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  • Protein
  • The results presented here identify for the first time a T. brucei protein that exhibits a PGF synthase activity capable of specifically converting PGH 2 to PGF 2α . (rupress.org)
  • L. Planelles, M. C. Thomas, C. Alonso, and M. C. López, "DNA immunization with Trypanosoma cruzi HSP70 fused to the KMP11 protein elicits a cytotoxic and humoral immune response against the antigen and leads to protection," Infection and Immunity , vol. 69, no. 10, pp. 6558-6563, 2001. (hindawi.com)
  • A. L. Edkins, M. H. Ludewig, and G. L. Blatch, "A Trypanosoma cruzi heat shock protein 40 is able to stimulate the adenosine triphosphate hydrolysis activity of heat shock protein 70 and can substitute for a yeast heat shock protein 40," International Journal of Biochemistry and Cell Biology , vol. 36, no. 8, pp. 1585-1598, 2004. (hindawi.com)
  • The surface of Trypanosoma brucei brucei insect forms is covered by an invariant protein coat consisting of procyclins. (acris-antibodies.com)
  • Protein glycosylation mutants of procyclic Trypanosoma brucei: defects in the asparagine-glycosylation pathway. (acris-antibodies.com)
  • However, in Trypanosoma brucei , disorganized arrays of microtubules are arranged into the axoneme structure by the later addition of preformed protein complexes. (elifesciences.org)
  • Trypanosoma brucei is an excellent model system to address this question because its two main surface protein genes, procyclin and variant surface glycoprotein ( VSG ), are transcribed by pol I and undergo distinct transcriptional activation or downregulation events during developmental differentiation. (rupress.org)
  • gene
  • a) A schematic representation of NTR gene deletion in the knockout T. brucei cell lines SKO HYG (top) and SKO PAC (bottom). (nih.gov)
  • We have observed that challenging Trypanosoma brucei cells with gene-specific double-stranded RNAs (dsRNAs) leads to specific degradation of the homologous mRNA. (pnas.org)
  • Here we show that TLF-1 resistance in T. b. brucei is caused by reduced expression of the Hp/Hb receptor gene (TbbHpHbR). (sigmaaldrich.com)
  • molecular
  • In Trypanosoma brucei , considerable progress has been made over recent years in identifying molecular regulators of the cell cycle and elucidating their functions, although many regulators undoubtedly remain to be identified, and there is still a long way to go with respect to determining signal transduction pathways. (pubmedcentralcanada.ca)
  • Further work is now required to determine the extent and frequency with which these abnormalities might occur, however these findings do highlight the potential instability of the molecular karyotype of T.brucei in prolonged in vitro culture. (gla.ac.uk)
  • Bloodstream
  • Bloodstream-form Trypanosoma brucei were selected for resistance to nifurtimox and fexinidazole by stepwise exposure to increasing drug concentrations. (nih.gov)
  • Bloodstream forms of T. brucei clone MITat 1.4 were isolated from infected rats as described previously ( 18 ). (rupress.org)
  • clone
  • The template genomic DNA was derived from WT T. brucei , SKO HYG clone 1 and SKO PAC clone 1. (nih.gov)
  • resistance
  • Ectopic expression of TbbHpHbR in TLF-1-resistant T. b. brucei rescued TLF-1 uptake, demonstrating that decreased TbbHpHbR expression conferred TLF-1 resistance. (sigmaaldrich.com)
  • cell
  • However, it is clear that cell cycle regulation in T. brucei is unusual in many respects. (pubmedcentralcanada.ca)
  • Although the cell division cycle in Trypanosoma brucei broadly follows this scheme, it possesses unique features and complexities [1,. (pubmedcentralcanada.ca)
  • T. brucei contains a number of single copy organelles and structures (e.g. nucleus, mitochondrion whose DNA is concentrated into a disc-like structure termed the kinetoplast, Golgi and basal body/flagellum complex), which must be accurately duplicated and segregated if cell division is to generate viable progeny. (pubmedcentralcanada.ca)
  • Expression
  • Ectopic expression of TbgHpHbR in TLF-1-resistant T. b. brucei failed to rescue TLF-1 killing, suggesting that coding sequence changes altered Hp/Hb receptor binding affinity for TLF-1. (sigmaaldrich.com)