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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
19 y replicating forms to sexual development in Plasmodium berghei, a malaria parasite of rodents.
20                In response to challenge with Plasmodium berghei, a malarial pathogen that models syst
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
26         In vitro invasion assays reveal that Plasmodium berghei and P. yoelii sporozoites attach to a
27                 Using rodent malaria models (Plasmodium berghei and P. yoelii), we were unable to sho
28                                              Plasmodium berghei and Plasmodium chabaudi are widely us
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
34 blood meal using the rodent malaria parasite Plasmodium berghei and rat complement as a model.
35                    TgAMA1 shows between 19% (Plasmodium berghei) and 26% (Plasmodium yoelii) overall
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
39 e species as follows: Plasmodium falciparum, Plasmodium berghei, and Plasmodium knowlesi.
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
44                                   The murine Plasmodium berghei ANKA (PbA) infection model has helped
45                             We have used the Plasmodium berghei ANKA (PbA) model in which mice develo
46                                       In the Plasmodium berghei ANKA (PbA) murine model, CM pathogene
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
49       The discovery that murine CM caused by Plasmodium berghei ANKA and human CM are both characteri
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.
52        To investigate this question, we used Plasmodium berghei ANKA blood-stage parasites for the in
53                  C57BL/6J mice infected with Plasmodium berghei ANKA develop neurological dysfunction
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
56       GSNOR knockout (KO) mice infected with Plasmodium berghei ANKA had significantly delayed mortal
57 nd arborization in brain cortex subjected to Plasmodium berghei ANKA infection compared to asymptomat
58                                              Plasmodium berghei ANKA infection induced CM in A 0/0 mi
59 ntal cerebral malaria (ECM) using the murine Plasmodium berghei ANKA infection model.
60                                              Plasmodium berghei ANKA infection of C57BL/6 mice is a w
61 f experimental cerebral malaria (ECM) during Plasmodium berghei ANKA infection of C57BL/6 mice.
62                                              Plasmodium berghei Anka infection of mice recapitulates
63                               Infection with Plasmodium berghei ANKA is a well-established model of h
64      Murine cerebral malaria (CM) induced by Plasmodium berghei ANKA kills susceptible mice within 24
65                                    Using the Plasmodium berghei ANKA murine model of ECM and mice def
66                                    Using the Plasmodium berghei ANKA murine model of experimental cer
67                                  We used the Plasmodium berghei ANKA murine model of experimental cer
68 an sulfate 500K to CBA/Ca mice infected with Plasmodium berghei ANKA reduced parasitemia and delayed
69                  Irbc of the rodent parasite Plasmodium berghei ANKA sequester in a fashion analogous
70               Additionally, mice with patent Plasmodium berghei ANKA strain infection treated with a
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
79 rain intravascular inflammation and protects Plasmodium berghei ANKA-infected mice from CM.
80                                              Plasmodium berghei ANKA-infected mice served as the posi
81 of malarial anemia in Plasmodium yoelii- and Plasmodium berghei ANKA-infected mice, similar to our pr
82 r infection with the rodent malaria parasite Plasmodium berghei ANKA.
83  mice with murine cerebral malaria caused by Plasmodium berghei ANKA.
84 CM), in which C57BL/6 mice are infected with Plasmodium berghei ANKA.
85 d-type (WT) C57BL/6J mice were infected with Plasmodium berghei ANKA.
86 ebral malaria (ECM) caused by infection with Plasmodium berghei ANKA.
87 lpha-/-) were as susceptible to CM caused by Plasmodium berghei (ANKA) as C57BL/6 mice, and died 6 to
88               Here, we used the TRAP gene of Plasmodium berghei as a target to test whether an ends-i
89 strated the ability of lead HHQs to suppress Plasmodium berghei blood-stage parasite proliferation.
90 odium falciparum and rodent malaria parasite Plasmodium berghei by up to 98%.
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)
93 he same preerythrocytic malaria antigen, the Plasmodium berghei circumsporozoite protein (CSP).
94 itope (DPPPPNPN)(2)D of the malaria parasite Plasmodium berghei circumsporozoite protein.
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
97             Combinatorial complementation of Plasmodium berghei CP genes with the orthologs from Plas
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
100                              Visualizing the Plasmodium berghei ER during liver stage development, we
101 ited oocyst development of P. falciparum and Plasmodium berghei expressing PfCelTOS in Anopheles gamb
102                             Using transgenic Plasmodium berghei expressing the repeat region of P. fa
103 f this QTL is important for encapsulation of Plasmodium berghei, F2 progeny were infected with P. ber
104                        We selected two vital Plasmodium berghei G-actin-binding proteins, C-CAP and p
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 (
108                                   Studying a Plasmodium berghei gene deletion mutant, we here provide
109 blood stages because we could not delete the Plasmodium berghei gene encoding GatA in blood stage par
110 ology arms for effective modification of the Plasmodium berghei genome.
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
114                          The rodent parasite Plasmodium berghei has served as a model for human malar
115                           In this study, the Plasmodium berghei homologues of antigens CSP and TRAP a
116        Here, a systematic knockout screen in Plasmodium berghei identified ten ApiAP2 genes that were
117 ng a population, transmission-based study of Plasmodium berghei in Anopheles stephensi to assess the
118 quired to detect the rodent malaria parasite Plasmodium berghei in blood.
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
122                              In vivo, versus Plasmodium berghei in the mouse, selected derivatives we
123 ounced in vitro and in vivo activity against Plasmodium berghei in the Thompson test.
124 ) (dihydrochloride), which is active against Plasmodium berghei in vivo (oral ID(50) of 25 micromol/k
125 d against Plasmodium falciparum in vitro and Plasmodium berghei in vivo.
126             Synergy is also observed against Plasmodium berghei in vivo.
127  tissue oxygenation were investigated during Plasmodium berghei-induced severe malaria in the hamster
128 nistration in two 60-day survival studies of Plasmodium berghei infected mice.
129 d and evaluated for antimalarial efficacy in Plasmodium berghei infected mice.
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
133                                              Plasmodium berghei-infected mice are a well-recognized m
134 d with 18 mg/kg of mefloquine hydrochloride, Plasmodium berghei-infected mice survived on average 29.
135                                              Plasmodium berghei-infected mice treated with IFN-beta d
136                 Compound 15 completely cured Plasmodium berghei-infected mice with a single oral dose
137                                              Plasmodium berghei-infected mice, a well-recognized mode
138 modium falciparum parasites and in vivo with Plasmodium berghei-infected mice.
139 flammation, was upregulated in the livers of Plasmodium berghei-infected mice; hepatic activin B was
140                                          The Plasmodium berghei-infected mouse model is a well-recogn
141                          An earlier study in Plasmodium berghei-infected rats showed an association b
142 und to be curative with all mice surviving a Plasmodium berghei infection after 30 days.
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
145 nopheles gambiae, and FREP1 is important for Plasmodium berghei infection of mosquitoes.
146 in the brain, lung, kidney, and heart during Plasmodium berghei infection, a well-recognized model fo
147  lactoferrin, or anti-LRP antibodies reduces Plasmodium berghei invasion by 60-70%.
148                                              Plasmodium berghei invasion of Anopheles stephensi midgu
149                               Infection with Plasmodium berghei is lethal to mice, causing high level
150                           The rodent malaria Plasmodium berghei is one of a small number of species o
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
154          Here, by gene targeting, we created Plasmodium berghei lines in which the single-copy CS gen
155 nd MHC class II molecules as determinants of Plasmodium berghei liver stage infection in mice.
156 more active than primaquine in vitro against Plasmodium berghei liver stage.
157 ate endocytic compartments accumulate around Plasmodium berghei liver-stage parasites during developm
158 ally and parenterally active in vivo against Plasmodium berghei malaria in mice.
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
163                       In this study, using a Plasmodium berghei model compatible with tracking anti-b
164 in vivo validation of this approach with the Plasmodium berghei model of murine malaria.
165 tive to monitoring liver stage burden in the Plasmodium berghei model.
166 dine and suppresses parasites in vivo in the Plasmodium berghei model.
167                                         In a Plasmodium berghei mouse infection model, one lead compo
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
170 ike strategy, was completely curative in the Plasmodium berghei mouse model at 4 x 50 mg/kg po.
171                 In contrast, efficacy in the Plasmodium berghei mouse model differed dramatically for
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
175                                       In the Plasmodium berghei mouse model, this series generally ex
176 lly at 50 mg/kg once daily for 4 days in the Plasmodium berghei mouse model, which is superior to the
177        We show that hepcidin upregulation in Plasmodium berghei murine malaria infection was accompan
178 lanization responses of Anopheles gambiae to Plasmodium berghei (murine malaria) has been established
179 iparum and in vivo by evolution of resistant Plasmodium berghei mutants.
180 ed with the reticulocyte-restricted parasite Plasmodium berghei NK65 1556Cl1.
181                         In this study, using Plasmodium berghei NK65 as a model of a systemic, proinf
182 IL-27R-deficient (WSX-1(-/-)) mice following Plasmodium berghei NK65 infection than in wild-type (WT)
183 ing IL-3-deficient (knockout [KO]) mice with Plasmodium berghei NK65.
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
186                  We previously reported that Plasmodium berghei oocysts in which the CS gene is inact
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
190                        Using the motility of Plasmodium berghei ookinetes as a signalling paradigm, w
191 pheles stephensi midgut epithelial cells and Plasmodium berghei ookinetes during invasion of the mosq
192        Infection of mice with sporozoites of Plasmodium berghei or Plasmodium yoelii has been used ex
193                    Immunization of mice with Plasmodium berghei or Plasmodium yoelii synthetic linear
194                        We also localized the Plasmodium berghei ortholog to the apicoplast in blood s
195 Surprisingly, the transcripts coding for the Plasmodium berghei orthologues of those genes are stored
196                    Unlike the rodent malaria Plasmodium berghei, P. falciparum sporozoites do not inf
197 P. vivax using a fully infectious transgenic Plasmodium berghei parasite expressing P. vivax TRAP to
198                 Moreover, we determined that Plasmodium berghei parasites are heterogeneous for midgu
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
203                            Here we show that Plasmodium berghei parasites infecting hepatic cells rel
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
207         Vaccination of mice with recombinant Plasmodium berghei PbSEA-1 significantly reduced parasit
208  parasites Plasmodium falciparum (PfVIT) and Plasmodium berghei (PbVIT).
209     Sporozoites expressing a mutated form of Plasmodium berghei PKG or carrying a deletion of the CDP
210       We report a functional analysis of the Plasmodium berghei protein phosphatome, which exhibits h
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
214 n and the rodent parasites P. falciparum and Plasmodium berghei, respectively.
215 orozoite protein (CSP) were evaluated in the Plasmodium berghei rodent malaria model system.
216  and mosquito bite challenge with transgenic Plasmodium berghei rodent sporozoites that incorporate t
217                                          The Plasmodium berghei scavenger receptor-like protein PbSR
218                              We identified a Plasmodium berghei secreted protein (PBANKA_131270) that
219 D8(+) T cell response in the liver following Plasmodium berghei sporozoite challenge.
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
223                                              Plasmodium berghei sporozoites attach to heparan sulphat
224 ies recognition of Plasmodium falciparum and Plasmodium berghei sporozoites by anti-Plasmodium vivax
225                                              Plasmodium berghei sporozoites delivered by mosquito bit
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
229 ct mice from infection with PfCSP transgenic Plasmodium berghei sporozoites.
230  C57BL/6 mice when they were challenged with Plasmodium berghei sporozoites.
231 ay rats previously immunized with irradiated Plasmodium berghei sporozoites.
232 ebral malaria by infecting C57BL/6 mice with Plasmodium berghei strain ANKA.
233 ed mortality after lethal challenge with the Plasmodium berghei strain ANKA.
234                                      Using a Plasmodium berghei strain expressing a bioluminescent ca
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
237          With both Plasmodium falciparum and Plasmodium berghei, the tryptophan metabolite xanthureni
238              We have cultured gametocytes of Plasmodium berghei through to infectious sporozoites wit
239                      We genetically modified Plasmodium berghei to express Pfs25 and demonstrated tha
240 either of these transgenes were impaired for Plasmodium berghei transmission.
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
243            Using the rodent malaria parasite Plasmodium berghei we show that SOAP is targeted to the
244      Here, using the rodent malaria parasite Plasmodium berghei, we identify and characterize the fir
245       Using a genetically targeted strain of Plasmodium berghei, we observed that the Plasmodium orth
246                    Using the rodent parasite Plasmodium berghei, we screened a panel of HIV PIs in vi
247            Using the rodent malaria parasite Plasmodium berghei, we show that CDPK1, which is known t
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
250       Mice infected with the NYU-2 strain of Plasmodium berghei were used to study the effect of chlo
251 bs21 is a surface protein of the ookinete of Plasmodium berghei, which can induce a potent transmissi

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