ライフサイエンスコーパス: Plasmodium berghei

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 measuring the growth of the rodent parasite, Plasmodium berghei.

7 idgut lumen are impaired for transmission of Plasmodium berghei.

8 e of the C-terminal hexapeptide of TRAP from Plasmodium berghei.

9 ere malaria (ESM) elicited by infection with Plasmodium berghei.

10 chitinase gene of a rodent malaria parasite, Plasmodium berghei.

11 dent malaria parasites Plasmodium yoelii and Plasmodium berghei.

12 -based fluorescence on the malarial parasite Plasmodium berghei.

13 le to no vivo activity in mice infected with Plasmodium berghei.

14 laria parasites Plasmodium yoelii yoelii and Plasmodium berghei.

15 modium falciparum clones and in vivo against Plasmodium berghei.

16 ein degradation tool in the malaria parasite Plasmodium berghei.

17 ria bacteria, and the mouse malaria parasite Plasmodium berghei.

18 release of eight flagellated microgametes in Plasmodium berghei.

19 5/5 cure @ <15 mpk x 3 in mice infected with Plasmodium berghei.

20 to ookinetes in the rodent malaria parasite Plasmodium berghei.

21 smodium falciparum, and rodent malaria model Plasmodium berghei, a large number of shared genes are d

22 00 plasmids designed to modify the genome of Plasmodium berghei, a malaria parasite of rodents, which

23 y replicating forms to sexual development in Plasmodium berghei, a malaria parasite of rodents.

24 In response to challenge with Plasmodium berghei, a malarial pathogen that models syst

25 ling of ookinetes from the malarial parasite Plasmodium berghei, a model for the human malarial paras

26 alciparum, the major human malaria parasite, Plasmodium berghei, a model rodent malaria parasite, and

27 subunit gene in the rodent malaria parasite, Plasmodium berghei, ablating the protein that converts A

28 PfSUB1 and displayed anti-P. falciparum and Plasmodium berghei activity in vitro and in vivo, respec

29 aries were constructed that are enriched for Plasmodium berghei and Anopheles stephensi genes express

30 bited promising activity against liver stage Plasmodium berghei and moderate antimethicillin-resistan

31 ffects on the rodent parasites P. yoelii and Plasmodium berghei and on the human malaria parasite Pla

32 In vitro invasion assays reveal that Plasmodium berghei and P. yoelii sporozoites attach to a

33 Using rodent malaria models (Plasmodium berghei and P. yoelii), we were unable to sho

34 Plasmodium berghei and Plasmodium chabaudi are widely us

35 alpha-AgAPN1 IgG strongly inhibited both Plasmodium berghei and Plasmodium falciparum development

36 nd IMD pathways are known to be induced upon Plasmodium berghei and Plasmodium falciparum infection,

37 antibody inhibits oocyst development of both Plasmodium berghei and Plasmodium falciparum, suggesting

38 bodies significantly blocked transmission of Plasmodium berghei and Plasmodium vivax to Anopheles gam

39 y rodent-infectious Plasmodium species, like Plasmodium berghei and Plasmodium yoelii, have been used

40 exoerythrocytic forms were observed for both Plasmodium berghei and Plasmodium yoelii, two different

41 blood meal using the rodent malaria parasite Plasmodium berghei and rat complement as a model.

42 facilitated genome-scale knockout screens in Plasmodium berghei and Toxoplasma gondii, in which poole

43 TgAMA1 shows between 19% (Plasmodium berghei) and 26% (Plasmodium yoelii) overall

44 -Plasmodium gallinaceum, Anopheles stephensi-Plasmodium berghei, and A. stephensi-P. gallinaceum, wer

45 was less pronounced in Plasmodium vivax and Plasmodium berghei, and absent in Plasmodium yoelii In P

46 in invasive stages of Toxoplasma gondii and Plasmodium berghei, and apical positioning of TgGAC depe

47 ne disruption in the rodent malaria parasite Plasmodium berghei, and distinctive features of fertiliz

48 e species as follows: Plasmodium falciparum, Plasmodium berghei, and Plasmodium knowlesi.

49 ll as protozoa, e.g., Trichomonas vaginalis, Plasmodium berghei, and sporozoites and blood-stage form

50 DC subset in an experimental CM model using Plasmodium berghei, and we provide strong evidence that

51 arum and were additionally tested in vivo in Plasmodium berghei- and/or Plasmodium yoelii-infected mi

52 SK3beta) in the brains of mice infected with Plasmodium berghei ANKA (PbA) compared to uninfected con

53 The murine Plasmodium berghei ANKA (PbA) infection model has helped

54 We have used the Plasmodium berghei ANKA (PbA) model in which mice develo

55 In the Plasmodium berghei ANKA (PbA) murine model, CM pathogene

56 response is required for the development of Plasmodium berghei ANKA (PbA)-induced experimental cereb

57 duced by infection with the rodent parasite, Plasmodium berghei ANKA (PbANKA) has been extensively us

58 lpha (alpha)-lactose into mice-infected with Plasmodium berghei ANKA (PbANKA) to block galectins and

59 The discovery that murine CM caused by Plasmodium berghei ANKA and human CM are both characteri

60 earance in CD47-deficient mice infected with Plasmodium berghei ANKA and in vitro phagocytosis of P.

61 gain selected for in vivo investigation in a Plasmodium berghei ANKA BALB/c mouse suppressive test.

62 To investigate this question, we used Plasmodium berghei ANKA blood-stage parasites for the in

63 C57BL/6J mice infected with Plasmodium berghei ANKA develop neurological dysfunction

64 oclonal antibody treatment and infected with Plasmodium berghei ANKA did not develop cerebral malaria

65 B2-encoding gene (Cnr2(-/-)) inoculated with Plasmodium berghei ANKA erythrocytes exhibited enhanced

66 of hits administered to the rodent parasite Plasmodium berghei ANKA exhibited up to 70% reduction in

67 GSNOR knockout (KO) mice infected with Plasmodium berghei ANKA had significantly delayed mortal

68 nd arborization in brain cortex subjected to Plasmodium berghei ANKA infection compared to asymptomat

69 Plasmodium berghei ANKA infection induced CM in A 0/0 mi

70 ntal cerebral malaria (ECM) using the murine Plasmodium berghei ANKA infection model.

71 Plasmodium berghei ANKA infection of C57BL/6 mice is a w

72 f experimental cerebral malaria (ECM) during Plasmodium berghei ANKA infection of C57BL/6 mice.

73 Plasmodium berghei Anka infection of mice recapitulates

74 Infection with Plasmodium berghei ANKA is a well-established model of h

75 Murine cerebral malaria (CM) induced by Plasmodium berghei ANKA kills susceptible mice within 24

76 In the Plasmodium berghei ANKA mouse model of malaria, accumula

77 Using the Plasmodium berghei ANKA murine model of ECM and mice def

78 Using the Plasmodium berghei ANKA murine model of experimental cer

79 We used the Plasmodium berghei ANKA murine model of experimental cer

80 an sulfate 500K to CBA/Ca mice infected with Plasmodium berghei ANKA reduced parasitemia and delayed

81 Irbc of the rodent parasite Plasmodium berghei ANKA sequester in a fashion analogous

82 ells are resistant to ECM when infected with Plasmodium berghei ANKA sporozoites, the liver-infective

83 nock-out (n = 5) mice were infected with the Plasmodium berghei ANKA strain from May 2016 to July 201

84 Additionally, mice with patent Plasmodium berghei ANKA strain infection treated with a

85 h cerebral malaria and in mice infected with Plasmodium berghei ANKA with or without the arginase gen

86 ematopoietic cells that were inoculated with Plasmodium berghei ANKA, a murine model of cerebral mala

87 (DCs) to purified Plasmodium falciparum and Plasmodium berghei ANKA, and by spleen macrophages and D

88 modial activity in vitro and in vivo against Plasmodium berghei ANKA, comparable to artesunate and ar

89 cranial window in the murine model of CM by Plasmodium berghei ANKA, we show that murine CM is assoc

90 fate of a single cohort of semisynchronous, Plasmodium berghei ANKA- or Plasmodium yoelii 17XNL-para

91 at a chronic T. gondii infection can prevent Plasmodium berghei ANKA-induced experimental cerebral ma

92 to the regulation of immune responses during Plasmodium berghei ANKA-induced experimental cerebral ma

93 c potential of IL-4 against fatal malaria in Plasmodium berghei ANKA-infected C57BL/6J mice, an exper

94 rain intravascular inflammation and protects Plasmodium berghei ANKA-infected mice from CM.

95 Plasmodium berghei ANKA-infected mice served as the posi

96 of malarial anemia in Plasmodium yoelii- and Plasmodium berghei ANKA-infected mice, similar to our pr

97 r infection with the rodent malaria parasite Plasmodium berghei ANKA.

98 mice with murine cerebral malaria caused by Plasmodium berghei ANKA.

99 CM), in which C57BL/6 mice are infected with Plasmodium berghei ANKA.

100 d-type (WT) C57BL/6J mice were infected with Plasmodium berghei ANKA.

101 ebral malaria (ECM) caused by infection with Plasmodium berghei ANKA.

102 lpha-/-) were as susceptible to CM caused by Plasmodium berghei (ANKA) as C57BL/6 mice, and died 6 to

103 Here, we used the TRAP gene of Plasmodium berghei as a target to test whether an ends-i

104 lasmodium falciparum and the rodent parasite Plasmodium berghei blocks sporozoite production inside o

105 strated the ability of lead HHQs to suppress Plasmodium berghei blood-stage parasite proliferation.

106 odium falciparum and rodent malaria parasite Plasmodium berghei by up to 98%.

107 We show that Plasmodium berghei CDK-related kinase 5 (CRK5), is a cri

108 hepatocytes by conditionally disrupting the Plasmodium berghei cGMP-dependent protein kinase in spor

109 ile protection (95%) in BALB/c mice required Plasmodium berghei circumsporozoite protein (CS(252-260)

110 he same preerythrocytic malaria antigen, the Plasmodium berghei circumsporozoite protein (CSP).

111 itope (DPPPPNPN)(2)D of the malaria parasite Plasmodium berghei circumsporozoite protein.

112 munization with pre-erythrocytic antigens of Plasmodium berghei, consisting of single dose priming wi

113 The genome of the rodent malaria parasite, Plasmodium berghei, contains two sets of variant ribosom

114 Combinatorial complementation of Plasmodium berghei CP genes with the orthologs from Plas

115 DNA plasmids expressing different amounts of Plasmodium berghei CSP were evaluated by immunizing BALB

116 onic and blood stage development and impairs Plasmodium berghei development inside hepatocytes, both

117 We also demonstrated that Plasmodium berghei DHFR promoter is recognized and funct

118 analysis of 35 orphan transport proteins of Plasmodium berghei during its life cycle in mice and Ano

119 Visualizing the Plasmodium berghei ER during liver stage development, we

120 ited oocyst development of P. falciparum and Plasmodium berghei expressing PfCelTOS in Anopheles gamb

121 Using transgenic Plasmodium berghei expressing the repeat region of P. fa

122 f this QTL is important for encapsulation of Plasmodium berghei, F2 progeny were infected with P. ber

123 adily distinguished mosquitoes infected with Plasmodium berghei from non-infected.

124 We selected two vital Plasmodium berghei G-actin-binding proteins, C-CAP and p

125 DHHC10, translationally repressed in female Plasmodium berghei gametocytes, is activated translation

126 required for CD8(+) T cell responses to the Plasmodium berghei GAP5040-48 epitope in mice expressing

127 ave isolated and sequenced the corresponding Plasmodium berghei gene and shown it encodes an enzyme (

128 Studying a Plasmodium berghei gene deletion mutant, we here provide

129 blood stages because we could not delete the Plasmodium berghei gene encoding GatA in blood stage par

130 ology arms for effective modification of the Plasmodium berghei genome.

131 ocks by creating a high-integrity library of Plasmodium berghei genomic DNA (>77% A+T content) in a b

132 unted after prime-boost immunization against Plasmodium berghei glideosome-associated protein 5041-48

133 stephensi, which are resistant partially to Plasmodium berghei, had higher fitness than non-transgen

134 The rodent parasite Plasmodium berghei has served as a model for human malar

135 In this study, the Plasmodium berghei homologues of antigens CSP and TRAP a

136 Here, a systematic knockout screen in Plasmodium berghei identified ten ApiAP2 genes that were

137 ng a population, transmission-based study of Plasmodium berghei in Anopheles stephensi to assess the

138 quired to detect the rodent malaria parasite Plasmodium berghei in blood.

139 unodominant CSP-derived epitope SYIPSAEKI of Plasmodium berghei in both sporozoite- and vaccine-induc

140 ionally, in vivo Thompson test results using Plasmodium berghei in mice showed that these 4(1H)-quino

141 al compounds also displayed activity against Plasmodium berghei in mice, the most potent being 2,7-di

142 ed for in vivo biological evaluation against Plasmodium berghei in the mouse model and for metabolism

143 In vivo, versus Plasmodium berghei in the mouse, selected derivatives we

144 ounced in vitro and in vivo activity against Plasmodium berghei in the Thompson test.

145 ) (dihydrochloride), which is active against Plasmodium berghei in vivo (oral ID(50) of 25 micromol/k

146 d against Plasmodium falciparum in vitro and Plasmodium berghei in vivo.

147 Synergy is also observed against Plasmodium berghei in vivo.

148 tissue oxygenation were investigated during Plasmodium berghei-induced severe malaria in the hamster

149 odium falciparum infected Anopheles gambiae, Plasmodium berghei infected Anopheles stephensi, and P.

150 nistration in two 60-day survival studies of Plasmodium berghei infected mice.

151 d and evaluated for antimalarial efficacy in Plasmodium berghei infected mice.

152 t for at most 15% of platelet destruction as Plasmodium berghei-infected B cell-deficient mice exhibi

153 delineate host-pathogen interactions across Plasmodium berghei-infected liver tissues.

154 even higher levels when mosquitoes are fed a Plasmodium berghei-infected meal, indicating that the ox

155 ding parasitemia in Plasmodium chabaudi- and Plasmodium berghei-infected mice and the 48-hour in vitr

156 Plasmodium berghei-infected mice are a well-recognized m

157 stages and demonstrates in vivo efficacy in Plasmodium berghei-infected mice at 4 x 50 mg.kg(-1) ora

158 In vivo efficacy studies in Plasmodium berghei-infected mice revealed that the front

159 d with 18 mg/kg of mefloquine hydrochloride, Plasmodium berghei-infected mice survived on average 29.

160 Plasmodium berghei-infected mice treated with IFN-beta d

161 In the present study Plasmodium berghei-infected mice were transfused intrape

162 Compound 15 completely cured Plasmodium berghei-infected mice with a single oral dose

163 Plasmodium berghei-infected mice, a well-recognized mode

164 modium falciparum parasites and in vivo with Plasmodium berghei-infected mice.

165 flammation, was upregulated in the livers of Plasmodium berghei-infected mice; hepatic activin B was

166 Following exposure to PfCSP-expressing Plasmodium berghei-infected mosquitoes, PfAg-immunized i

167 The Plasmodium berghei-infected mouse model is a well-recogn

168 An earlier study in Plasmodium berghei-infected rats showed an association b

169 und to be curative with all mice surviving a Plasmodium berghei infection after 30 days.

170 y influences the prevalence and intensity of Plasmodium berghei infection in adults, whereby Nishikoi

171 d for evaluation of in vivo efficacy against Plasmodium berghei infection in mice on the basis of the

172 al that the pathogenic response of mice to a Plasmodium berghei infection is dominated by a Vbeta8.1

173 nopheles gambiae, and FREP1 is important for Plasmodium berghei infection of mosquitoes.

174 In the absence of PRL2 in myeloid cells, Plasmodium berghei infection results in augmented lung i

175 progenitors (stem cells and enteroblasts) to Plasmodium berghei infection was investigated in Anophel

176 in the brain, lung, kidney, and heart during Plasmodium berghei infection, a well-recognized model fo

177 lactoferrin, or anti-LRP antibodies reduces Plasmodium berghei invasion by 60-70%.

178 Plasmodium berghei invasion of Anopheles stephensi midgu

179 Infection with Plasmodium berghei is lethal to mice, causing high level

180 The rodent malaria Plasmodium berghei is one of a small number of species o

181 scale generation and phenotypic analysis of Plasmodium berghei knockout (KO) lines, characterizing 2

182 itive growth rates in mice of 2,578 barcoded Plasmodium berghei knockout mutants, representing >50% o

183 Knockout of Plasmodium berghei LDH2 expression reduces the number an

184 We examined MyoA expression throughout the Plasmodium berghei life cycle in both mammalian and inse

185 solution transcriptional atlas of the entire Plasmodium berghei life cycle.

186 Here, by gene targeting, we created Plasmodium berghei lines in which the single-copy CS gen

187 nd MHC class II molecules as determinants of Plasmodium berghei liver stage infection in mice.

188 more active than primaquine in vitro against Plasmodium berghei liver stage.

189 ium falciparum asexual blood-stage (ABS) and Plasmodium berghei liver-stage (LS) parasites, next-gene

190 ate endocytic compartments accumulate around Plasmodium berghei liver-stage parasites during developm

191 ally and parenterally active in vivo against Plasmodium berghei malaria in mice.

192 otoxicity toward HeLa cells and in vivo in a Plasmodium berghei malaria model as well as in the SCID

193 exoerythrocytic stage of the murine strain, Plasmodium berghei malaria, was CD8+ T cell-dependent.

194 urther reported that the IgG response to the Plasmodium berghei malarial circumsporozoite (CS) protei

195 ble in mice, exhibits activity in the murine Plasmodium berghei model and efficacy comparable to that

196 In this study, using a Plasmodium berghei model compatible with tracking anti-b

197 in vivo validation of this approach with the Plasmodium berghei model of murine malaria.

198 tive to monitoring liver stage burden in the Plasmodium berghei model.

199 dine and suppresses parasites in vivo in the Plasmodium berghei model.

200 In a Plasmodium berghei mouse infection model, one lead compo

201 lay potent oral antimalarial activity in the Plasmodium berghei mouse malaria model associated with f

202 monstrated promising in vivo efficacy in the Plasmodium berghei mouse model and will be further evalu

203 ike strategy, was completely curative in the Plasmodium berghei mouse model at 4 x 50 mg/kg po.

204 In contrast, efficacy in the Plasmodium berghei mouse model differed dramatically for

205 d plasma exposure and better efficacy in the Plasmodium berghei mouse model of the disease than previ

206 analogues exhibited in vivo activity in the Plasmodium berghei mouse model when administered orally.

207 emonstrated in part curative activity in the Plasmodium berghei mouse model when administered peroral

208 In the Plasmodium berghei mouse model, this series generally ex

209 lly at 50 mg/kg once daily for 4 days in the Plasmodium berghei mouse model, which is superior to the

210 ve activity after oral administration in the Plasmodium berghei mouse model, without apparent signs o

211 We show that hepcidin upregulation in Plasmodium berghei murine malaria infection was accompan

212 lanization responses of Anopheles gambiae to Plasmodium berghei (murine malaria) has been established

213 iparum and in vivo by evolution of resistant Plasmodium berghei mutants.

214 ng regions of PbANKA and the closely related Plasmodium berghei NK65 (PbNK65), that does not cause EC

215 ed with the reticulocyte-restricted parasite Plasmodium berghei NK65 1556Cl1.

216 In this study, using Plasmodium berghei NK65 as a model of a systemic, proinf

217 IL-27R-deficient (WSX-1(-/-)) mice following Plasmodium berghei NK65 infection than in wild-type (WT)

218 ing IL-3-deficient (knockout [KO]) mice with Plasmodium berghei NK65.

219 y of ED(50)/ED(90) of 1.87/4.72 mg/kg versus Plasmodium berghei (NS Strain) in a murine model of mala

220 Importantly, transgene expression reduced Plasmodium berghei oocyst formation by 87% on average an

221 We previously reported that Plasmodium berghei oocysts in which the CS gene is inact

222 d for sequences expressed in differentiating Plasmodium berghei ookinetes and another enriched for se

223 cited a potent melanization response against Plasmodium berghei ookinetes and exhibited significantly

224 Here, we characterize a novel SPN protein of Plasmodium berghei ookinetes and sporozoites named G2 (g

225 Using the motility of Plasmodium berghei ookinetes as a signalling paradigm, w

226 pheles stephensi midgut epithelial cells and Plasmodium berghei ookinetes during invasion of the mosq

227 lasmodium falciparum erythrocytic stages and Plasmodium berghei ookinetes have identified proteolysis

228 Infection of mice with sporozoites of Plasmodium berghei or Plasmodium yoelii has been used ex

229 Immunization of mice with Plasmodium berghei or Plasmodium yoelii synthetic linear

230 We also localized the Plasmodium berghei ortholog to the apicoplast in blood s

231 Surprisingly, the transcripts coding for the Plasmodium berghei orthologues of those genes are stored

232 Unlike the rodent malaria Plasmodium berghei, P. falciparum sporozoites do not inf

233 P. vivax using a fully infectious transgenic Plasmodium berghei parasite expressing P. vivax TRAP to

234 protection against infection with transgenic Plasmodium berghei parasite expressing PfCSP in mice.

235 Moreover, we determined that Plasmodium berghei parasites are heterogeneous for midgu

236 development and characterization of chimeric Plasmodium berghei parasites bearing the type I repeat r

237 zyme is not essential for parasite growth as Plasmodium berghei parasites carrying a complete deletio

238 infection by isolating luciferase-expressing Plasmodium berghei parasites directly from the salivary

239 igen-specific T-cell responses, we generated Plasmodium berghei parasites expressing the model antige

240 Here we show that Plasmodium berghei parasites infecting hepatic cells rel

241 calization on the surface of midgut-invading Plasmodium berghei parasites, targeting them for destruc

242 binantly expressed and purified homolog from Plasmodium berghei (Pb), leading to the identification o

243 orin (PfAQP) in the rodent malaria parasite, Plasmodium berghei (PbAQP), and examined the biological

244 rotein kinase of the rodent malaria parasite Plasmodium berghei, Pbmap-2, in male sexual differentiat

245 Vaccination of mice with recombinant Plasmodium berghei PbSEA-1 significantly reduced parasit

246 parasites Plasmodium falciparum (PfVIT) and Plasmodium berghei (PbVIT).

247 Sporozoites expressing a mutated form of Plasmodium berghei PKG or carrying a deletion of the CDP

248 We report a functional analysis of the Plasmodium berghei protein phosphatome, which exhibits h

249 on of mosquito midgut screen candidate 2), a Plasmodium berghei protein with structural similarities

250 nctional studies in the rodent malaria model Plasmodium berghei recently showed the map-2 gene to be

251 ite CS proteins of Plasmodium falciparum and Plasmodium berghei, respectively, and a green fluorescen

252 d rodent parasites Plasmodium falciparum and Plasmodium berghei, respectively.

253 n and the rodent parasites P. falciparum and Plasmodium berghei, respectively.

254 l deregulation of PV5 in the rodent parasite Plasmodium berghei results in inordinate elongation of h

255 orozoite protein (CSP) were evaluated in the Plasmodium berghei rodent malaria model system.

256 and mosquito bite challenge with transgenic Plasmodium berghei rodent sporozoites that incorporate t

257 The Plasmodium berghei scavenger receptor-like protein PbSR

258 We identified a Plasmodium berghei secreted protein (PBANKA_131270) that

259 D8(+) T cell response in the liver following Plasmodium berghei sporozoite challenge.

260 lay an important albeit nonessential role in Plasmodium berghei sporozoite infectivity for the rodent

261 ne malaria model; (3) prevention of in vitro Plasmodium berghei sporozoite-induced development in hum

262 resence of a phospholipase on the surface of Plasmodium berghei sporozoites (P. berghei phospholipase

263 , multiple exposures to radiation-attenuated Plasmodium berghei sporozoites (Pb gamma-spz) induce lon

264 Plasmodium berghei sporozoites attach to heparan sulphat

265 ies recognition of Plasmodium falciparum and Plasmodium berghei sporozoites by anti-Plasmodium vivax

266 Plasmodium berghei sporozoites delivered by mosquito bit

267 mosquitoes with salivary gland infections of Plasmodium berghei sporozoites expressing a red fluoresc

268 liver Trm or protect against challenge with Plasmodium berghei sporozoites in mice, addition of an a

269 tion induced by radiation-attenuated (gamma) Plasmodium berghei sporozoites is linked to MHC class I-

270 erize the gene expression profiles of 16,038 Plasmodium berghei sporozoites isolated throughout their

271 In addition, we also demonstrate that arg- Plasmodium berghei sporozoites show significantly decrea

272 C57BL/6 mice when they were challenged with Plasmodium berghei sporozoites.

273 ay rats previously immunized with irradiated Plasmodium berghei sporozoites.

274 ct mice from infection with PfCSP transgenic Plasmodium berghei sporozoites.

275 ebral malaria by infecting C57BL/6 mice with Plasmodium berghei strain ANKA.

276 ed mortality after lethal challenge with the Plasmodium berghei strain ANKA.

277 Using a Plasmodium berghei strain expressing a bioluminescent ca

278 s to mice that were then coinfected with two Plasmodium berghei strains, only one of which could be r

279 ll mice at the age of 4 months infected with Plasmodium berghei survive longer during the initial pha

280 ontrast to the rodent model malaria parasite Plasmodium berghei that can become completely melanized

281 In Plasmodium berghei, the transcription factor AP2-G is re

282 With both Plasmodium falciparum and Plasmodium berghei, the tryptophan metabolite xanthureni

283 We have cultured gametocytes of Plasmodium berghei through to infectious sporozoites wit

284 We genetically modified Plasmodium berghei to express Pfs25 and demonstrated tha

285 the ability of Anopheles gambiae to transmit Plasmodium berghei to mice.

286 either of these transgenes were impaired for Plasmodium berghei transmission.

287 on of PIMMS43 in the rodent malaria parasite Plasmodium berghei triggers robust complement activation

288 rasite P. falciparum and the rodent parasite Plasmodium berghei using gene targeting strategies.

289 g sexual proliferation of the rodent malaria Plasmodium berghei, using a combination of super-resolut

290 n increase in survival of mice infected with Plasmodium berghei was observed when compared to control

291 Using the rodent malaria parasite Plasmodium berghei we show that SOAP is targeted to the

292 Here, using the rodent malaria parasite Plasmodium berghei, we identify and characterize the fir

293 Using a genetically targeted strain of Plasmodium berghei, we observed that the Plasmodium orth

294 Using the rodent parasite Plasmodium berghei, we screened a panel of HIV PIs in vi

295 Using the rodent malaria parasite Plasmodium berghei, we show that CDPK1, which is known t

296 ene disruption in the rodent malaria species Plasmodium berghei, we show that PbIMC1a is involved in

297 tial of trophozoites of the malaria parasite Plasmodium berghei were assayed in situ after permeabili

298 Mice infected with the NYU-2 strain of Plasmodium berghei were used to study the effect of chlo

299 bs21 is a surface protein of the ookinete of Plasmodium berghei, which can induce a potent transmissi

300 Plasmodium berghei Yop1 (PbYop1) is a REEP5 homolog in P