27 March 2007
Vol 2007, Issue 379
  • Contents

    • Perspective

    • Editors' Choice

      • Better Without Bax?

        Preserving ovarian function may improve the health of aging female mice.

      • Making a New Tail

        The H+ pump and membrane voltage play crucial roles in Xenopus tail regeneration.

      • Does Actin Give the Nod2 to NF-κB Activation?

        Association of Nod2 with cytoskeletal structures may represent a sequestration mechanism that allows its ready mobilization to activate NF-κB.

      • IL-2 Antagonizes Th17 Differentiation

        The cytokine formerly known as T cell growth factor appears to attenuate the differentiation of T helper 17 (Th17) cells.

      • Division Decisions

        Upon antigen binding, immune cells generate pathogen-fighting cells from daughters arising close to the antigen and memory cells from daughters away from it.

      • Making Bone with Oxysterols

        Activation of the Hedgehog pathway is one way oxysterols promote osteoblast differentiation.

      • Plant Hormone Signaling Receptor

        The cell surface receptor for an important growth regulator in plants binds to its ligand with high affinity and activates downstream targets.

      • Calpain Cleaves a Memory Inhibitor

        SCOP cleavage by calpain allows activation of mitogen-activated protein kinases and gene expression that promotes memory formation.

      • Modeling Competence

        A genetic circuit for bacterial cell differentiation exhibits a surprisingly varied repertoire of dynamic responses that depend on the amount of noise in the component biochemical reactions.

      • Staying in Charge

        The crystal structure of a key metabolic regulator reveals how it senses the ratio of ATP to AMP, initiating feedback processes to optimize ATP levels in the cell.

About The Cover

Cover image expansion

COVER This week features a Perspective on nonconventional functions of the phagocytic NADPH oxidase (NOX2). The image depicts a neutrophil extracellular trap (NET), formation of which depends on reactive oxygen species generated through NOX2 activity. [Image: Volker Brinkmann, Max-Planck Institute for Infection Biology, 10117 Berlin, Germany]