This message contains My NCBI what's new results from the National Center for Biotechnology Information (NCBI) at the U.S. National Library of Medicine (NLM).
Do not reply directly to this message.
Sender's message:
Sent on Saturday, 2010 Jan 30Search kinetoplastids OR kinetoplastid OR Kinetoplastida OR "trypanosoma brucei" OR leishmania OR brucei OR leishmaniasis OR "African trypanosomiasis"
Click here to view complete results in PubMed. (Results may change over time.)
To unsubscribe from these e-mail updates click here.
| PubMed Results |
| 1. | Curr Opin Investig Drugs. 2010 Feb;11(2):147-56.Apicomplexa, trypanosoma and parasitic nematode protein kinases as antiparasitic therapeutic targets.Liotta F, Siekierka JJ.Montclair State University, Sokol Institute of Pharmaceutical Life Sciences and Department of Chemistry and Biochemistry, 1 Normal Avenue, Montclair, NJ 07043, USA. siekierkaj@mail.montclair.edu. Parasitic infections caused by Plasmodium, Trypanosoma, Leishmania, Toxoplasma and parasitic nematodes affect hundreds of millions of individuals worldwide and are the cause of significant mortality and morbidity, particularly in developing countries. These diseases also have an impact on individuals from developed countries; for example, some US troops in Iraq and Afghanistan have been infected with Leishmania. The annual mortality associated with parasitic infections is estimated to be 1.5 million deaths. The socioeconomic impact of the morbidity associated with parasitic infections is significant, and the development of new drugs, aimed at novel targets, is urgently needed to develop effective treatments for these diseases. The small-molecule inhibitors discussed in this review constitute useful tools with which to explore the relevance of kinase inhibition in inducing antiparasitic activity. The aim of recent target-based approaches used in the development of parasite kinase inhibitors is to identify novel antiparasitic agents with therapeutic potential. |
| PMID: 20112164 [PubMed - in process] | |
| 2. | PLoS One. 2010 Jan 27;5(1):e8913.The Zinc-Fingers of KREPA3 Are Essential for the Comp lete Editing of Mitochondrial mRNAs in Trypanosoma brucei.Guo X, Ernst NL, Carnes J, Stuart KD.Seattle Biomedical Research Institute, Seattle, Washington, United States of America. Most mitochondrial mRNAs in trypanosomes undergo uridine insertion/deletion editing that is catalyzed by approximately 20S editosomes. The editosome component KREPA3 is essential for editosome structural integrity and its two zinc finger (ZF) motifs are essential for editing in vivo but not in vitro. KREPA3 function was further explored by examining the consequence of mutation of its N- and C- terminal ZFs (ZF1 and ZF2, respectively). Exclusively expressed myc-tagged KREPA3 with ZF2 mutation resulted in lower KREPA3 abundance and a relative increase in KREPA2 and KREL1 proteins. Detailed analysis of edited RNA products revealed the accumulation of partially edited mRNAs with less insertion editing compared to the partially edited mRNAs found in the cells with wild type KREPA3 expression. Mutation of ZF1 in TAP-tagged KREPA3 also resulted in accumulation of partially edited mRNAs that were shorter and only edited in the 3'-terminal editing region. Mutation of both ZFs essentially eliminated partially edited mRNA. The mutations did not affect gRNA abundance. These data indicate that both ZFs are essential for the progression of editing and perhaps its accuracy, which suggests that KREPA3 plays roles in the editing process via its ZFs interaction with editosome proteins and/or RNA substrates. |
| PMID: 20111718 [PubMed - in process] | |
| 3. | Ann Dermatol Venereol. 2009 Dec;136S7:S393-S406.[What's new in clinical dermatology?][Article in French] Morand JJ.Service de dermatologie, Hôpital militaire Alphonse Laveran, Institut de médecine tropicale du service de santé des armées, Pharo, 13384 Marseille, France. The actuality in clinical dermatology is, to our opinion, dominated by the emergent or reemergent infections (arboviruses, poxviruses, mycobacteria, leishmania, staphylococcus, papillomaviruses, bedbugs...) and their involvement in certain diseases (atopia, psoriasis), tumours or syndromes with dermatologic signs (IRIS). The cutaneous adverse side effects of the targeted chemotherapies and biotherapies are consequently better surrounded. Some rare new anatomoclinical entities are identified but <<classics>> (Lipschütz ulcer, pityriasis rosea, deep dissecting hematoma, puffy hand syndrome, disseminata alopecia areata) are rediscovered and better represented thanks to help, sometimes, by new techniques. Copyright © 2009 Elsevier Masson SAS. All rights reserved. |
| PMID: 20110055 [PubMed - as supplied by publisher] | |
| 4. | Exp Parasitol. 2010 Jan 25. [Epub ahead of print]Trypanosoma brucei: Trypanosome-specific endoplasmic reticulum proteins involved in variant surface glycoprotein expression.Wang YN, Wang M, Field MC.Department of Pathology, University of Cambridge, Tennis Court Road, Cambridge, CB2 1QP, UK; College of Veterinary Medicine, China Agricultural University, Beijing 100193, China. In Trypanosoma brucei the GPI-anchored variant surface glycoprotein (VSG) represents approximately 90% of cell surface protein and a major proportion of endoplasmic reticulum (ER) biosynthetic output. We identified four trypanosomatid-specific genes encoding candidate ER-resident proteins; all were required for normal proliferation. For Tb11.01.2640 and Tb11.01.8120, an increase in VSG abundance was found on silencing, while the protein products localized to the ER; we designated these ERAP32 and ERAP18 for ER-associated protein of 32kDa and 18kDa. Silencing ERAP32 or ERAP18 did not alter expression levels of ISG65 or ISG75, the major surface trans-membrane domain proteins. Surface biotinylation or immunoflorescence did not identify intracellular VSG accumulation, while FACS and fluorescence microscopy indicated that the cells were not increased in size, arguing for increased VSG density on the cell surface. Therefore, ERAP32 and ERAP18 are trypanosome-specific ER-localized proteins with a major role in VSG protein export and, contrary to current paradigms, VSG is not saturated on the cell surface. Copyright © 2010. Published by Elsevier Inc. |
| PMID: 20109450 [PubMed - as supplied by publisher] | |
| 5. | Exp Parasitol. 2010 Jan 25. [Epub ahead of print]Activation of Leishmania (Leishmania) amazonensis arginase at low temperature by binuclear Mn(2+) center formation of the immobilized enzyme on a Ni(2+) resin.Silva ER, Floeter-Winter LM.Faculdade de Zootecnia e Engenharia de Alimentos, Universidade de São Paulo, São Paulo, SP, Brazil. In Leishmania, arginase is responsible for the production of ornithine, a precursor of polyamines required for proliferation of the parasite. In this work, the activation kinetics of immobilized arginase enzyme from L. (L.) amazonensis were studied by varying the concentration of Mn(2+) applied to the nickel column at 23 C. The intensity of the binding of the enzyme to the Ni(2+) resin was directly proportional to the concentration of Mn(2+). Conformational changes of the enzyme may occur when the enzyme interacts with immobilized Ni(2+), allowing the following to occur: 1) entrance of Mn(2+) and formation of the metal bridge; 2) stabilization and activation of the enzyme at 23 C; and 3) an increase in the affinity of the enzyme to Ni(2+) after the Mn(2+) activation step. The conformational alterations can be summarized as follows: the interaction with the Ni(2+) simulates thermal heating in the artificial activation by opening a channel for Mn(2+) to enter. Copyright © 2010. Published by Elsevier Inc. |
| PMID: 20109449 [PubMed - as supplied by publisher] | |
| 6. | Exp Parasitol. 2010 Jan 25. [Epub ahead of print]Trypanosoma brucei: Reduction of GPI-phospholipase C Protein During Differentiation is Dependent on Replication of Newly-Transformed Cells.Subramanya S, Armah DA, Mensa-Wilmot K.Department of Cellular Biology, The University of Georgia, 724 Biological Sciences, Athens, Georgia 30602. The protozoan parasite Trypanosoma brucei lives in the bloodstream of vertebrates or in a tsetse fly. Expression of a GPI-phospholipase C polypeptide (GPI-PLCp) in the parasite is restricted to the bloodstream form. Events controlling the amount of GPI-PLCp expressed during differentiation are not completely understood. Our metabolic "pulse-chase" analysis reveals that GPI-PLCp is stable in bloodstream form. However, during differentiation of bloodstream to insect stage (procyclic) T. brucei, translation GPI-PLC mRNA ceases within 8 h of initiating transformation. GPI-PLCp is not lost precipitously from newly-transformed procyclic trypanosomes. Nascent procyclics contain 400-fold more GPI-PLCp than established insect stage T. brucei. Reduction of GPI-PLCp in early-stage procyclics is linked to parasite replication. Sixteen cell divisions are required to reduce the amount of GPI-PLCp in newly-differentiated procyclics to levels present in the established procyclic. GPI-PLCp is retained in strains of T. brucei that fail to replicate after differentiation of the bloodstream to the procyclic form. Thus, at least two factors control levels of GPI-PLCp during differentiation of bloodstream T. brucei; (i) repression of GPI-PLC mRNA translation, and (ii) sustained replication of newly-transformed procyclic T. brucei. These studies illustrate the importance of repeated cell divisions in controlling the steady-state amount of GPI-PLCp during differentiation of the African trypanosome. Copyright © 2010. Published by Elsevier Inc. |
| PMID: 20109448 [PubMed - as supplied by publisher] | |
| 7. | Parasitology. 2010 Jan 29:1-11. [Epub ahead of print]Bloodstream form trypanosome plasma membrane proteins: antigenic variation and invariant antigens.Schwede A, Carrington M.Department of Biochemistry, University of Cambridge, 80 Tennis Court Road, Cambridge CB2 1GA, UK. SUMMARYTrypanosoma brucei is exposed to the adaptive immune system and complement in the blood of its mammalian hosts. The aim of this review is to analyse the role and regulation of the proteins present on the external face of the plasma membrane in the long-term persistence of an infection and transmission. In particular, the following are addressed: (1) antigenic variation of the variant surface glycoprotein (VSG), (2) the formation of an effective VSG barrier shielding invariant surface proteins, and (3) the rapid uptake of VSG antibody complexes combined with degradation of the immunoglobulin and recycling of the VSG. |
| PMID: 20109254 [PubMed - as supplied by publisher] | |
| 8. | Parasitology. 2010 Jan 29:1-12. [Epub ahead of print]The potential of metabolomics for Leishmania research in the post-genomics era.Scheltema RA, Decuypere S, T'kindt R, Dujardin JC, Coombs GH, Breitling R.Groningen Bioinformatics Centre, Groningen Biomolecular Sciences and Biotechnology Institute, University of Groningen, Kerklaan 30, 9751 NN Haren, The Netherlands. SUMMARYThe post-genomics era has provided researchers with access to a new generation of tools for the global characterization and understanding of pathogen diversity. This review provides a critical summary of published Leishmania post-genomic research efforts to date, and discusses the potential impact of the addition of metabolomics to the post-genomic toolbox. Metabolomics aims at understanding biology by comprehensive metabolite profiling. We present an overview of the design and interpretation of metabolomics experiments in the context of Leishmania research. Sample preparation, measurement techniques, and bioinformatics analysis of the generated complex datasets are discussed in detail. To illustrate the concepts and the expected results of metabolomics analyses, we also present an overview of comparative metabolic profiles of drug-sensitive and drug-resistant Leishmania donovani clinical isolates. |
| PMID: 20109253 [PubMed - as supplied by publisher] | |
| 9. | Parasitology. 2010 Jan 29:1-11. [Epub ahead of print]Development and evaluation of different PCR-based typing methods for discrimination of Leishmania donovani isolates from Nepal.Bha ttarai NR, Dujardin JC, Rijal S, DE Doncker S, Boelaert M, VAN DER Auwera G.Institute of Tropical Medicine Antwerp, Antwerp, Belgium. SUMMARYIntroduction. Leishmania donovani, the causative agent of visceral leishmaniasis in the Indian subcontinent, has been reported to be genetically homogeneous. In order to support ongoing initiatives to eliminate the disease, highly discriminative tools are required for documenting the parasite population and dynamics. Methods. Thirty-four clinical isolates of L. donovani from Nepal were analysed on the basis of size and restriction endonuclease polymorphisms of PCR amplicons from kinetoplast minicircle DNA, 5 nuclear microsatellites, and nuclear loci encoding glycoprotein 63, cysteine proteinase B, and hydrophilic acylated surface protein B. We present and validate a procedure allowing standardized analysis of kDNA fingerprint patterns. Results. Our results show that parasites are best discriminated on the basis of kinetoplast minicircle DNA (14 genotypes) and 1 microsatellite defining 7 genotypes, while the remaining markers discriminated 2 groups or were monomorphic. Combination of all nuclear markers revealed 8 genotypes, while extension with kDNA data yielded 18 genotypes. Conclusion. We present tools that allow discrimination of closely related L. donovani strains circulating in the Terai region of Nepal. These can be used to study the micro-epidemiology of parasite populations, determine the geographical origin of infections, distinguish relapses from re-infection, and monitor the spread of particular variants. |
| PMID: 20109247 [PubMed - as supplied by publisher] | |
| 10. | Parasitol Int. 2009 Jun;58(2):187-92. Epub 2009 Feb 3.Cloning and characterization of a DNA polymerase beta gene from Trypanosoma cruzi.Venegas JA, Aslund L, Solari A.Programa de Biología Celular y Molecular, ICBM, Universidad de Chile, Casilla 70086, Santiago-7, Chile. jvenega@med.uchile.cl A gene coding for a DNA polymerase beta from the Trypanosoma cruzi Miranda clone, belonging to the TcI lineage, was cloned (Miranda Tcpol beta), using the information from eight peptides of the T. cruzi beta-like DNA polymerase purified previously. The gene encodes for a protein of 403 amino acids which is very similar to the two T. cruzi CL Brener (TcIIe lineage) sequences published, but has three different residues in highly conserved segments. At the amino acid level, the identity of TcI-pol beta with mitochondrial pol beta and pol beta-PAK from other trypanosomatids was between 68-80% and 22-30%, respectively. Miranda Tc-pol beta protein has an N-terminal sequence similar to that described in the mitochondrial Crithidia fasciculata pol beta, which suggests that the TcI-pol beta plays a role in the organelle. Northern and Western analyses showed that this T. cruzi gene is highly expressed both in proliferative and non-proliferative developmental forms. These results suggest that, in addition to replication of kDNA in proliferative cells, this enzyme may have another function in non-proliferative cells, such as DNA repair role similar to that which has extensively been described in a vast spectrum of eukaryotic cells. |
| PMID: 19567232 [PubMed - indexed for MEDLINE] | |
| Related articles | |
 | |
Publication Types:
MeSH Terms:
Substances:
|
No comments:
Post a Comment