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.
The tumour suppressor p53 is subject to complex regulation and arginine methylation is now shown to provide an additional level of control. The protein arginine methyltransferase (PRMT) 5 is recruited by Strap to methylate p53 in response to DNA damage, governing the p53 response.
The anti-apoptotic regulators XIAP and c-IAPs promote turnover of the cRAF kinase to control cell migration. XIAP binding facilitates ubiquitylation of cRAF through the ubiquitin ligase CHIP.
P-ATPases in plants are typically thought to act at the plasma membrane. In contrast, PH5, a P-type H+ ATPase functions within the vacuolar membrane to control acidification during flower coloration.
Ubiquitin-dependent degradation of Cdc20 by the APC/C ligase is a conserved mechanism essential for maintaining the spindle assembly checkpoint activated by unattached chromosomes.
Quantitative analysis and mathematical modelling show that cortical tension anisotropy at apical cell junctions drives cell neighbour exchanges that are responsible for elongation of Drosophila embryos. This anisotropy depends on myosin II activity.
In an unanticipated cross-talk between the steroid and insulin endocrine systems, the neuroactive steroid pregnenolone sulphate is found to activate the TRPM3 channel, leading to enhanced insulin secretion from pancreatic islets.
The general transcription factor TATA-binding protein (TBP) is retained at gene promoters during mitosis, where it recruits PP2A to inactivate condensin. Chromatin decondensation at promoters may be associated with gene bookmarking, a mechanism to re-establish gene activity patterns in daughter cells.
The chromatin mark H3K27me3 is transmitted during cell division by recruitment and binding of the PRC2 complex, which maintains the mark and leads to methylation of H3K27 on newly incorporated histones.
A ubiquitin binding domain in the IAP proteins binds Lys 63-linked poly-ubiquitin chains and is essential for the oncogenic potential of cIAP. This domain is also required for activating NF-κB, possibly by binding poly-ubiquitinated NEMO.
In a kinase-independent manner, PAK1 serves as a scaffold that regulates Akt recruitment to the membrane and its stimulation by PDK1, thus regulating efficiency, localization and specificity of the PDK1–Akt pathway.
Mono-ubiquitylation of histone H2B is required for methylation of histone H3K4. Ubiquitylation of H2B in turn promotes ubiquitylation of Swd2, a component of the SET1/COMPASS methyltransferase. Inhibiting Swd2 ubiquitylation impairs recruitment of the COMPASS subunit, which is essential for methylation, and results in reduced H3K4 methylation.
The large, multi-functional protein DENN/MADD is an important linker between Rab3 and the kinesin-3 motor proteins KIF1Bβ and KIF1A in the transport of synaptic vesicle precursors.
Abnormal relocalization of A-type lamins to the nuclear envelope in LAP2α-deficient mice impairs pRb-mediated regulation of progenitor cell proliferation and differentiation in highly regenerative tissues.
Mammalian hair follicles are aligned along the anterior–posterior axis. The planar cell polarity genes Vangl2 and Celsr1 are essential for hair follicle polarization and orientation.
A genome-wide screen reveals that the transcription factor Elf5 is epigenetically silenced in the embryonic cell lineage and that its expression is restricted to the trophoblast, where it creates a positive-feedback loop with Cdx2 and Eomes.
In mammalian oocytes, cell polarity is established when meiosis I chromosomes move from the egg centre to the cortex. This translocation is dependent on actin filaments trailing behind the chromosomes, and on the actin-nucleating activity of the formin Fmn2.
ING proteins bind to lamin A. ING1 expression and localization is perturbed in lamin A-null cells. Data from Hutchinson-Gilford progeria syndrome (HGPS) cells, which carry mutations in lamin A, suggest that loss of lamin A–ING interaction may contribute to the HGPS phenotype.
The production of chemoattractants in the pre-metastatic lung can be induced by distant primary tumours. The chemoattractants S100A8 and S100A9 induce serum amyloid A3 and TLR4 activation and cause an inflammation-like state that facilitates metastasis.
Regulatory loops between transcriptional activators and repressors control the circadian clock. A minimal synthetic combination of these transcription factors is sufficient to drive a robust circadian rhythm.