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Peer review is an essential aspect of the publishing process; journals and the research community have a shared interest in it being a constructive process.
CRACR2A is a newly discovered Ca2+-binding protein that regulates store-operated Ca2+ entry (SOCE). CRACR2A enhances SOCE by promoting the binding of the endoplasmic reticulum Ca2+ sensor STIM to Orai, a Ca2+ channel located in the plasma membrane. As intracellular Ca2+ levels rise, CRACR2A binds Ca2+ and triggers SOCE inactivation by dissociating from the Orai–STIM complex.
Although all cells within a colon cancer may harbour adenomatous polyposis coli (APC) or β-catenin mutations, activation of Wnt signalling is limited to a subpopulation of cells that display cancer stem cell properties. This activation requires a co-stimulatory signal mediated by hepatocyte growth factor, which is produced by tumour-associated myofibroblasts.
Formation of multivesicular bodies (MVBs) from endosomes or budding of enveloped virus such as HIV-I from the plasma membrane require the ESCRT (endosomal sorting complex required for transport) complexes. An in vitro reconstitution assay unambiguously identifies the function of each ESCRT complex in the sequential events of MVB morphogenesis, from cargo clustering and membrane bud formation to sequestration of cargoes in vesicles, and fission of the vesicles into the lumen of the endosome.
Instability in the structure and number of chromosomes is a trait common to cells from most epithelial cancers. A role in chromosome segregation for a pathway previously implicated in the DNA damage response reveals new connections between the tumour suppressive processes that maintain chromosome integrity.
Electron tomography provides unprecedented three-dimensional images of lamellipodial actin in frozen, ‘live’ cells. The vast majority of actin filaments at the leading edge are unbranched, requiring a re-examination of the role of Arp2/3-mediated branching in vivo.
The calcium-binding protein CRACR2A positively regulates the activity of CRAC channels. CRACR2A is a ternary complex which binds to, and stabilizes, the interaction between STIM1 and Orai1, and disassociates as intracellular calcium levels rise.
Cytoplasmic polyadenylation-driven translational control is known to regulate the expression of stored maternal mRNA in meiosis and early embryonic divisions. CPEB proteins mediate cell cycle phase-specific changes in polyadenylation that are also required for cell proliferation and mitotic entry in other actively dividing cells.
A complex containing the oncogene Myc, Skp2 E3 ligase and the coactivators Miz1 and p300 promotes transcription of RhoA. Overexpression of this complex increases RhoA levels and is detected in metastatic human cancers.
Cancer stem cell activity may not merely be an intrinsic characteristic of a subset of cancer cells and could be regulated by environmental cues. High Wnt activity in human colorectal cancer designates a tumour-initiating population and is orchestrated by the microenvironment.
Rho guanine nucleotide dissociation inhibitors (RhoGDIs) bind to inactive Rho GTPases in the cytosol, but their function remains unclear. Several Rho GTPases are now shown to compete for RhoGDI binding and this is crucial for regulating Rho GTPase turnover and activation.
GEMC1 is a newly discovered protein required for initiation of DNA replication in Xenopus. xGEMC1 interacts with the replication factors TopBP1 and Cdk2 and promotes TopBP1- and Cdk2-dependent loading of Cdc45 onto replication origins.
The DNA-damage checkpoint kinase Chk2 is a candidate tumour suppressor. Independently of DNA damage, Chk2 regulates spindle assembly and maintenance of chromosomal stability through phosphorylation of BRCA1.
Before meiosis II, centromeric sister chromatid cohesion is protected by shugoshin and protein phosphatase 2A, but the identity of the antagonising kinase has remained unclear. Casein kinase 1 is found to phosphorylate cohesin to promote its cleavage during fission yeast meiosis.
The cystic fibrosis transmembrane conductance regulator (CFTR) is expressed in dynamic environments, such as the lung. CFTR is known to be activated by ligand binding. Here, it is also found to be activated by mechanical stretching of cellular membranes.
Viral infection is shown to trigger CREB-mediated upregulation of miR-132. The interferon response is then downregulated by miR-132 through direct targeting of p300, a transcriptional co-activator, thereby facilitating viral replication.
