Review
Importing Mitochondrial Proteins: Machineries and Mechanisms
Agnieszka Chacinska1,2, Carla M. Koehler3, Dusanka Milenkovic1, 2, Trevor Lithgow4 and Nikolaus Pfanner1, 2,
1Institut für Biochemie und Molekularbiologie, ZBMZ, Universität Freiburg, 79104 Freiburg, Germany
2Centre for Biological Signalling Studies, Universität Freiburg, 79104 Freiburg, Germany
3Department of Chemistry and Biochemistry, University of California, Los Angeles, Los Angeles, CA 90095, USA
4Department of Biochemistry and Molecular Biology, Monash University, Victoria 3800, Australia
Most mitochondrial proteins are synthesized on cytosolic ribosomes and must be imported across one or both mitochondrial membranes. There is an amazingly versatile set of machineries and mechanisms, and at least four different pathways, for the importing and sorting of mitochondrial precursor proteins. The translocases that catalyze these processes are highly dynamic machines driven by the membrane potential, ATP, or redox reactions, and they cooperate with molecular chaperones and assembly complexes to direct mitochondrial proteins to their correct destinations. Here, we discuss recent insights into the importing and sorting of mitochondrial proteins and their contributions to mitochondrial biogenesis.
Sunday, August 30, 2009
sliding β clamp subunit
Preview
Clamping Down on Transposon Targeting
Mick Chandler
1Laboratoire de Microbiologie et Génétique Moléculaire UMR 5100, CNRS, 31062 Toulouse CEDEX, France
Cell, Volume 138, Issue 4, 21 August 2009, Pages 685-695,
Adam R. Parks, Zaoping Li, Qiaojuan Shi, Roisin M. Owens, Moonsoo M. Jin, Joseph E. Peters
The sliding β clamp subunit of the DNA replication machinery in the bacterium Escherichia coli coordinates multiple functions in the cell beyond genome duplication. In this issue, Parks et al. (2009) find that the β clamp interacts with the transposition protein TnsE to target the Tn7 transposon to discontinuously replicating DNA at the replication fork.
Clamping Down on Transposon Targeting
Mick Chandler
1Laboratoire de Microbiologie et Génétique Moléculaire UMR 5100, CNRS, 31062 Toulouse CEDEX, France
Cell, Volume 138, Issue 4, 21 August 2009, Pages 685-695,
Adam R. Parks, Zaoping Li, Qiaojuan Shi, Roisin M. Owens, Moonsoo M. Jin, Joseph E. Peters
The sliding β clamp subunit of the DNA replication machinery in the bacterium Escherichia coli coordinates multiple functions in the cell beyond genome duplication. In this issue, Parks et al. (2009) find that the β clamp interacts with the transposition protein TnsE to target the Tn7 transposon to discontinuously replicating DNA at the replication fork.
Monday, August 10, 2009
सेल Volume 138, Issue 2, 23 July 2009, Pages 271-285
Article
CD47 Is Upregulated on Circulating Hematopoietic Stem Cells and Leukemia Cells to Avoid Phagocytosis
Cell, Volume 138, Issue 2, 23 July 2009, Pages 271-285
References and further reading may be available for this article. To view references and further reading you must purchase this article.
Siddhartha Jaiswal1, Corresponding Author Contact Information, E-mail The Corresponding Author, Catriona H.M. Jamieson2, Wendy W. Pang1, Christopher Y. Park1, Mark P. Chao1, Ravindra Majeti1, David Traver3, Nico van Rooijen4 and Irving L. Weissman1
Summary
Macrophages clear pathogens and damaged or aged cells from the blood stream via phagocytosis. Cell-surface CD47 interacts with its receptor on macrophages, SIRPα, to inhibit phagocytosis of normal, healthy cells. We find that mobilizing cytokines and inflammatory stimuli cause CD47 to be transiently upregulated on mouse hematopoietic stem cells (HSCs) and progenitors just prior to and during their migratory phase, and that the level of CD47 on these cells determines the probability that they are engulfed in vivo. CD47 is also constitutively upregulated on mouse and human myeloid leukemias, and overexpression of CD47 on a myeloid leukemia line increases its pathogenicity by allowing it to evade phagocytosis. We conclude that CD47 upregulation is an important mechanism that provides protection to normal HSCs during inflammation-mediated mobilization, and that leukemic progenitors co-opt this ability in order to evade macrophage killing.
CD47 Is Upregulated on Circulating Hematopoietic Stem Cells and Leukemia Cells to Avoid Phagocytosis
Cell, Volume 138, Issue 2, 23 July 2009, Pages 271-285
References and further reading may be available for this article. To view references and further reading you must purchase this article.
Siddhartha Jaiswal1, Corresponding Author Contact Information, E-mail The Corresponding Author, Catriona H.M. Jamieson2, Wendy W. Pang1, Christopher Y. Park1, Mark P. Chao1, Ravindra Majeti1, David Traver3, Nico van Rooijen4 and Irving L. Weissman1
Summary
Macrophages clear pathogens and damaged or aged cells from the blood stream via phagocytosis. Cell-surface CD47 interacts with its receptor on macrophages, SIRPα, to inhibit phagocytosis of normal, healthy cells. We find that mobilizing cytokines and inflammatory stimuli cause CD47 to be transiently upregulated on mouse hematopoietic stem cells (HSCs) and progenitors just prior to and during their migratory phase, and that the level of CD47 on these cells determines the probability that they are engulfed in vivo. CD47 is also constitutively upregulated on mouse and human myeloid leukemias, and overexpression of CD47 on a myeloid leukemia line increases its pathogenicity by allowing it to evade phagocytosis. We conclude that CD47 upregulation is an important mechanism that provides protection to normal HSCs during inflammation-mediated mobilization, and that leukemic progenitors co-opt this ability in order to evade macrophage killing.
Subscribe to:
Posts (Atom)