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1 cal disease caused by the protozoan parasite Trypanosoma brucei .
2 nzamides (CNBs) against bloodstream forms of Trypanosoma brucei .
3 tozoa (Leishmania spp., Plasmodium spp., and Trypanosoma brucei).
4 ke and the modulation of drug sensitivity in Trypanosoma brucei.
5 generates functional mitochondrial mRNAs in Trypanosoma brucei.
6 telomeric ESs and VSG antigenic switching in Trypanosoma brucei.
7 characterize the non-snRNP PRP19 complex of Trypanosoma brucei.
8 and the early diverging parasitic protozoan, Trypanosoma brucei.
9 lar activity against the bloodstream form of Trypanosoma brucei.
10 all lysine residues for all core histones of Trypanosoma brucei.
11 ut not CD8(+), T cells in mice infected with Trypanosoma brucei.
12 . Leishmania donovani, Trypanosoma cruzi and Trypanosoma brucei.
13 ganisation of transcription in the genome of Trypanosoma brucei.
14 essential for retrograde cargo transport in Trypanosoma brucei.
15 ,3-d]pyrimidines are inhibitors of PTR1 from Trypanosoma brucei.
16 tion of 19 kinetochore proteins (KKT1-19) in Trypanosoma brucei.
17 cycle, and development in the model parasite Trypanosoma brucei.
18 glycoprotein (VSG) expression sites (ESs) of Trypanosoma brucei.
19 somiasis is caused by the eukaryotic microbe Trypanosoma brucei.
20 cytokinesis in the early-branching eukaryote Trypanosoma brucei.
21 were found to be essential for the growth of Trypanosoma brucei.
22 aused by a single-celled protozoan parasite, Trypanosoma brucei.
23 can trypanosomiasis caused by the protozoan, Trypanosoma brucei.
24 y diverged protist and significant pathogen, Trypanosoma brucei.
25 s (HAT) is caused by the parasitic protozoan Trypanosoma brucei.
26 All three proteins are essential for Trypanosoma brucei.
27 ugar nucleotide GDP-mannose is essential for Trypanosoma brucei.
28 in tRNAs from Bacillus subtilis, plants and Trypanosoma brucei.
29 death (PCD) in the human protozoan parasite Trypanosoma brucei.
30 ogue of SSNA1 in the kinetoplastid parasite, Trypanosoma brucei.
31 ), which is caused by the parasitic protozoa Trypanosoma brucei.
32 and brain infections caused by the parasite Trypanosoma brucei.
33 r of Procyclin surface antigen expression in Trypanosoma brucei.
34 orthologue, PNT1, in the parasitic protozoon Trypanosoma brucei.
35 by RNA polymerase I (Pol I) in the parasite Trypanosoma brucei.
36 diting in kinetoplastid protists typified by Trypanosoma brucei.
37 ents in the large ribosomal subunit (60S) of Trypanosoma brucei.
38 e boundaries of previously annotated CDSs in Trypanosoma brucei.
39 As and is unique for kinetoplastids, such as Trypanosoma brucei.
41 ng their function in the protozoan parasite, Trypanosoma brucei, a causative agent of African trypano
44 rganisms belonging to the phylum euglenozoa: Trypanosoma brucei, a lethal human parasite, and Euglena
46 and condition-specific metabolic network of Trypanosoma brucei, a parasitic protozoan responsible fo
51 sites such as the sleeping sickness pathogen Trypanosoma brucei adapt to different host environments,
52 er unexpected functional differences between Trypanosoma brucei ADAT2/3 (TbADAT2/3) and its bacterial
55 rominent defence of the unicellular parasite Trypanosoma brucei against the host immune system is a d
60 e biosynthesis pathway of the human parasite Trypanosoma brucei, an early branching eukaryote that la
61 otein localizing to the nuclear periphery of Trypanosoma brucei and a candidate nucleoskeletal compon
63 el can be applied to the characterization of Trypanosoma brucei and Leishmania spp. ribosomes as well
65 zation of this channel to acidocalcisomes of Trypanosoma brucei and suggest that caution should be ex
67 roducts exhibit significant activity against Trypanosoma brucei and T. cruzi, featuring favorable dru
68 interference (RNAi) has been investigated in Trypanosoma brucei and to a lesser extent in Leishmania
69 o be essential for survival and virulence of Trypanosoma brucei and, in Trypanosoma cruzi, PDEC2 was
72 ological process for the bloodstream form of Trypanosoma brucei as the parasite would otherwise accum
73 y a pivotal role in life-cycle regulation of Trypanosoma brucei, as the translocation of a protein ph
76 itional null mutant of PdxK was generated in Trypanosoma brucei bloodstream forms showing that this e
77 h a single-digit micromolar activity against Trypanosoma brucei brucei (EC50 = 2.97 muM), thus being
78 HAP) by triosephosphate isomerase (TIM) from Trypanosoma brucei brucei (Tbb) has been investigated.
79 Glu-167 of triosephosphate isomerase from Trypanosoma brucei brucei (TbbTIM) acts as the base to d
81 ine transport activities in bloodstream form Trypanosoma brucei brucei found that these cells express
82 een of approximately 87000 compounds against Trypanosoma brucei brucei identified a number of promisi
84 responses in the penetration of T cells and Trypanosoma brucei brucei into the brain was studied in
85 ate immunity against the veterinary pathogen Trypanosoma brucei brucei is conferred by trypanosome ly
86 d low micromolar levels of inhibition of the Trypanosoma brucei brucei parasite grown in culture.
87 31-fold more active against bloodstream-form Trypanosoma brucei brucei trypomastigotes engineered to
88 ts: I172V, I172A, L232A, and P168A (TIM from Trypanosoma brucei brucei); a 208-TGAG for 208-YGGS loop
89 against the parasites Plasmodium falciparum, Trypanosoma brucei brucei, and Trypanosoma cruzi will be
90 everal African trypanosome species including Trypanosoma brucei brucei, but not the human-infective p
91 een of approximately 87000 compounds against Trypanosoma brucei brucei, we recently identified eight
92 omparable between Trypanosoma congolense and Trypanosoma brucei but is much lower in Trypanosoma viva
93 eotide-specific phosphodiesterases (PDEs) of Trypanosoma brucei, causative agent of the fatal human s
107 red the transcriptomes of cultured procyclic Trypanosoma brucei cells in early and late logarithmic p
108 kinase system of the kinetoplastid parasite Trypanosoma brucei, consisting of three highly similar a
109 tids, such as the sleeping sickness parasite Trypanosoma brucei, contain a approximately 20S RNA-edit
114 n addition, the binding mode of 14t with the Trypanosoma brucei CYP51 (TbCYP51) orthologue has been c
116 e tsetse fly-transmitted African trypanosome Trypanosoma brucei depends on maintenance and expression
118 ishmania displays striking conservation with Trypanosoma brucei, despite the latter parasite replicat
122 generates functional mitochondrial mRNAs in Trypanosoma brucei Editing is catalyzed by three distinc
123 ential for growth of the parasitic protozoan Trypanosoma brucei, enabling the study of its function i
126 ere, we report that TbVtc4 (Vtc4 ortholog of Trypanosoma brucei) encodes, in contrast, a short chain
129 l-infecting bloodstream stages as well as in Trypanosoma brucei evansi, a form of the latter stage la
131 screens were undertaken in bloodstream form Trypanosoma brucei exposed to the antifolates methotrexa
135 The bloodstream form of the human pathogen Trypanosoma brucei expresses oligomannose, paucimannose,
139 tivity against either human FPPS (HsFPPS) or Trypanosoma brucei FPPS (TbFPPS), the most active being
140 amides have been identified as inhibitors of Trypanosoma brucei from screening of a focused protease
141 ed by two subspecies of Trypanosoma brucei , Trypanosoma brucei gambiense , and Trypanosoma brucei rh
142 uman African trypanosomiasis (HAT) caused by Trypanosoma brucei gambiense can be diagnosed in the ear
145 to replace the current treatment regimen for Trypanosoma brucei gambiense infections, following a pos
146 is (HAT), Trypanosoma brucei rhodesiense and Trypanosoma brucei gambiense, have developed independent
149 on of both alleles of JGT from the genome of Trypanosoma brucei generates a cell line that completely
152 MM and a PAGM enzymes have been found in the Trypanosoma brucei genome, there is, surprisingly, no ca
155 tive agent of human African trypanosomiasis, Trypanosoma brucei, has already shown the utility of thi
156 inactive mutant of metacaspase 2 (MCA2) from Trypanosoma brucei, has been determined to a resolution
157 microbes, such as the kinetoplastid parasite Trypanosoma brucei, have a defined size, shape, and form
158 protists, such as the lethal human parasite Trypanosoma brucei, however, lack the heptad repeats and
159 context of the VSG layer, the dimensions of Trypanosoma brucei HpHbR and VSG have been determined by
160 In this study, we report the structure of Trypanosoma brucei HpHbR in complex with human haptoglob
161 ausative agent of African sleeping sickness, Trypanosoma brucei In mitochondria of this pathogen, mos
163 ed to TbKHC1, an orphan kinesin H chain from Trypanosoma brucei, inhibited T. musculi excreted/secret
164 ositol pyrophosphate biosynthetic pathway in Trypanosoma brucei: inositol polyphosphate multikinase (
167 del of glycolysis in the parasitic protozoan Trypanosoma brucei is a particularly well analysed examp
172 the current model for antigenic variation in Trypanosoma brucei is only one means by which these para
178 acterized in kinetoplastid parasites such as Trypanosoma brucei is Tim17 (TbTim17), which is essentia
180 receptor of the African trypanosome species, Trypanosoma brucei, is expressed when the parasite is in
182 g sickness, caused by the protozoan parasite Trypanosoma brucei, is universally fatal if untreated, a
183 s and can functionally replace homologues in Trypanosoma brucei, its SufCB protein has similar bioche
184 y, it was shown that the parasitic protozoon Trypanosoma brucei lacks a conventional Tom40 and instea
185 The mitochondrion of the parasitic protozoan Trypanosoma brucei lacks tRNA genes, and thus imports al
186 tive agent of human African trypanosomiasis, Trypanosoma brucei, lacks de novo purine biosynthesis an
187 screen with 176 individual bloodstream form Trypanosoma brucei lines identified PKs required for pro
194 DNA (kDNA), we identified an uncharacterized Trypanosoma brucei protein, named TbLOK1, required for m
196 on of the potentials of the redox centers in Trypanosoma brucei QSOX provides a context for understan
197 t that CRK1, a G1 cyclin-dependent kinase in Trypanosoma brucei, regulates anterograde protein traffi
199 ains of TR from the basal eukaryotic species Trypanosoma brucei, revealing the ancestry of TR compris
200 rence target sequencing (RIT-seq) screens in Trypanosoma brucei, revealing the transporters, organell
201 roove binders was evaluated in vitro against Trypanosoma brucei rhodesiense (8 compounds) and Plasmod
202 iprotozoal assays, ten of the oils inhibited Trypanosoma brucei rhodesiense (IC(50) 15.9-64.5 mug/mL)
203 ting against four other protozoan parasites: Trypanosoma brucei rhodesiense , Trypanosoma cruzi , Lei
204 ition of the cysteine proteases rhodesain of Trypanosoma brucei rhodesiense and falcipain-2 of Plasmo
205 .045 muM against the human pathogenic strain Trypanosoma brucei rhodesiense and is more than 4000 tim
206 brucei , Trypanosoma brucei gambiense , and Trypanosoma brucei rhodesiense and is one of Africa's ol
207 tent inhibitory effect against the parasites Trypanosoma brucei rhodesiense and Leishmania donovani w
208 t cause human African Trypanosomiasis (HAT), Trypanosoma brucei rhodesiense and Trypanosoma brucei ga
209 r proteins that contribute to virulence, and Trypanosoma brucei rhodesiense EVs contain the serum res
210 stance to most African trypanosomes, but not Trypanosoma brucei rhodesiense or T.b. gambiense, which
211 layed in vitro nanomolar IC50 values against Trypanosoma brucei rhodesiense STIB900 with selectivity
212 ctive (0.5 muM </= IC(50) < 6.0 muM) against Trypanosoma brucei rhodesiense trypomastigotes were 5-31
213 ural product displayed high activity against Trypanosoma brucei rhodesiense, a recalcitrant parasite
214 ch as Plasmodium falciparum, Lassa Virus and Trypanosoma brucei rhodesiense, has resulted in elevated
215 -stage HAT, and the only drug for late-stage Trypanosoma brucei rhodesiense, is intravenous melarsopr
216 ave additional trypanolytic activity against Trypanosoma brucei rhodesiense, the cause of acute Afric
217 orrelation with the human infective parasite Trypanosoma brucei rhodesiense, the most potent compound
218 st important human trypanosomatid pathogens (Trypanosoma brucei rhodesiense, Trypanosoma cruzi, and L
219 st important human trypanosomatid pathogens (Trypanosoma brucei rhodesiense, Trypanosoma cruzi, and L
220 c markers in CSF from patients infected with Trypanosoma brucei rhodesiense, using 1H nuclear magneti
221 ite concentrations in patients infected with Trypanosoma brucei rhodesiense, using liquid chromatogra
223 ved following RNAi-mediated silencing of the Trypanosoma brucei SODA ortholog suggests that SODA is e
230 nst several wild type and resistant lines of Trypanosoma brucei (T. b. rhodesiense STIB900, T. b. bru
231 we have shown that depletion of centrin1 in Trypanosoma brucei (T. brucei) displayed arrested organe
233 ng drug target within the parasitic protozoa Trypanosoma brucei (T. brucei), the causative agent for
236 e SAS-4 homolog in the flagellated protozoan Trypanosoma brucei, TbSAS-4, plays an unusual role in co
238 the procyclic and bloodstream form stages of Trypanosoma brucei that yields viable and proliferative
239 ing the cell cycle of the protozoan parasite Trypanosoma brucei The source of components required to
240 axoneme formation in the flagellate protist Trypanosoma brucei, the causal agent of African sleeping
241 ruzi, the causative agent of Chagas disease; Trypanosoma brucei, the causative agent of African sleep
245 the trypanocidal activity of nicotinamide on Trypanosoma brucei, the causative agent of African trypa
247 , which had been identified as a hit against Trypanosoma brucei, the causative agent of human African
248 mpound library for antiparasitic activity on Trypanosoma brucei, the causative agent of human African
249 of polyamine metabolism in bloodstream-form Trypanosoma brucei, the causative agent of human African
250 es (PKs) are a class of druggable targets in Trypanosoma brucei, the causative agent of Human African
254 play an important role in the life cycle of Trypanosoma brucei, the causative parasite of human Afri
260 tron microscopy structure of the ribosome of Trypanosoma brucei, the parasite that is transmitted by
261 nraveling the intricate interactions between Trypanosoma brucei, the protozoan parasite causing Afric
268 ow that cytosine 32 in the anticodon loop of Trypanosoma brucei tRNA(Thr) is methylated to 3-methylcy
269 ping sickness is caused by two subspecies of Trypanosoma brucei , Trypanosoma brucei gambiense , and
270 e diseases caused by the protozoan parasites Trypanosoma brucei, Trypanosoma cruzi, and Leishmania sp
271 nt parasites and include the human pathogens Trypanosoma brucei, Trypanosoma cruzi, and Leishmania sp
272 wth, and infectivity of the trypanosomatids: Trypanosoma brucei, Trypanosoma cruzi, and Leishmania.
273 pathway and its enzymes have been studied in Trypanosoma brucei, Trypanosoma cruzi, and various Leish
274 of evolution led to inactivation of PDEC in Trypanosoma brucei/Trypanosoma evansi/Trypanosoma congol
275 re we present a thorough kinetic analysis of Trypanosoma brucei TryS in a newly developed phosphate b
278 ghly motile and versatile protozoan pathogen Trypanosoma brucei undergoes a complex life cycle in the
284 its application to the pathogenic protozoan, Trypanosoma brucei, using hyperpolarized (13)C1 pyruvate
285 multiple ancestral VSG lineages, whereas in Trypanosoma brucei VSG have recent origins, and ancestra
286 re, in showing that the C-terminal domain of Trypanosoma brucei VSG plays a crucial role in facilitat
287 ve-site residues of PRMT7 from the protozoan Trypanosoma brucei We have designed 26 single and double
288 bitor of proliferation for the HAT pathogen (Trypanosoma brucei), we have now tested this class of an
289 e essentiality of pyrimidine biosynthesis in Trypanosoma brucei, we generated a umps double knockout
290 an and animal pathogenic protozoan parasite, Trypanosoma brucei, we generated conditional cardiolipin
291 ulation of glycosomes in live procyclic form Trypanosoma brucei When added to cells, this fluorescent
293 component of approximately 20S editosomes in Trypanosoma brucei which contains a degenerate, noncatal
297 idal activity against the protozoan parasite Trypanosoma brucei with IC50 < 5 muM, being each of thos
299 more potent than nifurtimox against in vitro Trypanosoma brucei with very low cytotoxicity against hu
300 in the causative agent of sleeping sickness, Trypanosoma brucei, with that of human erythrocytes, and
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