Expression site silencing and life-cycle progression appear normal in Argonaute1-deficient Trypanosoma brucei

Mol Biochem Parasitol. 2006 Sep;149(1):102-107. doi: 10.1016/j.molbiopara.2006.04.005. Epub 2006 May 12.

Authors

Christian J Janzen^#¹, Frederick van Deursen^#², Huafang Shi³, George A M Cross¹, Keith R Matthews², Elisabetta Ullu^{3

4}

Affiliations

¹ Laboratory of Molecular Parasitology, The Rockefeller University, Box 185, 1230 York Avenue, New York, NY 10021-6399, USA.
² Institute of Immunology and Infection Research, School of Biological Sciences, University of Edinburgh, West Mains Road, Edinburgh, EH9 3JT, UK.
³ Department of Internal Medicine, Yale Medical School, BCMM 136D, 295 Congress Avenue, Box 9812, New Haven, CT, 06536-8012, USA.
⁴ Department of Cell Biology, Yale Medical School, BCMM 136D, 295 Congress Avenue, Box 9812, New Haven, CT, 06536-8012, USA.

^# Contributed equally.

No abstract available

Publication types

Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

MeSH terms

Animals
Argonaute Proteins
Blood / parasitology
DNA, Mitochondrial / genetics
Gene Expression Regulation, Developmental
Life Cycle Stages
Membrane Glycoproteins / genetics
Mice
Mice, Inbred BALB C
Protozoan Proteins / genetics
RNA Interference*
RNA-Binding Proteins / genetics*
Trypanosoma brucei brucei / genetics*
Trypanosoma brucei brucei / growth & development
Trypanosomiasis, African / parasitology
Variant Surface Glycoproteins, Trypanosoma / genetics*

Substances

AGO1 protein, Trypanosoma brucei
Argonaute Proteins
DNA, Mitochondrial
Membrane Glycoproteins
Protozoan Proteins
RNA-Binding Proteins
Variant Surface Glycoproteins, Trypanosoma
procyclic acidic repetitive protein, Trypanosoma

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