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Volume 2 Issue 9, September 2000

Extensive branching of cellular processes, induced by overexpression of p120 catenin (green) in NIH3T3 cells. Actin filaments are shown in red. [Cover design: Majo Xeridat] [article, p.637]

Volume 2 Issue 9

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  • Covalent modification of the oncogene product Mdm2 by the ubiquitin-related protein SUMO1 protects it from ubiquitination and enhances its E3 ligase activity towards p53 in vitro. Disappearance of SUMO-modified Mdm2, which is observed upon radiation, may thus be a prerequisite for DNA-damage-induced accumulation of p53.

    • Frauke Melchior
    • Ludger Hengst
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  • The molecular pathways that mediate apoptosis are tightly regulated by a series of positive and negative signals, the balance of which determines whether or not cells commit suicide. New data from several laboratories now show that heat-shock proteins (HSPs) can influence this process through direct physical interaction with key components of the apoptotic machinery. These reports marry the survival (or death)-endowing properties of HSPs to the cell-death pathway.

    • Steven Xanthoudakis
    • Donald W. Nicholson
    News & Views

  • Acetylcholine calms the heartbeat by activating Gi-coupled receptors and G-protein-activated inwardly rectifying potassium (GIRK) channels. It also dampens the GIRK current by reducing PIP2 through Gq-coupled receptors. These two types of receptors seem to be engaged in an intriguingly specific form of crosstalk, which leads to desensitization of the GIRK current.

    • Lily Yeh Jan
    • Yuh Nung Jan
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  • Although it has long been appreciated that cAMP-related signalling can control cell growth, the mechanism by which this control is exerted has remained unknown. However, new findings now show how cAMP, acting through protein kinase A (PKA), maintains cells in an anchorage-dependent state by inhibiting mitogen-activated protein kinase (MAPK) signalling through p21-activated kinases (PAKs).

    • Steven M. Frisch
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