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1 (intracellular amastigotes and extracellular trypomastigotes).
2 d cocultures of PBMCs with epimastigotes and trypomastigotes.
3 s detected in both procyclic and bloodstream trypomastigotes.
4 nd subsequently failed to differentiate into trypomastigotes.
5  uniformly expressed at the cell surfaces of trypomastigotes.
6 iate host cell invasion by Trypanosoma cruzi trypomastigotes.
7 roxide dismutase in COL and SYL (versus TCC) trypomastigotes.
8 induced Ca2+ transients and cell invasion by trypomastigotes.
9 DNA, procyclic trypanosomes, and bloodstream trypomastigotes.
10 bout 2.3 kilobases was observed in procyclic trypomastigotes.
11 oscopy of L6E9 myoblasts exposed to T. cruzi trypomastigotes.
12 rk were enhanced in COL and SYL (versus TCC) trypomastigotes.
13 of primary murine cardiomyocytes by T. cruzi trypomastigotes.
14 d before differentiation of amastigotes into trypomastigotes.
15 ved trypomastigotes but 55 kDa in metacyclic trypomastigotes.
16 ut distributed intracellularly in metacyclic trypomastigotes.
17 nd lacking in N-linked glycans in metacyclic trypomastigotes.
18  on both recombinant Tc-1 and Tc-1 of intact trypomastigotes.
19  protein that is expressed only in infective trypomastigotes.
20 at these genes are up-regulated in procyclic trypomastigotes.
21  invasion and the intracellular retention of trypomastigotes.
22  whereas TcHA2 is expressed predominantly in trypomastigotes.
23 e inhibitors of T.b. brucei bloodstream form trypomastigotes.
24 hology so that the cells resemble mesocyclic trypomastigotes.
25 MP (cAMP), however, was unaltered in OPBnull trypomastigotes.
26                                  Exposure of trypomastigote and amastigote forms of T. cruzi to defen
27 d by the cloned genes as surface proteins in trypomastigote and/or amastigote stages of T. cruzi.
28 ruzi and provide data on the EVs produced by trypomastigotes and amastigotes (N.
29 pimastigotes readily converted to metacyclic trypomastigotes and efficiently infected mammalian cells
30 -3 binds to the surface of Trypanosoma cruzi trypomastigotes and human coronary artery smooth muscle
31 l-mediated immune responses to extracellular trypomastigotes and intracellular amastigotes.
32 t in vitro infections with TcUBP1-transgenic trypomastigotes and observed that TcUBP1 overexpression
33                 We report that both T. cruzi trypomastigotes and secreted parasite factor(s) antagoni
34         Invasion of host cells by TcLetm1-KD trypomastigotes and their intracellular replication is g
35 tudy, smooth muscle cells were infected with trypomastigotes, and immunoblot analysis revealed an inc
36  antigen-immunized groups, as well as higher trypomastigotes antibody-mediated lyses and cell invasio
37                            Trypanosoma cruzi trypomastigotes are exquisitely resistant to the lytic e
38                Trypanosoma cruzi blood stage trypomastigotes are highly resistant to complement-media
39           Host cells incubated with T. cruzi trypomastigotes are transiently wounded, show increased
40 opment of the parasite from amastigotes into trypomastigotes, are prevented by lactacystin, or by a p
41 A regulon comprising numerous transcripts of trypomastigote-associated cell-surface glycoproteins tha
42 ed by PDNF-expressing extracellular T. cruzi trypomastigotes at the start of host cell invasion.
43                                              Trypomastigotes avoid complement-mediated lysis by the p
44 lic trypomastigotes (MT), but not blood form trypomastigotes (BFT), are highly mucosally infective.
45 tes, amastigotes, and tissue culture-derived trypomastigotes but 55 kDa in metacyclic trypomastigotes
46 uced Ca2+ transients and myocyte invasion by trypomastigotes but are independent of Ca2+ entry into t
47 -kb transcript that is expressed in invasive trypomastigotes but not in noninvasive epimastigote form
48 y formed parasitophorous vacuoles containing trypomastigotes but not in the few parasite-containing v
49 ycoproteins are expressed by amastigotes and trypomastigotes but only amastigotes express the mannose
50 iferation of epimastigotes and was cidal for trypomastigotes but was not toxic for splenocytes.
51  cells exposed to both wild-type and OPBnull trypomastigotes, but the signals triggered by the mutant
52 tream form of Trypanosoma brucei rhodesiense trypomastigotes by bisphosphonates.
53 n is uniformly distributed on the surface of trypomastigotes by direct immunofluorescence.
54                               The killing of trypomastigotes by NO in cell-free medium is blocked by
55 a developmentally regulated gene of T. cruzi trypomastigotes can be expressed in noninfectious epimas
56 n of TbFPPS double-stranded RNA in procyclic trypomastigotes caused specific degradation of mRNA.
57          The TSF-induced Ca2+ transients and trypomastigote cell invasion could not be inhibited by a
58 , TcCLC and TcCHC at the posterior region of trypomastigote cells, coincident with the flagellar pock
59 th a T. cruzi expression vector carrying the trypomastigote CRP cDNA and produced fully functional re
60 e studies demonstrate the critical role that trypomastigote CRP plays in the protection of parasites
61 gas disease is compromised by very low blood trypomastigote densities, which fluctuate close to or be
62 gene in both the epimastigote and metacyclic trypomastigote developmental stages.
63 nonreplicating insect stage (epimastigote to trypomastigote differentiation).
64                  We discovered that T. cruzi trypomastigotes discard their flagella via an asymmetric
65   During T. cruzi infection, amastigotes and trypomastigotes disseminate in the mammalian host and in
66                           Infective T. cruzi trypomastigotes elicit Ca2+ signaling in mammalian host
67 t bloodstream-form Trypanosoma brucei brucei trypomastigotes engineered to overexpress reduced nicoti
68 omes to the host cell periphery, and reduced trypomastigote entry.
69                   Immunoblots of solubilized trypomastigotes, epimastigotes, and amastigotes probed w
70  results were obtained with bloodstream form trypomastigotes, except that the RNAi system in this cas
71  results were obtained with bloodstream form trypomastigotes, except that the RNAi system was leaky a
72 ve polymerase chain reaction (qPCR), and IgM-trypomastigote excreted-secreted antigen (TESA) blot at
73 itative PCR (qPCR), and immunoglobulin (Ig)M trypomastigote excreted-secreted antigen (TESA)-blots at
74  using the micromethod, qPCR analysis, and a trypomastigote excretory secretory antigen (TESA) blot f
75 ults of the IgG-TESA-blot (Western blot with trypomastigote excretory-secretory antigen), and the Cha
76 restricted to infective and nonproliferative trypomastigotes explaining decreased proliferation and b
77             Electron microscopic analysis of trypomastigotes exposed to defensin alpha-1 revealed por
78      Separation of bloodstream and procyclic trypomastigote extracts on Percoll gradients yielded fra
79 naling induced in normal rat kidney cells by trypomastigote extracts.
80 e a by T. cruzi epimastigotes and metacyclic trypomastigote extracts.
81 AZ filament, and depletion of TbSAS-4 in the trypomastigote form disrupts the elongation of the new F
82                 Depletion of cAMP-BP1 in the trypomastigote form of T. brucei causes major morphology
83 agellum in contact with the cell body of the trypomastigote form of Trypanosoma cruzi has been isolat
84 ect vector the parasite transitions from the trypomastigote form to the epimastigote form by repositi
85 100% inhibition of growth of the bloodstream trypomastigote forms of T. brucei at a concentration of
86  exhibited trypanolytic activity against the trypomastigote forms of T. cruzi, a property known to co
87                       Depletion of ClpGM6 in trypomastigote forms produces cells with long free flage
88  of the insect (epimastigote) and infective (trypomastigote) forms by two-dimensional gel electrophor
89 tarts in the skin after an insect bite, when trypomastigotes get through the extracellular matrix to
90                                The bioactive trypomastigote GPI fraction was compared with a relative
91  is essential for the extreme potency of the trypomastigote GPI fraction, which is at least as active
92                                          The trypomastigote GPI structures were found to contain addi
93  synthase activity, and AMP/ATP ratio, while trypomastigotes had reduced ability to efficiently infec
94    The residual invasion capacity of OPBnull trypomastigotes in fibroblasts still involves lysosome r
95 racellular free Ca2+ transients triggered by trypomastigotes in host cells.
96 und suppression in the number of circulating trypomastigotes in mice with an acute infection of T. cr
97 ine orange uptake in permeabilized procyclic trypomastigotes in the presence of different substrates
98 precipitation of labeled surface proteins of trypomastigotes indicated that the 62-kDa protein is a s
99            We found that T. cruzi metacyclic trypomastigotes induced microvesicle release from blood
100 sion of several surface glycoproteins of the trypomastigote infective stage of the parasite.
101 e first immediately after differentiation of trypomastigotes into amastigotes and the second before d
102 ion is induced during the differentiation of trypomastigotes into amastigotes, where TcPI-PLC associa
103 stablished after the injection of metacyclic trypomastigotes into the skin dermis by the tsetse fly v
104 n the absence of mutant receptor expression, trypomastigotes invaded the cells at a low level.
105       Antibodies to Tc-1 effectively blocked trypomastigote invasion of host cells and consequently r
106 either chemotaxis or previously defined anti-trypomastigote mechanisms for the control of T. cruzi's
107 acted specifically with a 160-kDa protein in trypomastigote membrane protein preparations as well as
108 generally thought to be lethal (i.e., >10(6) trypomastigotes/ml), thus associating CD4+ T cell functi
109  of isolated myocytes with secreted/released trypomastigote molecules, is a common outcome of the car
110 ellular amastigote-like cells and metacyclic trypomastigotes more rapidly than wild-type parasites, s
111 M3 to promote FAZ elongation for maintaining trypomastigote morphology.
112                 Trypanosoma cruzi metacyclic trypomastigotes (MT), but not blood form trypomastigotes
113  nitric oxide-inducing activities of T.cruzi trypomastigote mucins were recovered quantitatively in a
114 n the hearts of male CD-1 mice infected with trypomastigotes of T. cruzi (Brazil strain).
115 ermeabilized amastigotes, epimastigotes, and trypomastigotes of T. cruzi.
116 endothelial cells (HUVEC) were infected with trypomastigotes of the Tulahuen strain of T. cruzi.
117 lular compartment in permeabilized procyclic trypomastigotes of Trypanosoma brucei, as measured by ac
118  that the transformation in axenic medium of trypomastigotes of Trypanosoma cruzi into amastigote-lik
119                      Preincubation of either trypomastigotes or myoblasts with CKII inhibitors blocke
120 hich is initiated by live infective T. cruzi trypomastigotes or stimulation of isolated myocytes with
121  MIP-1alpha, and MIP-1beta enhances T. cruzi trypomastigote phagocytosis in a dose peak response.
122  did not upon infection with the counterpart trypomastigote population expressing low trans-sialidase
123     Most interesting, HIMECs infected with a trypomastigote population expressing trans-sialidase eff
124 s Chagas disease, the elongated, flagellated trypomastigotes remodel into oval amastigotes with no ex
125        Short exposure of defensin alpha-1 to trypomastigotes shows that defensin alpha-1 binds to the
126                Extracellular mammalian stage trypomastigotes simultaneously express and release multi
127 e Amazon, based on expression of recombinant trypomastigote small surface antigen (gTSSA-I) in the eu
128 al 120-kDa alkaline peptidase contained in a trypomastigote soluble fraction (TSF) of Trypanosoma cru
129  identified as a member of a large family of trypomastigote-specific genes, and a complete cDNA was i
130                   The gene family encoding a trypomastigote-specific protein restricted to the part o
131 ngs provide evidence for a role of TcUBP1 in trypomastigote stage-specific gene regulation important
132 lian amastigote stages) and the non-dividing trypomastigote stage.
133 s the transition to the infective metacyclic trypomastigote stage.
134 tion from the epimastigote to the metacyclic trypomastigote stage.
135 ergo before they develop into the metacyclic trypomastigote stage.
136 cted with a 55-kDa TcGP63 form in metacyclic trypomastigotes, suggesting stage-specific expression of
137 f an H-2Kb-restricted CTL epitope within two trypomastigote surface Ags encoded by members of the T.
138 ce antiparasite protective immunity, and the trypomastigote surface antigen 1 (TSA-1), a target of an
139                                            A trypomastigote surface antigen, TSA-1, and two amastigot
140                       A previously described trypomastigote surface glycoprotein was shown to have bi
141 ek pouch topically exposed to tissue culture trypomastigotes (TCTs).
142 arly effects of defensin alpha-1 on invasive trypomastigotes that involve damage of the flagellar str
143 llular milieu of cultured cells by infective trypomastigotes, the enzyme is restricted to a small (20
144                                              Trypomastigotes, the highly motile infective forms of Tr
145                                              Trypomastigotes, the infectious stage of T. cruzi, activ
146                                              Trypomastigotes, the infective forms, are capable of inv
147             After removal of nonadherent TS- trypomastigotes, the TS+ trypomastigotes were isolated f
148 egulation of Unx1 reduces the infectivity of trypomastigotes, the Unx1 channels might be an attractiv
149 rt and long chain polyPs was detected during trypomastigote to amastigote differentiation and during
150 sion increases during the differentiation of trypomastigote to amastigote stages.
151 e plasma membrane, in the differentiation of trypomastigotes to amastigotes, an essential step for th
152 he inability of oligopeptidase B null mutant trypomastigotes to mobilize Ca2+ from thapsigargin-sensi
153 starved, were impeded in the epimastigote to trypomastigote transition.
154 unctival challenges with T. cruzi metacyclic trypomastigotes using a combination of immunohistochemic
155 m location was also found in amastigotes and trypomastigotes using a polyclonal antibody against a CO
156 f the OPB gene results in a marked defect in trypomastigote virulence, consistent with a greatly redu
157                          Protein turnover in trypomastigotes was proteasome and ATP-dependent and was
158 ich are associated with effective killing of trypomastigotes, was not affected in CCR2(-/-) mice.
159  muM) against Trypanosoma brucei rhodesiense trypomastigotes were 5-31-fold more active against blood
160                                    Infective trypomastigotes were found to contain a soluble Ca2+-sig
161  of nonadherent TS- trypomastigotes, the TS+ trypomastigotes were isolated from the beads by specific
162 stigotes were relatively avirulent while TS+ trypomastigotes were more virulent than unfractionated p
163  the murine model of Chagas' disease, as TS- trypomastigotes were relatively avirulent while TS+ tryp
164                             Preincubation of trypomastigotes with a concentration of defensin alpha-1
165                             Preincubation of trypomastigotes with defensin alpha-1 followed by exposu
166                             Preincubation of trypomastigotes with either TcGP63 antiserum or a purifi

 
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