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1 Plasmodium falciparum ) and in vivo (against Plasmodium berghei ).
2 a bacterial RecA homolog during sporogony in Plasmodium berghei.
3 mosquitoes infected with the rodent parasite Plasmodium berghei.
4 lele into the rodent model malarial parasite Plasmodium berghei.
5 rane fusion reaction in the malaria organism Plasmodium berghei.
6 release of eight flagellated microgametes in Plasmodium berghei.
7 measuring the growth of the rodent parasite, Plasmodium berghei.
8 idgut lumen are impaired for transmission of Plasmodium berghei.
9 e of the C-terminal hexapeptide of TRAP from Plasmodium berghei.
10 ere malaria (ESM) elicited by infection with Plasmodium berghei.
11 chitinase gene of a rodent malaria parasite, Plasmodium berghei.
12 dent malaria parasites Plasmodium yoelii and Plasmodium berghei.
13 -based fluorescence on the malarial parasite Plasmodium berghei.
14 le to no vivo activity in mice infected with Plasmodium berghei.
15 laria parasites Plasmodium yoelii yoelii and Plasmodium berghei.
16 modium falciparum clones and in vivo against Plasmodium berghei.
17 5/5 cure @ <15 mpk x 3 in mice infected with Plasmodium berghei.
18 00 plasmids designed to modify the genome of Plasmodium berghei, a malaria parasite of rodents, which
21 ling of ookinetes from the malarial parasite Plasmodium berghei, a model for the human malarial paras
22 subunit gene in the rodent malaria parasite, Plasmodium berghei, ablating the protein that converts A
23 PfSUB1 and displayed anti-P. falciparum and Plasmodium berghei activity in vitro and in vivo, respec
24 aries were constructed that are enriched for Plasmodium berghei and Anopheles stephensi genes express
25 ffects on the rodent parasites P. yoelii and Plasmodium berghei and on the human malaria parasite Pla
29 alpha-AgAPN1 IgG strongly inhibited both Plasmodium berghei and Plasmodium falciparum development
30 nd IMD pathways are known to be induced upon Plasmodium berghei and Plasmodium falciparum infection,
31 antibody inhibits oocyst development of both Plasmodium berghei and Plasmodium falciparum, suggesting
32 bodies significantly blocked transmission of Plasmodium berghei and Plasmodium vivax to Anopheles gam
33 exoerythrocytic forms were observed for both Plasmodium berghei and Plasmodium yoelii, two different
36 -Plasmodium gallinaceum, Anopheles stephensi-Plasmodium berghei, and A. stephensi-P. gallinaceum, wer
37 in invasive stages of Toxoplasma gondii and Plasmodium berghei, and apical positioning of TgGAC depe
38 ne disruption in the rodent malaria parasite Plasmodium berghei, and distinctive features of fertiliz
40 ll as protozoa, e.g., Trichomonas vaginalis, Plasmodium berghei, and sporozoites and blood-stage form
41 DC subset in an experimental CM model using Plasmodium berghei, and we provide strong evidence that
42 arum and were additionally tested in vivo in Plasmodium berghei- and/or Plasmodium yoelii-infected mi
43 SK3beta) in the brains of mice infected with Plasmodium berghei ANKA (PbA) compared to uninfected con
47 response is required for the development of Plasmodium berghei ANKA (PbA)-induced experimental cereb
48 lpha (alpha)-lactose into mice-infected with Plasmodium berghei ANKA (PbANKA) to block galectins and
50 earance in CD47-deficient mice infected with Plasmodium berghei ANKA and in vitro phagocytosis of P.
51 gain selected for in vivo investigation in a Plasmodium berghei ANKA BALB/c mouse suppressive test.
54 oclonal antibody treatment and infected with Plasmodium berghei ANKA did not develop cerebral malaria
55 B2-encoding gene (Cnr2(-/-)) inoculated with Plasmodium berghei ANKA erythrocytes exhibited enhanced
57 nd arborization in brain cortex subjected to Plasmodium berghei ANKA infection compared to asymptomat
68 an sulfate 500K to CBA/Ca mice infected with Plasmodium berghei ANKA reduced parasitemia and delayed
71 h cerebral malaria and in mice infected with Plasmodium berghei ANKA with or without the arginase gen
72 ematopoietic cells that were inoculated with Plasmodium berghei ANKA, a murine model of cerebral mala
73 (DCs) to purified Plasmodium falciparum and Plasmodium berghei ANKA, and by spleen macrophages and D
74 modial activity in vitro and in vivo against Plasmodium berghei ANKA, comparable to artesunate and ar
75 cranial window in the murine model of CM by Plasmodium berghei ANKA, we show that murine CM is assoc
76 fate of a single cohort of semisynchronous, Plasmodium berghei ANKA- or Plasmodium yoelii 17XNL-para
77 to the regulation of immune responses during Plasmodium berghei ANKA-induced experimental cerebral ma
78 at a chronic T. gondii infection can prevent Plasmodium berghei ANKA-induced experimental cerebral ma
81 of malarial anemia in Plasmodium yoelii- and Plasmodium berghei ANKA-infected mice, similar to our pr
87 lpha-/-) were as susceptible to CM caused by Plasmodium berghei (ANKA) as C57BL/6 mice, and died 6 to
89 strated the ability of lead HHQs to suppress Plasmodium berghei blood-stage parasite proliferation.
91 hepatocytes by conditionally disrupting the Plasmodium berghei cGMP-dependent protein kinase in spor
92 ile protection (95%) in BALB/c mice required Plasmodium berghei circumsporozoite protein (CS(252-260)
95 munization with pre-erythrocytic antigens of Plasmodium berghei, consisting of single dose priming wi
96 The genome of the rodent malaria parasite, Plasmodium berghei, contains two sets of variant ribosom
98 DNA plasmids expressing different amounts of Plasmodium berghei CSP were evaluated by immunizing BALB
99 analysis of 35 orphan transport proteins of Plasmodium berghei during its life cycle in mice and Ano
101 ited oocyst development of P. falciparum and Plasmodium berghei expressing PfCelTOS in Anopheles gamb
103 f this QTL is important for encapsulation of Plasmodium berghei, F2 progeny were infected with P. ber
105 DHHC10, translationally repressed in female Plasmodium berghei gametocytes, is activated translation
106 required for CD8(+) T cell responses to the Plasmodium berghei GAP5040-48 epitope in mice expressing
107 ave isolated and sequenced the corresponding Plasmodium berghei gene and shown it encodes an enzyme (
109 blood stages because we could not delete the Plasmodium berghei gene encoding GatA in blood stage par
111 ocks by creating a high-integrity library of Plasmodium berghei genomic DNA (>77% A+T content) in a b
112 unted after prime-boost immunization against Plasmodium berghei glideosome-associated protein 5041-48
113 stephensi, which are resistant partially to Plasmodium berghei, had higher fitness than non-transgen
117 ng a population, transmission-based study of Plasmodium berghei in Anopheles stephensi to assess the
119 ionally, in vivo Thompson test results using Plasmodium berghei in mice showed that these 4(1H)-quino
120 al compounds also displayed activity against Plasmodium berghei in mice, the most potent being 2,7-di
121 ed for in vivo biological evaluation against Plasmodium berghei in the mouse model and for metabolism
124 ) (dihydrochloride), which is active against Plasmodium berghei in vivo (oral ID(50) of 25 micromol/k
127 tissue oxygenation were investigated during Plasmodium berghei-induced severe malaria in the hamster
130 t for at most 15% of platelet destruction as Plasmodium berghei-infected B cell-deficient mice exhibi
131 even higher levels when mosquitoes are fed a Plasmodium berghei-infected meal, indicating that the ox
132 ding parasitemia in Plasmodium chabaudi- and Plasmodium berghei-infected mice and the 48-hour in vitr
134 d with 18 mg/kg of mefloquine hydrochloride, Plasmodium berghei-infected mice survived on average 29.
139 flammation, was upregulated in the livers of Plasmodium berghei-infected mice; hepatic activin B was
143 y influences the prevalence and intensity of Plasmodium berghei infection in adults, whereby Nishikoi
144 al that the pathogenic response of mice to a Plasmodium berghei infection is dominated by a Vbeta8.1
146 in the brain, lung, kidney, and heart during Plasmodium berghei infection, a well-recognized model fo
151 scale generation and phenotypic analysis of Plasmodium berghei knockout (KO) lines, characterizing 2
152 itive growth rates in mice of 2,578 barcoded Plasmodium berghei knockout mutants, representing >50% o
153 We examined MyoA expression throughout the Plasmodium berghei life cycle in both mammalian and inse
157 ate endocytic compartments accumulate around Plasmodium berghei liver-stage parasites during developm
159 otoxicity toward HeLa cells and in vivo in a Plasmodium berghei malaria model as well as in the SCID
160 exoerythrocytic stage of the murine strain, Plasmodium berghei malaria, was CD8+ T cell-dependent.
161 urther reported that the IgG response to the Plasmodium berghei malarial circumsporozoite (CS) protei
162 ble in mice, exhibits activity in the murine Plasmodium berghei model and efficacy comparable to that
168 lay potent oral antimalarial activity in the Plasmodium berghei mouse malaria model associated with f
169 monstrated promising in vivo efficacy in the Plasmodium berghei mouse model and will be further evalu
172 d plasma exposure and better efficacy in the Plasmodium berghei mouse model of the disease than previ
173 analogues exhibited in vivo activity in the Plasmodium berghei mouse model when administered orally.
174 emonstrated in part curative activity in the Plasmodium berghei mouse model when administered peroral
176 lly at 50 mg/kg once daily for 4 days in the Plasmodium berghei mouse model, which is superior to the
178 lanization responses of Anopheles gambiae to Plasmodium berghei (murine malaria) has been established
182 IL-27R-deficient (WSX-1(-/-)) mice following Plasmodium berghei NK65 infection than in wild-type (WT)
184 y of ED(50)/ED(90) of 1.87/4.72 mg/kg versus Plasmodium berghei (NS Strain) in a murine model of mala
185 Importantly, transgene expression reduced Plasmodium berghei oocyst formation by 87% on average an
187 d for sequences expressed in differentiating Plasmodium berghei ookinetes and another enriched for se
188 cited a potent melanization response against Plasmodium berghei ookinetes and exhibited significantly
189 Here, we characterize a novel SPN protein of Plasmodium berghei ookinetes and sporozoites named G2 (g
191 pheles stephensi midgut epithelial cells and Plasmodium berghei ookinetes during invasion of the mosq
195 Surprisingly, the transcripts coding for the Plasmodium berghei orthologues of those genes are stored
197 P. vivax using a fully infectious transgenic Plasmodium berghei parasite expressing P. vivax TRAP to
199 development and characterization of chimeric Plasmodium berghei parasites bearing the type I repeat r
200 zyme is not essential for parasite growth as Plasmodium berghei parasites carrying a complete deletio
201 infection by isolating luciferase-expressing Plasmodium berghei parasites directly from the salivary
202 igen-specific T-cell responses, we generated Plasmodium berghei parasites expressing the model antige
204 calization on the surface of midgut-invading Plasmodium berghei parasites, targeting them for destruc
205 orin (PfAQP) in the rodent malaria parasite, Plasmodium berghei (PbAQP), and examined the biological
206 rotein kinase of the rodent malaria parasite Plasmodium berghei, Pbmap-2, in male sexual differentiat
209 Sporozoites expressing a mutated form of Plasmodium berghei PKG or carrying a deletion of the CDP
211 on of mosquito midgut screen candidate 2), a Plasmodium berghei protein with structural similarities
212 nctional studies in the rodent malaria model Plasmodium berghei recently showed the map-2 gene to be
213 ite CS proteins of Plasmodium falciparum and Plasmodium berghei, respectively, and a green fluorescen
216 and mosquito bite challenge with transgenic Plasmodium berghei rodent sporozoites that incorporate t
220 lay an important albeit nonessential role in Plasmodium berghei sporozoite infectivity for the rodent
221 resence of a phospholipase on the surface of Plasmodium berghei sporozoites (P. berghei phospholipase
222 , multiple exposures to radiation-attenuated Plasmodium berghei sporozoites (Pb gamma-spz) induce lon
224 ies recognition of Plasmodium falciparum and Plasmodium berghei sporozoites by anti-Plasmodium vivax
226 mosquitoes with salivary gland infections of Plasmodium berghei sporozoites expressing a red fluoresc
227 tion induced by radiation-attenuated (gamma) Plasmodium berghei sporozoites is linked to MHC class I-
228 In addition, we also demonstrate that arg- Plasmodium berghei sporozoites show significantly decrea
235 s to mice that were then coinfected with two Plasmodium berghei strains, only one of which could be r
236 ll mice at the age of 4 months infected with Plasmodium berghei survive longer during the initial pha
241 rasite P. falciparum and the rodent parasite Plasmodium berghei using gene targeting strategies.
242 n increase in survival of mice infected with Plasmodium berghei was observed when compared to control
244 Here, using the rodent malaria parasite Plasmodium berghei, we identify and characterize the fir
248 ene disruption in the rodent malaria species Plasmodium berghei, we show that PbIMC1a is involved in
249 tial of trophozoites of the malaria parasite Plasmodium berghei were assayed in situ after permeabili
251 bs21 is a surface protein of the ookinete of Plasmodium berghei, which can induce a potent transmissi
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