ライフサイエンスコーパス: T. brucei

1 T. brucei and other trypanosomatid pathogens require a d

2 T. brucei brucei cells exposed to peroxides or thiol-bin

3 T. brucei cells expressing only analogue-sensitive TbPLK

4 T. brucei cells overexpressing TbHrg displayed up-regula

5 T. brucei cultivated in the presence of deoxyadenosine a

6 T. brucei cycles between its mammalian host (bloodstream

7 T. brucei has a single flagellum whose base contains a b

8 T. brucei lacks many evolutionarily conserved centriolar

9 T. brucei methylthioadenosine phosphorylase (TbMTAP) was

10 T. brucei regularly switches its major surface antigen,

11 T. brucei TatD nuclease showed intrinsic DNase activity,

12 T. brucei telomerase plays a key role in maintaining tel

13 T. brucei TK was primarily monomeric but can be consider

14 arasite proliferation (e.g., VUF13525 (20b): T. brucei rhodesiense IC(5)(0) = 60 nM, T. brucei brucei

15 convolution analysis using a selection of 29 T. brucei mutants that overexpress known essential prote

16 phs showed that T. brucei, L. mexicana and a T. brucei RNAi morphology mutant have a range of shape a

17 ulatory genes, of which one can complement a T. brucei QS signal-blind mutant to restore stumpy forma

18 In AT, T. cruzi resides inside adipocytes, T. brucei is found in the interstitial spaces between ad

19 f 1 resulted in 10e (0.19 muM EC(50) against T. brucei and 990 muM aqueous solubility).

20 and displayed antiparasitic activity against T. brucei (IC50 49 muM).

21 TR1 inhibition and in vitro activity against T. brucei and amastigote Leishmania infantum.

22 gue (7) was identified with activity against T. brucei as low as 70 nM and a selectivity index of 72.

23 inhibitor with interesting activity against T. brucei in a phenotypic screen.

24 mane scaffold has promising activity against T. brucei rhodesiense and L. donovani.

25 er of pinobanksin with high activity against T. brucei whereas in the case of T. congolense high acti

26 ) and low muM antiparasitic activity against T. brucei.

27 rexate when evaluated in combination against T. brucei, with a potentiating index between 1.2 and 2.7

28 e design of a safe and specific drug against T. brucei.

29 Both compounds show in vitro effects against T. brucei and in vivo curative activity in a mouse model

30 hibitors that show nanomolar potency against T. brucei bloodstream forms, Leishmania and Trypanosoma

31 7b, that exhibited nanomolar potency against T. brucei with excellent selectivity for parasite cells

32 variants of human APOL1 that protect against T. brucei rhodesiense have recapitulated molecular signa

33 nt with Old World monkeys, protected against T. brucei rhodesiense due in part to reduced SRA binding

34 -AAG and 17-DMAG were most selective against T. brucei as compared to mammalian cells.

35 ifferent chemotherapeutic strategies against T. brucei were investigated using this model and interru

36 Twelve compounds showed EC50 values against T. brucei below 10 muM.

37 We also analyzed T. brucei extracts for the presence of inositol phosphat

38 hich human-infective T. brucei gambiense and T. brucei rhodesiense have evolved resistance.

39 key role in maintaining telomere length, and T. brucei telomeres terminate in a single-stranded 3' G-

40 ivity against the enzyme (IC(50) = 2 nM) and T. brucei (EC(50) = 2 nM) in culture.

41 nfective pathogens T. brucei rhodesiense and T. brucei gambiense, which are resistant to lysis by hum

42 In B. subtilis and T. brucei, ms2ct6A disappeared and remained to be ms2t6A

43 the role of T. brucei centrin2 (TbCen2) and T. brucei 3 (TbCen3) in the early events of T. brucei pr

44 ance of T. brucei PS synthase 2 (TbPSS2) and T. brucei PS decarboxylase (TbPSD), two key enzymes invo

45 aintaining high potency against TbrPDEB1 and T. brucei.

46 Using anti-T. brucei ABQs as chemical probes, we demonstrated that

47 the structure-activity relationships around T. brucei for a series of benzoxazepinoindazoles previou

48 ences in structure, processing and assembly, T. brucei ribosomes may require biogenesis factors not f

49 The interaction between T. brucei and its host is substantially more dynamic and

50 In the host bloodstream T. brucei scavenges heme via haptoglobin-hemoglobin (HpH

51 pyrrolopyrimidine AEE788 killed bloodstream T. brucei in vitro with GI(50) in the low micromolar ran

52 s inhibited the proliferation of bloodstream T. brucei with EC(50) values down to <1 muM and exerted

53 depletion of centrin1 in Trypanosoma brucei (T. brucei) displayed arrested organelle segregation resu

54 Trypanosoma brucei (T. brucei) is responsible for the fatal human disease ca

55 n the parasitic protozoa Trypanosoma brucei (T. brucei), the causative agent for human African trypan

56 protein p67 was observed in Deltatbnst4 BSF T. brucei.

57 role for indolepyruvate in immune evasion by T. brucei.

58 nce-associated protein, which is produced by T. brucei rhodesiense and prevents trypanosome lysis by

59 Rhodesain is required by T. brucei to cross the blood-brain barrier, degrade host

60 This suggests the chiral T. brucei cell shape (associated with the lateral attach

61 ional drug design targeting BILBO1 to combat T. brucei infections.

62 Consequently, T. brucei grown in the presence of adenine demonstrated

63 ion of T cells and trypanosomes, and control T. brucei brucei load in the brain by molecules distinct

64 Moreover, NMT inhibitors effectively cure T. brucei infection in rodents.

65 ble EbS analogues were synthesized and cured T. brucei brucei infection in mice when used together wi

66 A-resistant trypanocidal compound that cured T. brucei infection in mice.

67 Cytoplasmic T. brucei aaRSs were organized in a multiprotein complex

68 n both tsetse fly-derived and mammal-derived T. brucei, and we show that BRCA2 loss has less impact o

69 er organisms, is only seen in mammal-derived T. brucei.

70 GM6 repeats (ClpGM6) involved in determining T. brucei cell shape, size, and form.

71 interest for nucleoside analog development, T. brucei TK was less discriminative against purines tha

72 Previously, we identified a highly divergent T. brucei N-acetylglucosaminyltransferase I (TbGnTI) amo

73 in the context of IFN-gamma and IL-10 during T. brucei infections.

74 ed in the synthesis of IgG antibodies during T. brucei infections.

75 chanisms governing edited mRNA levels during T. brucei development and the first to interrogate U-ind

76 reby human trypanolytic APOL1 variants evade T. brucei rhodesiense virulence factor serum resistance-

77 pressure, we generated VSG double-expresser T. brucei lines, which have disrupted monoallelic exclus

78 erting ectopic VSG117 into VSG221 expressing T. brucei.

79 5A levels and found that it is essential for T. brucei growth.

80 ever, subtelomere integrity is essential for T. brucei viability.

81 s identify the adipose tissue as a niche for T. brucei during its mammalian life cycle and could pote

82 ssue constitutes a third major reservoir for T. brucei.

83 in the series were exquisitely selective for T. brucei over a panel of other protozoan parasites, sho

84 EbS was more toxic for T. brucei than for Trypanosoma cruzi, probably due to lo

85 nockdown of RCCP or FYRP in bloodstream form T. brucei results in derepression of silent variant surf

86 e and VSG gene silencing in bloodstream form T. brucei.

87 levels of VSG expression in bloodstream form T. brucei.

88 ar potency in vitro against bloodstream-form T. brucei; novobiocin had micromolar activity.

89 e activity improved growth of procyclic form T. brucei during oxidative challenges with hydrogen pero

90 ly decreased growth (>90%) of procyclic form T. brucei under standard culture conditions and was leth

91 encodes this vital pyruvate transporter from T. brucei.

92 thesis of both complex and hybrid N-glycans, T. brucei TbGT11 null mutants expressed atypical "pseudo

93 y checkpoint, and nothing is known about how T. brucei controls its cell cycle checkpoints.

94 This helps to explain how T. brucei escapes 'wholesale deamination' of its genome

95 In T. brucei, spliced leader (SL)-mediated trans-splicing o

96 In T. brucei, we show that this protein is localized to the

97 Here, we report that TBsRNA-10 in T. brucei is a vtRNA, based on its association with TEP1

98 Ca(2+) release channel of acidocalcisomes in T. brucei.

99 TbORC1/CDC6-interacting factors also act in T. brucei nuclear DNA replication and demonstrate that T

100 yb domain tolerates well the bulky J base in T. brucei telomere DNA, and the DNA-binding affinity of

101 n essential role in basal body biogenesis in T. brucei Further investigation of the functional interp

102 essential roles in basal body biogenesis in T. brucei, but how they cooperate in the regulation of b

103 mechanism for assembly of the basal body in T. brucei.

104 Although QS is characterized in T. brucei, co-infections with other trypanosome species

105 , DNA damage-induced metaphase checkpoint in T. brucei.

106 This showed quantitatively how chirality in T. brucei cell shape confers highly directional swimming

107 ate dependence of deoxyadenosine cleavage in T. brucei cell extracts and increased deoxyadenosine sen

108 ppear to form a single major ISWI complex in T. brucei (TbIC).

109 we report that the gamma-tubulin complex in T. brucei is composed of gamma-tubulin and three GCP pro

110 entified an unusual gamma-tubulin complex in T. brucei, uncovered an essential role of gammaTuSC in c

111 nithine uptake has important consequences in T. brucei, but the transporters have not been identified

112 nclear how ES transcription is controlled in T. brucei.

113 tructures that facilitate gene conversion in T. brucei and mechanisms underlying its antigenic divers

114 st and therefore suggest that cytokinesis in T. brucei could potentially be exploited as a new drug t

115 Initiation of cytokinesis in T. brucei is regulated by two evolutionarily conserved p

116 telomeric transcript, TERRA, was detected in T. brucei previously.

117 We suggest all proliferative divisions in T. brucei and related organisms will involve non-equival

118 e set of gRNAs necessary for mRNA editing in T. brucei, we used Illumina deep sequencing of purified

119 Potential specialized functions for eIF5A in T. brucei in translation of variable surface glycoprotei

120 To evaluate the function of eIF5A in T. brucei, we used RNA interference (RNAi) to knock down

121 C (TbPLC) derepresses numerous silent ESs in T. brucei bloodstream forms.

122 Polyamine biosynthesis is essential in T. brucei, and the polyamine spermidine is required for

123 However, the dynamics of VSG expression in T. brucei during an infection are poorly understood.

124 ween antigenic variation and cell fitness in T. brucei.

125 resents the unique route for PS formation in T. brucei.

126 celerates differentiation to stumpy forms in T. brucei, which is also QS dependent.

127 hat, in vitro, approximately 10% of genes in T. brucei are expressed with a circadian rhythm.

128 functional specialization of Arl3-GTPases in T. brucei These results establish the function of TbUnc1

129 peroxide, known to be constitutively high in T. brucei, enhanced the EbS inhibition of TryR.

130 arrier protein Unc119 has been identified in T. brucei genome, but its function in lipidated protein

131 n Orc1/Cdc6 homologue has been identified in T. brucei, but its role in DNA replication has not been

132 ctional analyses of other NSTs identified in T. brucei.

133 ed features of DNA replication initiation in T. brucei, providing new insight into this key stage of

134 of endogenous and exogenous myo-inositol in T. brucei is strictly segregated.

135 3 ), and inositol hexakisphosphate (IP6 ) in T. brucei different stages.

136 ical roles of the different TbAK isoforms in T. brucei are further discussed.

137 In contrast, loss of J in T. brucei did not lead to genome-wide termination defect

138 spectrometry, we analyzed protein levels in T. brucei procyclic forms at different time points durin

139 racellular ornithine and polyamine levels in T. brucei, thereby decreasing sensitivity to eflornithin

140 Conditional repression of MCP2 in T. brucei bloodstream forms resulted in reduced parasite

141 s localized in the mitochondrial membrane in T. brucei.

142 gh which TbPLK directs cell morphogenesis in T. brucei.

143 ection among the single-copied organelles in T. brucei, a strategy employed by the parasite for order

144 the existence of more replication origins in T. brucei than previously appreciated.

145 ht the existence of a cytokinesis pathway in T. brucei that is different from that of its mammalian h

146 the presence of a conserved LIFT pathway in T. brucei.

147 cers previously demonstrated to cause PCD in T. brucei.

148 This functional complex is also present in T. brucei, and conditional knock-out studies indicate th

149 t TbTim62, a unique mitochondrial protein in T. brucei, is required for the formation of a stable TbT

150 TIM complex consisting of novel proteins in T. brucei and is critical for mitochondrial protein impo

151 for genes encoding putative CAE proteins in T. brucei, we identified a single ORF, Tb927.9.8780, as

152 s identify two new cytokinesis regulators in T. brucei and integrate them into the CIF1-mediated cyto

153 perimental characterization of ribokinase in T. brucei showed that very low enzyme levels are suffici

154 inal domain (NTD) plays an essential role in T. brucei FPC biogenesis and is thus vital for the paras

155 of TbPLK, SPBB1, and its essential roles in T. brucei.

156 most complete model of pyrimidine salvage in T. brucei to date, supported by genome-wide profiling of

157 TL6), is important for ribosome stability in T. brucei.

158 specific elaboration of axoneme structure in T. brucei reflects adaptations to support unique motilit

159 arger being identified as a TFIIH subunit in T. brucei.

160 ES transcription and antigenic switching in T. brucei by epigenetic regulation of telomere silencing

161 Depletion of TbTim17 in T. brucei impairs the mitochondrial import of cytochrome

162 Here we show that in T. brucei in vivo import of tRNAs requires four subunits

163 We showed that in T. brucei the TPR structural motifs, highly conserved be

164 tory factor to maintain the levels of TIM in T. brucei mitochondria.

165 inner membrane (TIM) consisting of Tim17 in T. brucei.

166 50 proteins from fungi and mammals, Tim50 in T. brucei (TbTim50) possesses a mitochondrial targeting

167 te the dynamic nature of tRNA trafficking in T. brucei and its potential impact not only on the avail

168 protein facilitating Pol I transcription in T. brucei.

169 dy positioning and life cycle transitions in T. brucei.

170 to lower levels of TryR and trypanothione in T. brucei.

171 A key regulator of RAD51 is BRCA2, which in T. brucei contains a dramatic expansion of a motif that

172 e is restricted to Leishmania spp., while in T. brucei it regulates termination and gene expression a

173 l development of Hsp90 inhibitors to include T. brucei.

174 We have found that four parasites, including T. brucei, contain genes where two or four thymidine kin

175 HbHpR polymorphism unique to human infective T. brucei gambiense has been shown to be sufficient to r

176 actors (TLFs), against which human-infective T. brucei gambiense and T. brucei rhodesiense have evolv

177 Interestingly, T. brucei-infected mice also had a reduced homeostatic s

178 ce-associated PKs provides new insights into T. brucei-host interaction and reveals novel potential p

179 Moreover, ADP/ATP exchange in isolated T. brucei mitochondria was eliminated upon TbMCP5 deplet

180 could be a promising drug target in not just T. brucei but in other eukaryotic pathogens.

181 (GW572016, 1) and canertinib (CI-1033) kill T. brucei with low micromolar EC50 values.

182 tivate a subset of human CDXG kinases, kills T. brucei in culture and in infected mice.

183 tes with seven unique as well as a few known T. brucei mitochondrial proteins.

184 appears to do so independently of two known T. brucei telomere proteins, TbRAP1 and TbTRF.

185 We demonstrate that a major T. brucei PRMT, TbPRMT1, functions as a heterotetrameric

186 d adaptor ligation assay, we found that most T. brucei telomere G-overhangs end in 5' TTAGGG 3', whil

187 0b): T. brucei rhodesiense IC(5)(0) = 60 nM, T. brucei brucei IC(5)(0) = 520 nM, T. cruzi = 7.6 muM),

188 e separation of function between two nuclear T. brucei RNase H enzymes during RNA Pol II transcriptio

189 to make and screen numerous conditional null T. brucei bloodstream form cell lines that express rando

190 determined using metabolomic assessments of T. brucei clonal lines adapted to high levels of these p

191 nes et al. report on the characterization of T. brucei pyridoxal kinase (PdxK), an enzyme required fo

192 eport, we show that the non-canonical CTD of T. brucei RNA pol II is important for normal protein-cod

193 n the glycosome, and TbAK3 in the cytosol of T. brucei.

194 two daughters of a proliferative division of T. brucei are non-equivalent and enables more refined mo

195 me in vitro The upstream essential domain of T. brucei TR, termed the template core, constitutes thre

196 ural data, we identified distinct domains of T. brucei A1 which specifically recognize A6 and L2.

197 T. brucei 3 (TbCen3) in the early events of T. brucei procyclic cell cycle.

198 ere we show that silencing the expression of T. brucei cdc2-related kinase 9 (CRK9) leads to a loss o

199 The bloodstream form of T. brucei excretes significant amounts of aromatic ketoa

200 ized cell system for the bloodstream form of T. brucei, we show that down-regulated vtRNA levels impa

201 inesis initiation in the bloodstream form of T. brucei.

202 nces between insect and bloodstream forms of T. brucei were also investigated.

203 ressed in bloodstream and procyclic forms of T. brucei, while the total cellular arginine kinase acti

204 Curiously, the genome of T. brucei does not encode EGFR or VEGFR, indicating that

205 and annotation of the kinetoplast genome of T. brucei.

206 n over variant surface coat glycoproteins of T. brucei, which impair effective host immune responses.

207 essential role of NST(s) in glycosylation of T. brucei.

208 We now reveal the importance of T. brucei PS synthase 2 (TbPSS2) and T. brucei PS decarb

209 cured mice of a normally lethal infection of T. brucei.

210 tities that are active against infections of T. brucei.

211 nalogue of ebselen, is a potent inhibitor of T. brucei growth with a favorable selectivity index over

212 ass of potent, brain penetrant inhibitors of T. brucei NMT.

213 e processes are involved in TLF-1 killing of T. brucei brucei.

214 We now report that lack of T. brucei RFT1 (TbRFT1) not only affects protein N-glyco

215 Here we show that loss of T. brucei RNase H2 (TbRH2A) leads to growth and cell cyc

216 n complex from the mitochondrial membrane of T. brucei by tandem affinity chromatography revealed tha

217 tivity is essential, TbGnTII null mutants of T. brucei grow in culture and are still infectious to an

218 pounds have a clear effect on the S-phase of T. brucei cell cycle by inflicting specific damage on th

219 e add the pentose phosphate pathway (PPP) of T. brucei to the glycolytic model.

220 ain, a cathepsin L-like cysteine protease of T. brucei rhodesiense, is considered a potential target

221 ated that the major GPI-anchored proteins of T. brucei procyclic forms have truncated GPI anchor side

222 hat TbRP2 is required for the recruitment of T. brucei orthologs of MKS1 and MKS6, proteins that, in

223 Down-regulation of T. brucei vtRNA impairs mRNA splicing in a permeabilized

224 acts to maintain the huge VSG repository of T. brucei, and this function has necessitated the evolut

225 In this study we analyzed the role of T. brucei centrin2 (TbCen2) and T. brucei 3 (TbCen3) in

226 that, in the pathogenic bloodstream stage of T. brucei, the huge and energetically demanding apparatu

227 et against the mammalian life cycle stage of T. brucei.

228 ial effects between the life cycle stages of T. brucei that differentially edit mRNAs.

229 We here report the crystal structure of T. brucei brucei acidocalcisomal PPases in a ternary com

230 maintain an energized state, whereas that of T. brucei evansi also lacks a conventional proton-driven

231 Herein we delineate the effects of AEE788 on T. brucei using chemical biology strategies.

232 The analysis revealed 42 Psis on T. brucei snRNAs, which is the highest number reported s

233 rucei, but not the human-infective pathogens T. brucei rhodesiense and T. brucei gambiense, which are

234 Silencing of TbMCP5 expression in PCF T. brucei revealed that this ADP/ATP carrier is essentia

235 A stringent restriction mechanism prevents T. brucei from expressing multiple ESs at the same time,

236 How to prioritize T. brucei kinases and quantify their intracellular engag

237 n S17 were knocked down by RNAi in procyclic T. brucei.

238 lls of a proliferative division of procyclic T. brucei we used the recently identified constituents o

239 ngolense-conditioned culture medium promotes T. brucei stumpy formation in vitro, which is dependent

240 f-function models in the flagellated protist T. brucei and in M. musculus.

241 ansferase I (TbGnTI) among a set of putative T. brucei glycosyltransferase genes belonging to the bet

242 Activity of recombinant T. brucei PdxK was comparable to previously published wo

243 We show recombinant T. brucei GMPS efficiently catalyzes GMP formation.

244 methylation acts as a switch that regulates T. brucei gene expression.

245 y is non-essential to the medically relevant T. brucei life cycle stage.

246 ess at the plasma membrane, which sensitizes T. brucei brucei to oxidation-stimulated osmotic lysis.

247 Several T. brucei polyprolyl proteins are involved in flagellar

248 However, nothing is known about the single T. brucei CDS gene (Tb927.7.220/EC 2.7.7.41) or its acti

249 Surprisingly, T. brucei still contains a bona fide Pam18 orthologue th

250 er function after expression in a tbat1(-/-) T. brucei line.

251 Lapatinib bound to Tb927.4.5180 (termed T. brucei lapatinib-binding protein kinase-1 (TbLBPK1))

252 d with a basal transcription factor and that T. brucei relies on RNA Pol I for expressing the variant

253 and bloodstream form cells and we found that T. brucei DNA replication rate is similar to rates seen

254 p in gene expression, and we found here that T. brucei's vtRNA is highly enriched in a non-nucleolar

255 We showed by RNAi knockdown that T. brucei isoleucyl-tRNA synthetase is essential for the

256 Based on these findings, we postulate that T. brucei senses heme levels via the flagellar TbHrg pro

257 We propose that T. brucei has retained HSK and threonine synthase in ord

258 We report that T. brucei BBS proteins assemble into a BBSome that inter

259 Herein we show that T. brucei encodes three prozyme transcripts.

260 Here we show that T. brucei treated with 1 mm deoxyadenosine accumulates h

261 High speed videomicrographs showed that T. brucei, L. mexicana and a T. brucei RNAi morphology m

262 is apparently not expressed, suggesting that T. brucei takes up heme by a different, unknown route.

263 The T. brucei CTD, however, is phosphorylated and essential

264 The T. brucei genome encodes two cytosolic NADPH-producing p

265 Post assembly, the T. brucei transition zone alters structure and its assoc

266 C in vitro requires the presence of both the T. brucei m(3)C methyltransferase TRM140 and the deamina

267 late procyclin EP1, two proteins coating the T. brucei surface in the procyclic stage.

268 Recently we identified the T. brucei homologue of polo-like kinase (TbPLK) as an es

269 usly published genetic screen identified the T. brucei MCM-BP, which interacts with subunits of MCM h

270 Conversion of pyruvate to CO2 in the T. brucei bloodstream form provides new support for the

271 Depletion of PNT1 by RNAi in the T. brucei bloodstream form was lethal both in in vitro c

272 The important role of TbMCP5 in the T. brucei energy metabolism is further discussed.

273 applicable to the many kinases found in the T. brucei genome that lack an ascribed function.

274 ransferase I or II genes can be found in the T. brucei genome.

275 ed co-localization of BRCA2 and RAD51 in the T. brucei nucleus, and we show that BRCA2 mutants displa

276 controls reveal compartmentalization of the T. brucei genome in terms of the DNA-damage response and

277 oinformatics analysis showed that 15% of the T. brucei proteome contains 3 or more consecutive prolin

278 vage is important for the maintenance of the T. brucei ribosome in the observed structure.

279 letion causes extensive rearrangement of the T. brucei transcriptome, with increases and decreases in

280 s translate into differential impacts on the T. brucei transcriptome.

281 uts and a mouse infection model, we show the T. brucei BBSome is dispensable for flagellar assembly,

282 Sequence alignment reveals that the T. brucei enzyme is far removed from the metazoan GnTI f

283 We show that the T. brucei FACT complex contains the Pob3 and Spt16 subun

284 d PCR, we showed for the first time that the T. brucei telomere 5' end sequence - an important featur

285 ve and differentiation divisions through the T. brucei life cycle and in related parasitic trypanosom

286 ential pathways of the mitochondrion at this T. brucei life stage.

287 However, contrary to T. brucei, no siRNAs were detected from other genomic re

288 In contrast to T. brucei, Leishmania siRNAs are sensitive to 3' end oxi

289 Similarly to T. brucei, putative mobile elements and repeats constitu

290 Moreover, TLF-1-treated T. brucei brucei became rapidly susceptible to hypotonic

291 l-p-phenylenediamine protected TLF-1-treated T. brucei brucei from lysis.

292 Conversely, lysis of TLF-1-treated T. brucei brucei was increased by the addition of peroxi

293 Swelling of TLF-1-treated T. brucei brucei was reminiscent of swelling under hypot

294 We previously identified two T. brucei mitochondrial carrier family proteins, TbMCP5

295 a range of shape asymmetries, from wild-type T. brucei (highly chiral) to L. mexicana (near-axial sym

296 the essential and previously uncharacterized T. brucei RBP, DRBD18.

297 Unusually, T. brucei uses RNA polymerase I (Pol I) to transcribe th

298 We have previously validated T. brucei NMT as a promising druggable target for the tr

299 Although the mechanism by which T. brucei infection causes these changes remains to be d

300 the procyclic developmental stage, in which T. brucei is confined to the tsetse fly midgut, this rec

301 leep architecture of male mice infected with T. brucei and found that infected mice had drastically a