Monday, May 2, 2011

Hot off the presses! May 01 trends cell biol

The May 01 issue of the trends cell biol is now up on Pubget (About trends cell biol): if you're at a subscribing institution, just click the link in the latest link at the home page. (Note you'll only be able to get all the PDFs in the issue if your institution subscribes to Pubget.)

Latest Articles Include:

  • Editorial Board
    - trends cell biol 21(5):i (2011)
  • LRRK2 signaling pathways: the key to unlocking neurodegeneration?
    - trends cell biol 21(5):257-265 (2011)
    Mutations in PARK8, encoding leucine-rich repeat kinase 2 (LRRK2), are a major cause of Parkinson's disease. We contrast data suggesting that changes in LRRK2 activity cause alterations in mitogen-activated protein kinase, translational control, tumor necrosis factor α/Fas ligand and Wnt signaling pathways with the cell biological functions of LRRK2 such as vesicle trafficking. Despite scarce in vivo data on cell signaling, involvement in diverse cell biological functions suggests a role for LRRK2 as an upstream regulator in events leading to neurodegeneration. To stimulate discussion and give direction for future research, we further suggest that despite the importance of the catalytic activity for cytotoxicity, the main cellular function of LRRK2 is linked to assembly of signaling complexes.
  • Regulation of membrane traffic by integrin signaling
    - trends cell biol 21(5):266-273 (2011)
    Membrane trafficking pathways function to sort and transport cargoes to various intracellular compartments and to the plasma membrane. This allows precise spatiotemporal control of processes such as signal transduction, which in turn is crucial for complex cell functions such as cell division, migration and polarity. Recent studies identified cell–matrix adhesions as regulators of exocytosis, endocytosis and the recycling machinery, thus establishing a new layer of crosstalk between cell adhesion and signaling. This review discusses these findings and considers their implications for signaling events downstream of integrins and growth factor receptors.
  • Lonely death dance of human pluripotent stem cells: ROCKing between metastable cell states
    - trends cell biol 21(5):274-282 (2011)
    Two kinds of human pluripotent cells, human embryonic stem cells (hESCs) and human induced pluripotent stem cells (hiPSCs), promise new avenues for medical innovation. These human cells share many similarities with mouse counterparts, including pluripotency, and they exhibit several unique properties. This review examines the diversity of mammalian pluripotent cells from a perspective of metastable pluripotency states. An intriguing phenomenon unique to human pluripotent stem cells is dissociation-induced apoptosis, which has been a technical problem for various cellular manipulations. The discovery that this apoptosis is suppressed by ROCK inhibitors brought revolutionary change to this troublesome situation. We discuss possible links of the metastable pluripotent state to ROCK-dependent human embryonic stem cell apoptosis and summarize recent progress in molecular understandings of this phenomenon.
  • On the cutting edge: post-translational modifications in cytokinesis
    - trends cell biol 21(5):283-292 (2011)
    Cytokinesis represents the final stage in the cell cycle, in which two daughter cells, each with their complement of the duplicated genome, physically separate. At the core of this process sits highly conserved machinery responsible for specifying the plane of division, building a contractile apparatus and ultimately cleaving cells in two. Although the 'parts list' of contributing proteins has been well described, mechanisms by which these parts are spatially and temporally regulated are only beginning to be understood. With advancements in biochemical and proteomic analyses, recent work has uncovered multiple new roles for post-translational modifications in the regulation of cytokinesis. Here, we review these latest findings and interpret our current understanding of cytokinesis in light of relevant modifications.
  • The dynamic state of protein turnover: It's about time
    - trends cell biol 21(5):293-303 (2011)
    The continual destruction and renewal of proteins that maintain cellular homeostasis has been rigorously studied since the late 1930s. Experimental techniques for measuring protein turnover have evolved to measure the dynamic regulation of key proteins and now, entire proteomes. In the past decade, the proteomics field has aimed to discover how cells adjust their proteomes to execute numerous regulatory programs in response to specific cellular and environmental cues. By combining classical biochemical techniques with modern, high-throughput technologies, researchers have begun to reveal the synthesis and degradation mechanisms that shape protein turnover on a global scale. This review examines several recent developments in protein turnover research, emphasizing the combination of metabolic labeling and mass spectrometry.
  • Planarian stem cells: a simple paradigm for regeneration
    - trends cell biol 21(5):304-311 (2011)
    Planarians are capable of profound regenerative feats dependent upon a population of self-renewing adult stem cells called neoblasts. The key features of neoblasts are their capacity for indefinite self-renewal, their totipotency and the ability of their progeny to interpret differentiation and polarity signals and correctly replace lost structures after tissue damage. Regeneration in planarians offers a paradigm for understanding the molecular and cellular control of the repair and regeneration of animal tissues, and could provide valuable insights for the safe use of stem cells to repair damaged, diseased and ageing human tissues with little or no regenerative capacities. Here, I review recent progress in understanding neoblasts in regeneration and the growing potential this research has to be broadly informative for human biology.
  • Regulation of cell differentiation by the DNA damage response
    - trends cell biol 21(5):312-319 (2011)
    When faced with DNA double-strand breaks (DSBs), vertebrate cells activate DNA damage response (DDR) programs that preserve genome integrity and suppress malignant transformation. Three established outcomes of the DDR include transient cell cycle arrest coupled with DNA repair, apoptosis, or senescence. However, recent studies in normal and cancer precursor or stem cells suggest that a fourth potential outcome, cell differentiation, is under the influence of DDR programs. Here we review and discuss the emerging evidence that supports the linkage of signaling from DSBs to the regulation of differentiation, including some of the molecular mechanisms driving this under-appreciated DDR outcome. We also consider the physiologic and pathologic consequences of defects in DDR signaling on cell differentiation and malignant transformation.

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