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The tumour suppressor p53 inhibits cancer cell proliferation and induces apoptosis. A new tumour-suppressive effect of p53 is to induce MDM2-dependent degradation of the tumour invasion factor Slug, resulting in reduced metastasis.
It is unclear how the growth rate and size of asymmetrically dividing stem cells are regulated. The U3snoRNP component Wicked, required for pre-ribosomal RNA maturation and thus ribosome formation, is localized asymmetrically and is critical for stem cell maintenance and function.
The ubquitin ligase Rad18 is a central mediator of cell cycle checkpoint activation by DNA damage. Now Rad18 turns out to directly regulate homologous recombination repair by interacting with Rad51C
The tumour suppressor p53 can mediate both cell-cycle arrest and apoptosis. Apak binds and acetylates p53 by recruiting KAP-1 and HDAC1 to specifically suppress p53 regulated pro-apoptotic genes. Stress-induced phosphorylation of Apak by ATM relieves this inhibition.
The 'somatic growth axis' involving IGF-1 and growth hormone is implicated in longevity. Persistent transcription-blocking DNA damage attenuates growth hormone and IGF-1 receptor expression and precipitates other ageing associated transcriptional changes, as well as inhibiting somatic growth.
How temporal signals from the steroid hormone ecdysone are integrated with JAK/STAT-mediated spatial control of Drosophila border-cell migration has been unclear. JAK/STAT represses Abrupt, which in turn attenuates ecdysone signalling by interacting with the ecdysone receptor coactivator Taiman.
SCAI is novel protein that inhibits the transcription factor MAL and represses the expression of β1-integrin. Reduced SCAI levels also correlate with increased invasive cell migration.
The actin severing factor cofilin is activated by the slingshot phosphatases. Phosphorylation of slingshot 1L by protein kinase D is found to block the association of slingshot 1L with actin, thereby inhibiting cofilin activation and directed cell migration.
The kinase DYRK2 regulates the assembly of a ubiquitin ligase complex in a phosphorylation-independent manner, while also phosphorylating the target for the ligase. Thus, ligase assembly and target ubiquitylation appear to be physically linked processes.
Beclin 1 is an essential mediator of mammalian autophagy that has anti-tumour activity. Beclin 1 associates with Atg14L and Rubicon to regulate autophagosome formation and maturation, respectively.
Skp2 is a known component of the SCF ubiquitin ligase that targets the cell-cycle regulator p27. Akt kinase phosphorylates Skp2 and regulates its stability and cytoplasmic localization.
Skp2 is a known component of the SCF ubiquitin ligase that ubiquitylates the cell-cycle regulator p27. Akt kinase directly phosphorylates Skp2 and regulates SCF complex assembly and ligase activity, Skp2 cytoplasmic localization and Skp2-dependent regulation of cell proliferation and migration.
Lamin B is a component of a membranous matrix thought to be essential for spindle assembly. The dynein motor and its interacting protein Nudel are required for the recruitment of lamin B to the spindle matrix.
By preventing G-actin accumulation, Rho-GTPase promotes the transcriptional activity of myocardin-related transcription factors (MRTFs), known co-factors of serum response factor (SRF). Rho-dependent MRTF expression is required for injected metastatic cell lines to colonize the lung.
The DNA-binding chromodomain helicase CHD8 regulates gene expression but how it acts on specific genes has been unclear. During early embryogenesis in mice, CHD8 recruits histone H1 to the p53-dependent promotors of apoptotic genes and thereby prevents massive cell death at this stage of development.
Pin1 interacts with Notch1 to increases its cleavage by γ-secretase and thus its transcriptional activity. In a feedback loop, Notch1 controls Pin1 expression, which results in enhanced Notch1 tumorigenic activity.
The intracellular fragment of the adhesion molecule EpCAM, which is generated by the proteases TACE and presenilin-2, increases cell proliferation and acts in a complex with β-catenin and Lef-1 to regulate gene expression.
NF-κB signalling protein NEMO is the first physiological substrate for linear head-to-tail polyubiquitin chains. The heterodimeric ubiquitin ligase LUBAC catalyses the reaction and mice lacking a LUBAC subunit show defects in NF-κB signalling.
RCAN1, the regulator of calcineurin phosphatase, interacts with TAK1 kinase binding protein 2 (TAB2). This leads to formation of the signalling complex TAK1-TAB1-TAB2, which phosphorylates RCAN1 and converts it to an activator of the calcineurin-NFAT pathway. Activated calcineurin then switches the signal off by dephopshorylating TAK1 and TAB1.