete
180 ng, revamping Wnt5a signaling can inhibit L. donovani infection, irrespective of drug sensitivity or
181 afficking and hepatic inflammation during L. donovani infection, it is not essential for immunity aga
182 sults showed that compared with wild-type L. donovani infection, LdCen(-/-) parasites induce signific
183 luation in a mouse model of acute Leishmania donovani infection, one phenylpyridine derivative (37) s
184 cell responses during the early stages of L. donovani infection.
185 rotective manner to animals with existing L. donovani infection.
186 nflammation and granuloma formation after L. donovani infection.
187 nfirming that Wnt5a signaling antagonizes L. donovani infection.
188 lationship of Wnt5a signaling and Leishmania donovani infection.
189                                   Leishmania donovani infects macrophages, disrupting immune homeosta
190            The initial macrophage-Leishmania donovani interaction results in the formation of membran
191 ound with modest activity against Leishmania donovani intracellular amastigotes and excellent selecti
192 une evasion strategies adopted by Leishmania donovani involve the exploitation of suppressor of cytok
193                                   Leishmania donovani is a protozoan parasite.
194                                   Leishmania donovani is an intracellular parasite that infects profe
195 The pathogenic protozoan parasite Leishmania donovani is capable of both de novo pyrimidine biosynthe
196  or absent expression of parasite ISP2 in L. donovani is necessary to preserve the activation of the
197 r contribution to host resistance against L. donovani is not clear.
198                East Africa, where Leishmania donovani is prevalent, faces the highest burden world-wi
199 he lymph node barrier to dissemination of L. donovani is related to insufficient numbers of lymph nod
200 l leishmaniasis (PKDL), caused by Leishmania donovani is the dermal sequel of Visceral Leishmaniasis
201  mice with the protozoan parasite Leishmania donovani, is characterized by focal accumulation of infl
202                                           L. donovani isolates separated into five groups that largel
203  regulation in which the parasite Leishmania donovani (Ld) causes mitochondrial depolarization, reduc
204 characterization of two new biomarkers of L. donovani (Ld-mao1 and Ld-ppi1) present in the urine of V
205 by a live attenuated centrin gene-deleted L. donovani (LdCen(-/-) ) parasite vaccine.
206 e attenuated centrin gene-deleted Leishmania donovani (LdCen(-/-) ) parasites through induction of Th
207 er a live attenuated centrin gene-deleted L. donovani (LdCen1(-/-)) parasite can persist and be both
208  genes in laboratory-maintained resistant L. donovani lines.
209 solution significantly suppressed Leishmania donovani liver parasite burdens (p<0.05) but could not i
210 aken together, these results suggest that L. donovani may exploit SOCS for subverting macrophage apop
211                These results suggest that L. donovani might exploit host A20 to inhibit the TLR2-medi
212                   However, in the Leishmania donovani model of pathogen persistence, Il10(-/-)/hIL10B
213     In this study, we showed that Leishmania donovani modulates the TLR2-mediated pathway in macropha
214                              In a Leishmania donovani mouse model, two racemic phenylpyridines (71 an
215  which was classified as ABCC2 or Leishmania donovani multidrug resistance protein 2 (LdMRP2).
216                                           L. donovani mutants deficient in de novo pyrimidine biosynt
217                    These studies validate L. donovani NMT as a potential target for development of ne
218                 The open reading frame of L. donovani NMT has been amplified and used to overproduce
219 resulting in novel, highly potent Leishmania donovani NMT inhibitors with good selectivity over the h
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 n ab initio model of a homologous Leishmania donovani nucleoside transporter.
223 tly, we have demonstrated that a Deltaodc L. donovani null mutant lacking ornithine decarboxylase (OD
224      Collectively, our results imply that L. donovani orchestrates different SOCS isoforms to impair
225  using a transgenic luciferase-expressing L. donovani parasite and longitudinally quantified the infe
226 etically modified live-attenuated Leishmania donovani parasite cell lines (LdCen(-/-) and Ldp27(-/-))
227 our PfCENs in a centrin knock-out Leishmania donovani parasite line that exhibited a severe growth de
228 sis (VL), a disease caused by the Leishmania donovani parasite.
229  vaccines such as centrin deleted Leishmania donovani parasites (LdCen (-/-)) showed protective immun
230                                   Leishmania donovani parasites are the cause of visceral leishmanias
231 onstrate the potential of live-attenuated L. donovani parasites as pan-Leishmania species vaccines.
232                     Starvation of Leishmania donovani parasites for purines leads to a rapid amplific
233                                            L donovani parasites were serially passaged in mice expose
234 tes (compared to that with wild-type [WT] L. donovani parasites) induced significantly higher product
235 e shown that genetically modified Leishmania donovani parasites, here described as live attenuated pa
236 ulated proteins in purine-starved Leishmania donovani parasites.
237 M s) and CD4(+) T cells, we observed that L. donovani preferentially upregulates SOCS1 and SOCS3 expr
238 sary for the viability and growth of both L. donovani promastigotes and amastigotes and intimate that
239 fectively inhibited the growth of Leishmania donovani promastigotes and amastigotes, and iron did not
240                       In the first phase, L. donovani promastigotes induce activation of acid sphingo
241                               In fact, in L. donovani promastigotes, we verified for 7 a decrease of
242 s is an essential nutritional pathway for L. donovani promastigotes.
243 ity catalyzed by the beta5 subunit of the L. donovani proteasome.
244 ; EC 4.2.1.1) enzyme expressed in Leishmania donovani protozoa.
245 eral leishmaniasis (VL) caused by Leishmania donovani requires interferon-gamma production by CD4+ T
246 ive protozoan pathogen of humans, Leishmania donovani, resides and multiplies in highly restricted mi
247 tant of L. donovani that establishes that L. donovani salvages purines primarily through hypoxanthine
248 Infection with antimony-resistant Leishmania donovani (Sb(R)LD) induces aggressive pathology in the m
249 r mechanism of antimony-resistant Leishmania donovani (Sb(R)LD)-driven up-regulation of IL-10 and mul
250  infected with antimony-resistant Leishmania donovani (Sb(R)LD).
251 ompared with ones with antimony-sensitive L. donovani (Sb(S)LD) infection.
252 val of the intracellular parasite Leishmania donovani Screening of macrophage antioxidant enzymes dur
253 rts extensive skin infection with Leishmania donovani, spatial analyses at macro-(quantitative PCR) a
254 h Dakota) and infection caused by Leishmania donovani species complex.
255 ted individuals (qualified as positive forL. donovani-specific antibodies by direct agglutination tes
256           Previous efforts to generate an L. donovani strain deficient in both hypoxanthine-guanine p
257 istance in two clinically derived Leishmania donovani strains with different inherent resistance to a
258 bisbenzofurans displayed activity against L. donovani superior to that of pentamidine.
259 pite the development of a functional anti-L. donovani Th1 response that can mediate granuloma formati
260   Five congeners were more active against L. donovani than pentamidine.
261 acellular replication of residual Leishmania donovani that escape chemotherapy evolves to a host mech
262 nal lethal Deltahgprt/Deltaxprt mutant of L. donovani that establishes that L. donovani salvages puri
263 sis is a deadly illness caused by Leishmania donovani that provokes liver and spleen inflammation and
264 parasites Leishmania infantum and Leishmania donovani The gold standard diagnostic test for VL is the
265 polyamine biosynthetic pathway of Leishmania donovani, the causal agent of visceral leishmaniasis, ar
266 In this study the interactions of Leishmania donovani, the causative agent of visceral Leishmaniasis,
267 ens against the tropical parasite Leishmania donovani, the causative agent of visceral leishmaniasis.
268                          Unlike wild type L. donovani, the Deltahgprt/Deltaxprt knock-out cannot grow
269                      However, for Leishmania donovani, the DNA-binding activity and the majority of r
270 t, IL-12p40 expression is not elicited by L. donovani, the etiological agent of deadly visceral leish
271 polyamine biosynthetic pathway of Leishmania donovani, the etiological agent of visceral leishmaniasi
272 d a proof-of-concept of SL-seq in Leishmania donovani, the main causative agent of visceral leishmani
273 stigated the interactions between Leishmania donovani, the main etiological agent of visceral leishma
274 ation of a phenotypic hit against Leishmania donovani, the major causative organism of VL.
275 o transmit Leishmania infantum or Leishmania donovani to hamsters.
276  by the intra-macrophage parasite Leishmania donovani to protect their "home" from actinomycin D-indu
277 ans were quantified and the sensitivity of L donovani to sodium stibogluconate assessed at each passa
278 y in Leishmania, has not been analyzed in L. donovani To test ARG function in intact parasites, we ge
279 A crystal structure of an active truncated L.donovani TOP1L/TOP1S heterodimer bound to nicked double-
280 t relevant to human disease, i.e. Leishmania donovani, Trypanosoma cruzi and Trypanosoma brucei.
281 involving Schistosoma mansoni and Leishmania donovani, two important human pathogens affecting the li
282  highlights the non-canonical function of L. donovani tyrosyl-tRNA synthetase.
283 e Ufm1-mediated modifications, we made an L. donovani Ufm1 null mutant (Ufm1(-/-)).
284          In this work we demonstrate that L. donovani UMPS (LdUMPS) is an essential enzyme in promast
285  it is not essential for immunity against L. donovani, unlike L. major.
286        Genetic analysis has authenticated L. donovani uracil phosphoribosyltransferase (LdUPRT), an e
287 eral leishmaniasis (VL) caused by Leishmania donovani using an experimental mouse model.
288 ease from the parasitic protozoan Leishmania donovani, using ab initio computation.
289                           We propose that L. donovani utilizes the host NE-TLR machinery to induce IF
290 ease (SUB; Clan SB, family S8) of Leishmania donovani was cloned and found to possess a unique cataly
291 ease from the parasitic protozoan Leishmania donovani was modeled using ab initio computation.
292  significant uptake of L. tropica by MCs, L. donovani was not phagocytosed.
293          To test this hypothesis, Leishmania donovani was serially passaged in mice exposed to arseni
294 n mice infected with the parasite Leishmania donovani, we identified a transcriptomic network operati
295 th antimony drug-sensitive and -resistant L. donovani, we noted disruption in the steady-state level
296 is expressed in both life cycle stages of L. donovani, whereas subcellular fractionation and immunofl
297  antileishmanial activity against Leishmania donovani with an IC50 value of 9.22 muM.
298 exhibited potent activity against Leishmania donovani with IC(50) values ranging from 3.75 to 10.37 m
299 rypanosoma brucei rhodesiense and Leishmania donovani with IC50 values of 1.55 and 0.22 muM, respecti
300  3.75 muM, respectively) forms of Leishmania donovani with negligible cytotoxicity toward the host (J

 
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