期刊
CELL REPORTS
卷 17, 期 3, 页码 660-670出版社
CELL PRESS
DOI: 10.1016/j.celrep.2016.09.041
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资金
- Spanish Ministerio de Ciencia e Innovacion [SAF2015-71444]
- Junta de Andalucia [CTS-5841]
- Subdireccion General de Redes y Centros de Investigacion Cooperativa (RICET) [RD12/0018/0015]
- NIH [R01AI114685]
During infection in mammals, the protozoan parasite Trypanosoma brucei transforms from a proliferative bloodstream form to a quiescent form that is pre-adapted to host transition. AMP analogs are known to induce quiescence and also inhibit TbTOR4. To examine the role of AMP-activated kinase (AMPK) in the regulation of this developmental transition, we characterized trypanosome TbAMPK complexes. Expression of a constitutively active AMPK alpha 1 induces quiescence of the infective form, and TbAMPK alpha 1 phosphorylation occurs during differentiation of wild-type pleomorphic trypanosomes to the quiescent stumpy form in vivo. Compound C, a well-known AMPK inhibitor, inhibits parasite differentiation in mice. We also provide evidence linking oxidative stress to TbAMPK alpha 1 activation and quiescent differentiation, suggesting that TbAMPK alpha 1 activation balances quiescence, proliferation, and differentiation.
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