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 four histone variants: H2AZ, H2BV, H3V, an

8 T. brucei is unusual in controlling gene expression pred

9 T. brucei methylthioadenosine phosphorylase (TbMTAP) was

10 T. brucei TatD nuclease showed intrinsic DNase activity,

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

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

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

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

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

16 ral proteins, including NOPP44/46, accompany T. brucei development.

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

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

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

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

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

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

23 7b, that exhibited nanomolar potency against T. brucei with excellent selectivity for parasite cells

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

48 e pathways being integrated and exploited by T. brucei to carefully coordinate energy demands to tran

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

65 ort that, although glycosome-resident enzyme T. brucei hexokinase 1 (TbHK1) protein levels are mainta

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

67 erting ectopic VSG117 into VSG221 expressing T. brucei.

68 5A levels and found that it is essential for T. brucei growth.

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

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

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

72 ruzain for T. cruzi and TbCatB/rhodesain for T. brucei.

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

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

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

76 ar to be active in cultured bloodstream form T. brucei, and it is not upregulated even when the Kenne

77 LP is key for ES control in bloodstream form T. brucei, as NLP knockdown results in 45- to 65-fold de

78 silent VSG ES promoters in bloodstream form T. brucei, with derepression specific to the G2/M cell c

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

80 t but not active VSG ESs in bloodstream form T. brucei.

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

82 In insect form T. brucei TbSpt16 knock-down results in 16- to 25-fold V

83 e arrest in both bloodstream and insect form T. brucei.

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

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

86 ed in its transcriptionally active form from T. brucei extracts.

87 encodes this vital pyruvate transporter from T. brucei.

88 We therefore generated T. brucei lines expressing T. cruzi topoisomerase-II tru

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

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

91 However, T. brucei encodes two Nfs homologues, one cytoplasmic an

92 In T. brucei, four putative RAD51 paralogue genes have been

93 In T. brucei, the RNA is nicked prior to uridylate insertio

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

95 Thus the requirement for ACC in T. brucei is dependent upon the growth environment in tw

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

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

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

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

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

101 a novel TFIIH-associated protein complex in T. brucei (Med-T) consisting of nine subunits whose amin

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

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

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

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

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

107 he complete kinetoplast duplication cycle in T. brucei based on three-dimensional reconstructions fro

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

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

110 erminant for the essential C to U editing in T. brucei.

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

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

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

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

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

116 We found that cardiolipin formation in T. brucei procyclic forms is catalyzed by a bacterial-ty

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

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

119 The essentiality of the single HisRS gene in T. brucei is shown by a severe depression of parasite gr

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

121 ough an RNAi screen for cytokinesis genes in T. brucei.

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

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

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

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

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

127 3 ), and inositol hexakisphosphate (IP6 ) in T. brucei different stages.

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

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

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

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

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

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

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

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

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

137 ficant resistance to the induction of PCD in T. brucei.

138 on of PK50 and a second NDR kinase, PK53, in T. brucei has not been determined to date, although tryp

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

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

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

142 l degradation machinery or its regulation in T. brucei.

143 ating that the Rad51 paralogue repertoire in T. brucei is unusually large among microbial eukaryotes

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

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

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

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

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

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

150 the molecular mechanism of VSG switching in T. brucei.

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

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

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

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

155 50 proteins from fungi and mammals, Tim50 in T. brucei (TbTim50) possesses a mitochondrial targeting

156 protein facilitating Pol I transcription in T. brucei.

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

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

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

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

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

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

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

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

165 oth animal infective and the human-infective T. brucei rhodesiense in vivo.

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

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

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

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

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

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

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

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

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

175 0b): T. brucei rhodesiense IC(5)(0) = 60 nM, T. brucei brucei IC(5)(0) = 520 nM, T. cruzi = 7.6 muM),

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

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

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

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

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

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

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

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

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

185 utes to cell growth in the procyclic form of T. brucei and functions as a cytochrome oxidase subunit

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

187 exocytic pathways in the bloodstream form of T. brucei.

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

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

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

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

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

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

194 Moreover, inactivation of T. brucei protein-tyrosine phosphatase 1 (TbPTP1) trigge

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

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

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

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

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

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

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

202 se blood, we find that, instead, motility of T. brucei is by the propagation of kinks, separating lef

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

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

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

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

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

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

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

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

211 Segregation of T. brucei minichromosomes in these stalled cells is impa

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

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

214 cultured bloodstream and procyclic stages of T. brucei has little effect on parasite growth or morpho

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

216 oodstream and procyclic life cycle stages of T. brucei.

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

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

219 provides an excellent tool for validation of T. brucei NMT as a drug target for HAT as well as a valu

220 docalcisomes and for growth and virulence of T. brucei.

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

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

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

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

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

226 ay of galactose metabolism, is one promising T. brucei drug target.

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

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

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

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

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

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

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

234 Several T. brucei polyprolyl proteins are involved in flagellar

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

236 The Trypanosoma brucei subspecies T. brucei brucei is non-human infective due to susceptib

237 The most potent inhibitors target T. brucei PTR1, and two compounds displayed antiparasite

238 Inhibition of this target-T. brucei N-myristoyltransferase-leads to rapid killing

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

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

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

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

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

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

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

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

247 Here, we show that T. brucei ACC shares the same enzyme architecture and mo

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

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

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

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

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

253 The T. brucei full-length enzyme as well as its two constitu

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

255 The T. brucei p22 protein was identified as one such accesso

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

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

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

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

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

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

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

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

264 wo additional TOR kinases are encoded in the T. brucei genome.

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

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

267 differences in catalytic specificity of the T. brucei enzyme family are controlled by natural variat

268 resent here suggests that sumoylation of the T. brucei enzyme is not required for centromere-specific

269 Here, we show that blocking synthesis of the T. brucei FACT subunit TbSpt16 triggers a G2/early M pha

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

271 In vitro and in vivo characterization of the T. brucei neutral sphingomyelinase demonstrates that it

272 ions, we solved the crystal structure of the T. brucei p22 protein to 2.0-A resolution.

273 control between two life cycle stages of the T. brucei parasite.

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

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

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

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

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

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

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

281 We also show that the T. brucei RAD51 paralogues interact, and that the comple

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

283 scription units (Pol II PTUs) throughout the T. brucei genome.

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

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

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

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

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

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

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

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

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

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

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

295 d in this way and it explains why, uniquely, T. brucei has been able to lose its PGM gene.

296 Our studies validate T. brucei N-myristoyltransferase as a promising therapeu

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

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

299 progression is essential for infections with T. brucei and that parasite Aurora kinases can be target

300 gn of selective inhibitors to interfere with T. brucei transmission.