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- Besnard, E, et al.
(author)
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The mTOR Complex Controls HIV Latency
- 2016
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In: Cell host & microbe. - : Elsevier BV. - 1934-6069 .- 1931-3128. ; 20:6, s. 785-797
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Journal article (peer-reviewed)
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6. |
- Billker, Oliver, et al.
(author)
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Calcium Builds Strong Host-Parasite Interactions
- 2015
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In: Cell Host and Microbe. - : Elsevier. - 1931-3128 .- 1934-6069. ; 18:1, s. 9-10
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Research review (peer-reviewed)abstract
- Apicomplexan parasite invasion of host cells is a multistep process, requiring coordinated events. In this issue of Cell Host & Microbe, Paul et al. (2015) and Philip and Waters (2015) leverage experimental genetics to show that the calcium-regulated protein phosphatase, calcinuerin, regulates invasion in multiple parasite species.
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7. |
- Billker, Oliver, et al.
(author)
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Calcium-dependent signaling and kinases in apicomplexan parasites
- 2009
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In: Cell Host and Microbe. - : Elsevier BV. - 1931-3128 .- 1934-6069. ; 5:6, s. 612-622
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Journal article (peer-reviewed)abstract
- Calcium controls many critical events in the complex life cycles of apicomplexan parasites including protein secretion, motility, and development. Calcium levels are normally tightly regulated and rapid release of calcium into the cytosol activates a family of calcium-dependent protein kinases (CDPKs), which are normally characteristic of plants. CDPKs present in apicomplexans have acquired a number of unique domain structures likely reflecting their diverse functions. Calcium regulation in parasites is closely linked to signaling by cyclic nucleotides and their associated kinases. This Review summarizes the pivotal roles that calcium- and cyclic nucleotide-dependent kinases play in unique aspects of parasite biology.
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- Billker, Oliver
(author)
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CRISPRing the elephant in the room
- 2018
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In: Cell Host and Microbe. - : Elsevier. - 1931-3128 .- 1934-6069. ; 24:6, s. 754-755
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Journal article (other academic/artistic)abstract
- The importance of guanylyl-cyclases (GCs) in apicomplexa has remained elusive due to the large size of the genes. Two recent studies, including Brown and Sibley, 2018 in this issue of Cell Host & Microbe, make elegant use of genome editing with CRISPR-Cas9 to characterize roles of GCs in Toxoplasma and Plasmodium.
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- Blomgran, Robert, et al.
(author)
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Mycobacterium tuberculosis inhibits neutrophil apoptosis, leading to delayed activation of naive CD4 T cells
- 2012
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In: Cell Host and Microbe. - : Elsevier. - 1931-3128 .- 1934-6069. ; 11:1, s. 81-90
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Journal article (peer-reviewed)abstract
- Mycobacterium tuberculosis promotes its replication by inhibiting the apoptosis of infected macrophages. A proapoptotic M. tuberculosis mutant lacking nuoG, a subunit of the type I NADH dehydrogenase complex, exhibits attenuated growth in vivo, indicating that this virulence mechanism is essential. We show that M. tuberculosis also suppresses neutrophil apoptosis. Compared to wild-type, the nuoG mutant spread to a larger number of lung phagocytic cells. Consistent with the shorter lifespan of infected neutrophils, infection with the nuoG mutant resulted in fewer bacteria per infected neutrophil, accelerated bacterial acquisition by dendritic cells, earlier trafficking of these dendritic cells to lymph nodes, and faster CD4 T cell priming. Neutrophil depletion abrogated accelerated CD4 T cell priming by the nuoG mutant, suggesting that inhibiting neutrophil apoptosis delays adaptive immunity in tuberculosis. Thus, pathogen modulation of apoptosis is beneficial at multiple levels, and enhancing phagocyte apoptosis promotes CD4 as well as CD8 T cell responses.
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