Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain
the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in
Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles
and JavaScript.
Although the flood of cell biological knowledge rises relentlessly, many databases face an uncertain future. Unless funding for essential bioinformatic resources is set in stone, the next storm may wash away the foundation of future cell biology research.
Regions of metazoan genomes replicate at defined times within S phase. This observation suggests that replication origins fire with a defined timing pattern that remains the same from cycle to cycle. However, an alterative model based on the stochastic firing of origins may also explain replication timing. This model assumes varying origin efficiency instead of a strict origin-timing programme. Here, we discuss the evidence for both models.
The BCL-2 oncogene promotes cancer progression by prohibiting cell death. BCL-2-related regulators were once thought to constitute a simple, two-class system of anti-death and pro-death factors. New data delineate a multistep hierarchy of BCL-2-family protein interactions that are driven by signal-dependent pathways.
A new study has revealed an unexpected role for eukaryotic translation initiation factor 4A (eIF4A) in suppressing Decapentaplegic (Dpp) signalling. On activation of Dpp signalling, eIF4A promotes degradation of the downstream signalling components Mad and Medea in a translation-independent manner.
Primary tumours release soluble factors, including VEGF-A, TGFβ and TNFα, which induce expression of the chemokines S100A8 and S100A9 in the myeloid and endothelial cells within the lung before tumour metastasis. These chemokine-activated premetastatic niches support adhesion and invasion of disseminating malignant cells, thereby establishing a fertile habitat for metastatic tumours.
The response of some G-protein coupled receptors (GPRCs) is affected by the voltage across the membrane in which they sit. A study now shows that gating currents, similar to those of ion channels, are associated with this alteration in GPRC activity. The currents depend on structural elements of the receptor that functionally couple to G proteins.
