Tuesday, November 23, 2010

Hot off the presses! Dec 01 Nat Rev Mol Cell Biol

The Dec 01 issue of the Nat Rev Mol Cell Biol is now up on Pubget (About Nat Rev Mol 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:

  • - Nat Rev Mol Cell Biol 11(12):815 (2010)
  • Cytoskeleton: Keeping minus ends stable | PDF (169 KB)
    - Nat Rev Mol Cell Biol 11(12):816 (2010)
    Reveals how Patronin caps and stabilizes microtubule minus ends.
  • Membrane Trafficking: On track for delivery | PDF (265 KB)
    - Nat Rev Mol Cell Biol 11(12):817 (2010)
    ILK directs a pathway that mediates caveolar trafficking by microtubules.
  • From MYOD1 to iPS cells | PDF (184 KB)
    - Nat Rev Mol Cell Biol 11(12):817 (2010)
    The identification of MYOD1 as a myogenic factor influenced the cellular reprogramming field.
  • Cell Migration: A new move for SUMO | PDF (210 KB)
    - Nat Rev Mol Cell Biol 11(12):818 (2010)
    A new sumoylation mechanism for regulating RAC1 activity.
  • Oxidative stress: ATM bonds under stress | PDF (207 KB)
    - Nat Rev Mol Cell Biol 11(12):818 (2010)
    Identification of a pathway for ATM activation that is dependent on oxidative stress.
  • Cell cycle: Disposing of SETD8 | PDF (227 KB)
    - Nat Rev Mol Cell Biol 11(12):819 (2010)
    SETD8 degradation is mediated by CRL4CDT2.
  • Gene expression: Patterning by piRNAs | PDF (243 KB)
    - Nat Rev Mol Cell Biol 11(12):820 (2010)
    Piwi-interacting RNAs can regulate embryonic patterning by controlling Nanos mRNA decay.
  • Cell signalling: Cilia downsize mTORC1 | PDF (206 KB)
    - Nat Rev Mol Cell Biol 11(12):820 (2010)
    Primary cilia under fluid flow downregulate mTOR signalling to inhibit cell size.
  • Monitoring MAPs | Fit for export | PDF (164 KB)
    - Nat Rev Mol Cell Biol 11(12):820 (2010)
    Monitoring MAPs The dynamic turnover of microtubule filaments, which consist of protofilaments of α-tubulinâ€"β-tubulin heterodimers that are bound head-to-tail, is controlled by microtubule-associated proteins (MAPs). MAPs can either stabilize or destabilize microtubules, but our understanding of the mechanistic basis of this is limited by a lack of structural insights into how MAPs associate with microtubules.
  • In the news | PDF (135 KB)
    - Nat Rev Mol Cell Biol 11(12):821 (2010)
    Making blood from skin Human skin fibroblasts can be converted into haematopoietic progenitors and mature blood cells, according to a study published in Nature (7 Nov 2010; doi:10.1038/nature09591).
  • The prion hypothesis: from biological anomaly to basic regulatory mechanism
    - Nat Rev Mol Cell Biol 11(12):823 (2010)
    Prions are unusual proteinaceous infectious agents that are typically associated with a class of fatal degenerative diseases of the mammalian brain. However, the discovery of fungal prions, which are not associated with disease, suggests that we must now consider the effect of these factors on basic cellular physiology in a different light. Fungal prions are epigenetic determinants that can alter a range of cellular processes, including metabolism and gene expression pathways, and these changes can lead to a range of prion-associated phenotypes. The mechanistic similarities between prion propagation in mammals and fungi suggest that prions are not a biological anomaly but instead could be a newly appreciated and perhaps ubiquitous regulatory mechanism.
  • MET signalling: principles and functions in development, organ regeneration and cancer
    - Nat Rev Mol Cell Biol 11(12):834 (2010)
    The MET tyrosine kinase receptor (also known as the HGF receptor) promotes tissue remodelling, which underlies developmental morphogenesis, wound repair, organ homeostasis and cancer metastasis, by integrating growth, survival and migration cues in response to environmental stimuli or cell-autonomous perturbations. The versatility of MET-mediated biological responses is sustained by qualitative and quantitative signal modulation. Qualitative mechanisms include the engagement of dedicated signal transducers and the subcellular compartmentalization of MET signalling pathways, whereas quantitative regulation involves MET partnering with adaptor amplifiers or being degraded through the shedding of its extracellular domain or through intracellular ubiquitylation. Controlled activation of MET signalling can be exploited in regenerative medicine, whereas MET inhibition might slow down tumour progression.
  • Asymmetric cell division: recent developments and their implications for tumour biology
    - Nat Rev Mol Cell Biol 11(12):849 (2010)
    The ability of cells to divide asymmetrically is essential for generating diverse cell types during development. The past 10 years have seen tremendous progress in our understanding of this important biological process. We have learned that localized phosphorylation events are responsible for the asymmetric segregation of cell fate determinants in mitosis and that centrosomes and microtubules play important parts in this process. The relevance of asymmetric cell division for stem cell biology has added a new dimension to the field, and exciting connections between asymmetric cell division and tumorigenesis have begun to emerge.
  • The SUMO pathway: emerging mechanisms that shape specificity, conjugation and recognition
    - Nat Rev Mol Cell Biol 11(12):861 (2010)
    Proteins of the small ubiquitin-related modifier (SUMO) family are conjugated to proteins to regulate such cellular processes as nuclear transport, transcription, chromosome segregation and DNA repair. Recently, numerous insights into regulatory mechanisms of the SUMO modification pathway have emerged. Although SUMO-conjugating enzymes can discriminate between SUMO targets, many substrates possess characteristics that facilitate their modification. Other post-translational modifications also regulate SUMO conjugation, suggesting that SUMO signalling is integrated with other signal transduction pathways. A better understanding of SUMO regulatory mechanisms will lead to improved approaches for analysing the function of SUMO and substrate conjugation in distinct cellular pathways.
  • Mitochondrial fusion and fission in cell life and death
    - Nat Rev Mol Cell Biol 11(12):872 (2010)
    Mitochondria are dynamic organelles that constantly fuse and divide. These processes (collectively termed mitochondrial dynamics) are important for mitochondrial inheritance and for the maintenance of mitochondrial functions. The core components of the evolutionarily conserved fusion and fission machineries have now been identified, and mechanistic studies have revealed the first secrets of the complex processes that govern fusion and fission of a double membrane-bound organelle. Mitochondrial dynamics was recently recognized as an important constituent of cellular quality control. Defects have detrimental consequences on bioenergetic supply and contribute to the pathogenesis of neurodegenerative diseases. These findings open exciting new directions to explore mitochondrial biology.
  • Peroxisomal protein import and ERAD: variations on a common theme
    - Nat Rev Mol Cell Biol 11(12):885 (2010)
    Despite their distinct biological functions, there is a surprising similarity between the composition of the machinery that imports proteins into peroxisomes and the machinery that degrades endoplasmic reticulum (ER)-associated proteins. The basis of this similarity lies in the fact that both machineries make use of the same basic mechanistic principle: the tagging of a substrate by monoubiquitylation or polyubiquitylation and its subsequent recognition and ATP-dependent removal from a membrane by ATPases of the ATPases associated with diverse cellular activities (AAA) family of proteins. We propose that the ER-associated protein degradation (ERAD)-like removal of the peroxisomal import receptor is mechanically coupled to protein translocation into the organelle, giving rise to a new concept of export-driven import.

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