ライフサイエンスコーパス: gondii

1 xan protozoan parasite Toxoplasma gondii (T. gondii).

2 to reveal the functions of many genes in T. gondii.

3 nfections in the world, caused by Toxoplasma gondii.

4 caused by the protozoan parasite Toxoplasma gondii.

5 a remarkable low level of conservation in T. gondii.

6 n 1 to stimulate autophagy and killing of T. gondii.

7 including the protozoan parasite Toxoplasma gondii.

8 H1 cells following infection with Toxoplasma gondii.

9 of how human cells detect and respond to T. gondii.

10 more effective, less toxic drugs against T. gondii.

11 idative stress as a mechanism for killing T. gondii.

12 e factors were involved in mRNA export in T. gondii.

13 PKA and PKG pathways to govern egress in T. gondii.

14 c toxoplasmosis after oral infection with T. gondii.

15 yme in the opportunistic pathogen Toxoplasma gondii.

16 c cycle of the protozoan parasite Toxoplasma gondii.

17 r visualising F-actin dynamics in Toxoplasma gondii.

18 snails are competent transport hosts for T. gondii.

19 ilar functions in host cell engagement by T. gondii.

20 to prevent reactivation of infection with T. gondii.

21 ty to virulent acute infection by Toxoplasma gondii.

22 and function in the centrosome of Toxoplasma gondii.

23 Plasmodium falciparum and related Toxoplasma gondii.

24 thogens Plasmodium falciparum and Toxoplasma gondii.

25 apicomplexan parasites, including Toxoplasma gondii.

26 e eukaryotic single-cell parasite Toxoplasma gondii.

27 ain-dwelling, protozoan parasite, Toxoplasma gondii.

28 with the intracellular protozoan Toxoplasma gondii(1).

29 ted H4K31 is enriched in the core body of T. gondii active genes but inversely correlates with transc

30 r, structural and biochemical analyses of T. gondii aldolase and aldolase-like proteins reveal divers

31 The growth of T. gondii aldolase crystals in acidic conditions enabled tr

32 cryotrapped in the active site of Toxoplasma gondii aldolase crystals to high resolution.

33 ic insight into the function of different T. gondii aldolases, we first determined the crystal struct

34 The cytoskeleton of Toxoplasma gondii, an important human parasite, contains at least f

35 Toxoplasma gondii, an obligate intracellular protozoan parasite, es

36 imary gestational infections with Toxoplasma gondii and congenital toxoplasmosis in Austria, a countr

37 producing innate cytokines in response to T. gondii and demonstrate an unappreciated requirement for

38 previously undescribed apical proteins in T. gondii and identify an essential component named conoid

39 chanism of inhibition of TLR signaling by T. gondii and IL-10 and suggest potential negative conseque

40 maging flow cytometry, we found that both T. gondii and IL-10 inhibited virus-induced nuclear translo

41 operative during the interaction between T. gondii and its host cell.

42 oan parasites (Trypanosoma cruzi, Toxoplasma gondii and Leishmania major), in which the Gzms generate

43 apical pole in invasive stages of Toxoplasma gondii and Plasmodium berghei, and apical positioning of

44 Apicomplexan parasites Toxoplasma gondii and Plasmodium spp. use latent stages to persist

45 n in promoting sterile protection against T. gondii and provide strong evidence for rhoptry-regulated

46 How the protozoan pathogen Toxoplasma gondii and related parasites shuttle proteins through th

47 The apical complex of Toxoplasma gondii and some other apicomplexans includes a cone-shap

48 e burdens at secondary sites colonized by T. gondii and succumb to infection.

49 esponses to herpes simplex virus, Toxoplasma gondii, and Citrobacter rodentium infections.

50 lenges, including H1N1 influenza, Toxoplasma gondii, and Ebola virus.

51 P, nucleic acid, proteins, and lipids) in T. gondii, and either of them is sufficient to ensure the p

52 s) are critical for resistance to Toxoplasma gondii, and infection with this pathogen leads to increa

53 otected against infection by T. cruzi and T. gondii, and survive infections that are lethal to wild-t

54 hat contributes to resistance to invading T. gondii, and they thus unveil new avenues for developing

55 pes simplex virus, rubella virus, Toxoplasma gondii, and Zika virus.

56 that seroprevalence of Brucella spp. and T. gondii antibodies likely increased through time, and pro

57 Paternal serum samples were tested for T. gondii antibodies with immunoglobulin (Ig) G dye test an

58 Strains of T. gondii are globally diverse, with more than 16 distinct

59 Plasmodium falciparum and Toxoplasma gondii are widely studied parasites in phylum Apicomplex

60 We further demonstrate that the T. gondii armadillo repeats-only protein (TgARO) mutant, wh

61 Here, we use Toxoplasma gondii as a model system to functionally characterize Tg

62 Here we establish that Toxoplasma gondii aspartyl protease 3 (ASP3) resides in the endosom

63 ne scaffold interrupts the lytic cycle of T. gondii at submicromolar concentration by targeting ASP3.

64 otential to revolutionize the analysis of T. gondii biology and help us to better develop new drugs a

65 naturally occurring peptides from Toxoplasma gondii bound by HLA-A*02:01.

66 the disrupted gene and protein are called T. gondii Brain Colonization Protein 1 (TgBCP1).

67 the motility apparatus of living Toxoplasma gondii by adhering a microsphere to the surface of an im

68 e intracellular vacuolar pathogen Toxoplasma gondii by inducing the destruction of the parasitophorou

69 rvention to combat chronic infection with T. gondii by targeting the persistent cysts of the parasite

70 lective inhibitor (compound 1) of Toxoplasma gondii calcium-dependent protein kinase 1 (TgCDPK1) that

71 It has been proposed that Toxoplasma gondii can cross biological barriers as a motile extrace

72 that systemic infectious agents, such as T. gondii, can induce long-term immune alterations associat

73 ction with the protozoan parasite Toxoplasma gondii causes a nonresolving Th1 myositis with prolonged

74 pyrazolopyrimidine inhibitors of Toxoplasma gondii CDPK1 demonstrated in vitro and in vivo efficacy.

75 ction, the intracellular parasite Toxoplasma gondii co-opts critical functions of its host cell to av

76 st potential negative consequences of HIV/T. gondii coinfection.

77 one-shaped assembly, the conoid, which in T. gondii comprises 14 spirally arranged fibers that are no

78 Following exposure to T. gondii-containing seawater, oocysts were detected by mic

79 monstrate higher than previously reported T. gondii contamination of California coastlines, and descr

80 ellular pathogens, especially for Toxoplasma gondii control.

81 The intracellular parasite Toxoplasma gondii converts from a rapidly replicating tachyzoite fo

82 e to the pathogens Brucella spp., Toxoplasma gondii, Coxiella burnetii, Francisella tularensis, and N

83 The Toxoplasma gondii cyst stage is resistant to drug therapy.

84 .2 chain have a potent activity to remove T. gondii cysts from the brain.

85 ed wild-type (WT) and CD73(-/-) mice with T. gondii cysts systemically by the intraperitoneal (i.p.)

86 n population is chronically infected with T. gondii cysts, the dormant form of the parasite.

87 tivate CD8(+) T cells capable of removing T. gondii cysts.

88 ated that the acute (tachyzoite) stage of T. gondii depends on cooperativity of glucose and glutamine

89 partially reversed by a deficiency in the T. gondii-derived ROP16 kinase, known to directly phosphory

90 expectedly, T-bet(-/-) mice infected with T. gondii develop a strong NK cell IFN-gamma response that

91 The protozoan parasite Toxoplasma gondii develops within a parasitophorous vacuole (PV) in

92 HC class II tetramer reagent specific for T. gondii did not recognize Tregs isolated from the CNS.

93 T. gondii differs substantially in its broad distribution f

94 ers of DCs, Flt3L(-/-) mice infected with T. gondii displayed an expansion of CD8alpha(+) and CD11b(l

95 In Toxoplasma gondii, disruption of the first, fifth, or sixth step of

96 Thirteen mussels (1.4%) had detectable T. gondii DNA and the presence of T. gondii in mussels was

97 ent proteins or targeted genes of Toxoplasma gondii, driven by N. caninum promoters, have yielded rob

98 to profile the transcriptomes of mice and T. gondii during acute and chronic stages of infection.

99 on of each gene from the parasite Toxoplasma gondii during infection of human fibroblasts.

100 When Toxoplasma gondii egresses from the host cell, glyceraldehyde-3-pho

101 We identify 195 T. gondii encoded ligands originating from both secreted an

102 Toxoplasma gondii encodes three protein kinase A catalytic (PKAc1-3

103 The genome of Toxoplasma gondii encodes ubiquitination machinery, but the roles o

104 oteins along the cortical microtubules of T. gondii, established during daughter biogenesis and regul

105 thogen, the apicomplexan parasite Toxoplasma gondii evades immune system-mediated clearance by underg

106 Although an association between T. gondii exposure and prey specialization on marine snails

107 In Toxoplasma gondii, extracellular potassium levels and other stimuli

108 In Toxoplasma gondii, fatty acid synthesis via the apicoplast-localize

109 utics, we screened insertional mutants of T. gondii for a reduced ability to form cysts in the brains

110 o facilitate drug development: EGS strain T. gondii forms cysts in vitro that induce oocysts in cats,

111 ide broad-based functional information on T. gondii genes and will facilitate future approaches to ex

112 ere we summarize the major strategies for T. gondii genetic manipulation including genetic crosses, i

113 e homologous type I or a distinct type II T. gondii genotypes.

114 of potent killer T cells to curb Toxoplasma gondii growth during latency.

115 determined that ZBP1 functions to control T. gondii growth.

116 ate immune responses to restrict cerebral T. gondii growth.

117 Recently, we showed that T. gondii harbors a novel AMA designated as TgAMA4 that sho

118 demonstrate that the apicomplexan Toxoplasma gondii harbors homologues of proteins from all the major

119 ated from ZBP1 deletion (ZBP1(-/-)) mice, T. gondii has an increased rate of replication and a decrea

120 , this study brings novel evidence on how T. gondii has devised a molecular weapon of choice to take

121 T. gondii has evolved mechanisms to timely counteract the h

122 Here, we characterized a unique T. gondii homologue of mammalian lecithin:cholesterol acylt

123 We demonstrate that a T. gondii homologue of Tom22 (TgTom22), a central component

124 We also identify and characterize a T. gondii homologue of Tom7 (TgTom7) that is important for

125 ive analysis of palmitoylated proteins in T. gondii, identifying a total of 282 proteins, including c

126 -agglutination and IgG avidity tests when T. gondii IgG and IgM results were positive and serum sampl

127 recent T gondii infection (a positive anti-T gondii IgM antibody test) from Erechim, Rio Grande do Su

128 ognitive assessments and had anti-Toxoplasma gondii immunoglobulin G (anti-Toxo IgG) measured by qual

129 n of IgG, IgM, and IgA antibodies against T. gondii in an approximately 1-mul serum or whole-blood sa

130 Using the zoonotic parasite Toxoplasma gondii in California, USA as a model for coastal pathoge

131 gnaling in the model apicomplexan Toxoplasma gondii In doing so, we took advantage of the phosphodies

132 tophagy and autophagic killing of Toxoplasma gondii in host cells.

133 ectable T. gondii DNA and the presence of T. gondii in mussels was significantly associated with prox

134 Studies in Plasmodium spp. and Toxoplasma gondii in particular have revealed that these parasites

135 galovirus, Epstein-Barr virus and Toxoplasma gondii in patients with uveitis.

136 ntify NLRP3 as an inflammasome sensor for T. gondii in primary human peripheral blood cells and to de

137 latency of chronic infection with Toxoplasma gondii in the brain.

138 to the intracellular replicative cycle of T. gondii including secretion of adhesins, motility, invasi

139 intracellular protozoan parasite Toxoplasma gondii induced an early IL-1beta response (within 4 h) i

140 sensor NLRP3 and for potassium efflux in T. gondii-induced IL-1beta production.

141 e (NECA) protected CD73(-/-) mice against T. gondii-induced immunopathology, suggesting that the abse

142 etic compartments contributes to limiting T. gondii-induced immunopathology.

143 rein we purify HLA-A*02:01 complexes from T. gondii infected cells and characterize the peptide ligan

144 al for CD8+ T-cell recognition of Toxoplasma gondii infected cells.

145 B1 allele that was recently documented in T. gondii-infected carnivores from California.

146 at whereas neutrophils and monocytes from T. gondii-infected infants display a combination of proinfl

147 SI + mode and 74 in ESI - mode in sera of T. gondii-infected mice compared to the control mice.

148 Upon stimulation, T. gondii-infected ZBP1(-/-) macrophages display increased

149 patients with serologic evidence of recent T gondii infection (a positive anti-T gondii IgM antibody

150 Similarly, Tregs in the CNS during T. gondii infection are Th1 polarized, as exemplified by th

151 However, prior T. gondii infection blocks IFN-gamma-dependent gene transcr

152 Toxoplasma gondii infection causes substantial morbidity and mortal

153 Interestingly, T. gondii infection did not induce an IL-1beta response in

154 latforms, as the serological diagnosis of T. gondii infection does not rely on the detection of a sin

155 454 individuals with serologic evidence of T gondii infection during the epidemic (positive IgM antib

156 Toxoplasma gondii infection has been described previously to cause

157 aled a high prevalence (29 of 81; 36%) of T. gondii infection in fathers, relative to the average ser

158 The course of Toxoplasma gondii infection in rats closely resembles that in human

159 Intrinsic to Toxoplasma gondii infection is the parasite-induced modulation of t

160 An early hallmark of Toxoplasma gondii infection is the rapid control of the parasite po

161 neither provided a protective response to T. gondii infection nor mediated autoimmune colitis.

162 mic and transcriptomic effects of Toxoplasma gondii infection on human host cells and demonstrate tha

163 ifestations were associated with paternal T. gondii infection status.

164 ocephalus secondary to congenital Toxoplasma gondii infection were identified and characterized for i

165 EW rat versus the BN rat, with or without T. gondii infection, in order to unravel molecular factors

166 es that infiltrate the brain upon chronic T. gondii infection, plays a decisive role in host defense.

167 actoriness of LEW rat peritoneal cells to T. gondii infection, resulting in proliferation of parasite

168 ctive in acute and latent mouse models of T. gondii infection, significantly reducing the amount of p

169 actions can be an initial manifestation of T gondii infection, with necrotizing retinochoroiditis occ

170 1beta cleavage and release in response to T. gondii infection, without affecting the release of TNF-a

171 ning to peptides that are presented after T. gondii infection.

172 ts into the roles of CDPKs during Toxoplasma gondii infection.

173 sing a mouse model for persistent Toxoplasma gondii infection.

174 ole for ZBP1 in assisting host control of T. gondii infection.

175 he metabolic profile of mouse sera during T. gondii infection.

176 tigenic recall in infants with congenital T. gondii infection.

177 vated macrophages, even in the absence of T. gondii infection.

178 and was not induced in macrophages during T. gondii infection.

179 people develop ocular disease soon after T. gondii infection.

180 acerbates ileitis induced by oral Toxoplasma gondii infection.

181 ferate to prevent reactivation of chronic T. gondii infection.

182 (NCCCTS) have a high incidence of Toxoplasma gondii infection.

183 for serologic evidence of recent Toxoplasma gondii infection.

184 L-22 in innate lymphoid cells (ILCs) upon T. gondii infection.

185 ons regulates their local behavior during T. gondii infection.

186 Lewis (LEW) rat is extremely resistant to T. gondii infection.

187 ill children reflecting brain damage and T. gondii infection.

188 gions of increased sentinel marine mammal T. gondii infection.

189 enitally infected children indicates that T. gondii infections cluster within families in North Ameri

190 alence of chronic and incidence of recent T. gondii infections in fathers of congenitally infected ch

191 However, T. gondii inhibited IFN-alpha and TNF-alpha produced in res

192 We now have identified TgIST (T. gondii inhibitor of STAT1 transcriptional activity) as a

193 l pellets, snails may facilitate entry of T. gondii into the nearshore marine food web.

194 uorescence microscopy, we determined that T. gondii invaded but did not induce IFN-alpha or TNF-alpha

195 Toxoplasma gondii is a classic model for studying obligate intracel

196 Toxoplasma gondii is a common parasite of humans and animals, which

197 oastal habitat contamination with Toxoplasma gondii is a health risk to humans and marine wildlife, w

198 f HIV type 1 replication, whereas Toxoplasma gondii is a life-threatening opportunistic infection in

199 Toxoplasma gondii is a protist parasite of warm-blooded animals tha

200 Toxoplasma gondii is a protozoan pathogen in the phylum Apicomplexa

201 Toxoplasma gondii is a widespread parasite of warm-blooded vertebra

202 Toxoplasma gondii is a widespread parasitic pathogen that infects o

203 Toxoplasma gondii is a widespread protozoan parasite infecting near

204 Infection with Toxoplasma gondii is acquired through consumption of undercooked in

205 Toxoplasma gondii is among the most prevalent parasites worldwide,

206 The parasite Toxoplasma gondii is an environmentally persistent pathogen that ca

207 Toxoplasma gondii is an intracellular parasite that causes dissemin

208 Toxoplasma gondii is an obligate intracellular parasite that invade

209 Toxoplasma gondii is an obligate intracellular protozoan parasite.

210 Toxoplasma gondii is an obligate, intracellular eukaryotic apicompl

211 rne infection with an atypical genotype of T gondii is associated with substantial risk of ocular inv

212 that the unusual population structure of T. gondii is characterized by clade-specific inheritance of

213 Toxoplasma gondii is considered to be one of the most successful in

214 ebral infection with the parasite Toxoplasma gondii is followed by activation of resident cells and r

215 of actinonin in P. falciparum and Toxoplasma gondii is FtsH1, a homolog of a bacterial membrane AAA+

216 ts animal counterparts, Skp1 from Toxoplasma gondii is hydroxylated by an O2-dependent prolyl-4-hydro

217 40-mediated autophagic killing of Toxoplasma gondii is known to require TNF-alpha.

218 ed the genomes of 62 globally distributed T. gondii isolates to several closely related coccidian par

219 nic functions during ileitis triggered by T. gondii, it was required for host defense against C. rode

220 f JNK, CaMKKbeta, AMPK, or ULK1 prevented T. gondii killing in CD40-activated macrophages.

221 factors directing robust and rapid early T. gondii-killing mechanisms in the LEW rat.

222 In mice, infection with Toxoplasma gondii leads to a Th1-polarized parasite-specific effect

223 Surprisingly, T. gondii ligands are significantly longer than uninfected

224 Toxoplasma gondii, like all apicomplexan parasites, uses Ca(2+) sig

225 ainst the intracellular pathogens Toxoplasma gondii, Listeria monocytogenes, and Mycobacterium tuberc

226 ith pathogens such as Zika virus, Toxoplasma gondii, Listeria monocytogenes, Treponema pallidium, par

227 tute the lytic cycle, as well as the ways T. gondii manipulates host cells to ensure its survival.

228 Bacillus anthracis lethal toxin, Toxoplasma gondii, muramyl dipeptide, and host intracellular ATP de

229 asive protozoal infections due to Toxoplasma gondii (n = 3), Trypanosoma cruzi, and Leishmania specie

230 mice challenged with the parasite Toxoplasma gondii, NK and T cell responses are characterized by mar

231 contribute most to the disease burden of T. gondii, ocular disease from acquired infection was recen

232 vestigated the impact of coinfection with T. gondii on the innate virus-directed responses of human p

233 plied as a method for confirming putative T. gondii oocysts detected in snail faeces and tissues by m

234 ed role of phagocytic cells in processing T. gondii oocysts, in line with non-classical routes of inf

235 -18) in intestinal epithelial cells after T. gondii or Citrobacter rodentium infection, but also main

236 Within 1 hour, greater numbers of T gondii or S typhimurium were present within mucosae of m

237 manipulation tools have been developed in T. gondii over the past 20 years.

238 fy an intrinsic role for autophagy in the T. gondii parasite and its close relatives.

239 double punch that can destroy the Toxoplasma gondii parasite and its niche inside cells.

240 Toxoplasma gondii parasites must actively invade host cells to prop

241 le of CD73 and extracellular adenosine in T. gondii pathogenesis, we infected wild-type (WT) and CD73

242 Bradyzoite forms of Toxoplasma gondii persist in tissue cysts for the lifetime of an in

243 veterinary importance, including Toxoplasma gondii, Plasmodium falciparum, and C. parvum In the pres

244 nslation initiation site preference for a T. gondii protein.

245 lmitoylation is ubiquitous throughout the T. gondii proteome and reveal insights into the biology of

246 B/c mice experimentally infected with the T. gondii Pru strain (Genotype II).

247 Thus, T. gondii PTMs are implicated as critical regulators of cel

248 Apicomplexan parasites such as Toxoplasma gondii rely on a unique form of locomotion known as glid

249 Toxoplasma gondii replicates asexually by a unique internal budding

250 Control of T. gondii replication by mGBP2 requires GTP hydrolysis and

251 the hypothesis that sustained immunity to T. gondii requires repeated antigenic stimulations.

252 a previously unknown modulator of Toxoplasma gondii resistance in vivo thereby extending host innate

253 A recent study in Toxoplasma gondii revealed a unique bipartite structure of the cent

254 reduction in invasiveness of the Toxoplasma gondii RH-AMA1 knockout (RH-AMA1(KO)) tachyzoite populat

255 e demonstrated that N. caninum expressing T. gondii's GRA15 and ROP16 kinase are biologically active

256 hardy free-living environmental stage of T. gondii shed in faeces of domestic and wild felids, are c

257 ort a novel function of the endolysosomal T. gondii sortilin-like receptor (TgSORTLR), which mediates

258 mounts of tachyzoite (acute stage form of T. gondii)-specific SAG1 mRNA and numbers of foci associate

259 ing gestation is made mostly by detecting T. gondii-specific antibodies, including IgG and IgM, indiv

260 Monoclonal T. gondii-specific CD8 T cells adoptively transferred into

261 tly proinflammatory profile upon in vitro T. gondii stimulation.

262 Transmissible stages of Toxoplasma gondii store energy in the form of the carbohydrate amyl

263 immunological phenotypes consistent with T. gondii strains.

264 ormed on the rat pineal gland and Toxoplasma gondii, successfully detecting known and previously vali

265 f modified CRISPR-Cas9 systems for use in T. gondii, such as regulation of gene expression, labeling

266 Taken together, our results indicate that T. gondii suppresses pDC activation by mimicking IL-10's re

267 e apicomplexan protozoan parasite Toxoplasma gondii (T. gondii).

268 cell completely replaces the l-Phe within T. gondii tachyzoites 7-9 hours after infection.

269 but not least, the observed physiology of T. gondii tachyzoites appears to phenocopy cancer cells, wh

270 T. gondii tachyzoites are capable of extracting l-Phe(D8) f

271 may underlie the promiscuous survival of T. gondii tachyzoites in diverse host cells.

272 context, IFN-gamma activates a variety of T. gondii-targeting activities in immune and nonimmune cell

273 ing the mitochondrion-associated DHODH of T. gondii (TgDHODH) failed.

274 ogy during intraperitoneal infection with T. gondii than WT mice.

275 caused by the protozoan parasite Toxoplasma gondii that can lead to severe sequelae in the fetus dur

276 ows strong antiparasitic activity against T. gondii The same compound inhibits invasion of the most l

277 Dictyostelium (a social amoeba), Toxoplasma gondii (the agent for human toxoplasmosis), and other pr

278 In apicomplexan parasites such as Toxoplasma gondii, the apical complex includes a spiral cap of tubu

279 Toxoplasma gondii, the causative agent of toxoplasmosis, is an intr

280 letal structures differs substantially in T. gondii, the molecular motor dependence of DG trafficking

281 Toxoplasma gondii, the most common parasitic infection of human bra

282 As a major natural host for Toxoplasma gondii, the mouse is widely used for the study of the im

283 ng invasion, egress, and cell division in T. gondii, the roles of most of these genes are unexplored.

284 lation of the host immune response allows T. gondii to not only dampen the ability of the host to eli

285 ifferent isoforms of these enzymes allows T. gondii to rapidly adapt to diverse metabolic requirement

286 ns, Heligsomosoides polygyrus and Toxoplasma gondii, to investigate the negative impact of helminthes

287 ns, Heligmosomoides polygyrus and Toxoplasma gondii, to investigate the negative impact of helminthes

288 It is believed that infection by Toxoplasma gondii triggers a lifelong protective immunity due to th

289 emic infection with the protozoan Toxoplasma gondii triggers not only a transient increase in activat

290 ar characterization revealed alleles from T. gondii types I, II/III, X at the B1 locus, and a novel a

291 ylum, such as Plasmodium spp. and Toxoplasma gondii, undergo complex life cycles involving multiple s

292 vation of cerebral infection with Toxoplasma gondii using a murine model.

293 Toxoplasma gondii was not detected in field-collected snails.

294 that regulate these processes in Toxoplasma gondii We found that microneme secretion was triggered i

295 valence and function of ubiquitination in T. gondii, we mapped the ubiquitin proteome of tachyzoites.

296 Salmonella typhimurium or Toxoplasma gondii were administered to knockout (KO) mice lacking e

297 Additionally, the odds of exposure to T. gondii were greater for bears that used land than for be

298 lassic cell-cycle regulators conserved in T. gondii were not detected in the ubiquitinome.

299 omplexan parasites, especially in Toxoplasma gondii where 14 separate genes encoding these enzymes ar

300 n was inhibited only in cells infected by T. gondii, which inhibited neither uptake of GFP-HSV nor lo

301 The survival of Toxoplasma gondii within its host cell requires protein release fro