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Intracellular force reconstruction of migrating epithelial cells by quantitative fluorescent speckle microscopy. Predicted force fields were derived from F-actin speckle data.
Silvio Berlusconi's government seems set on its course to reform Italy's troubled education system through heavy cuts in funding to schools, universities and scientific research, prompting a belated flurry of protests.
A surprising functional association between TRPM3, a mysterious member of the family of transient receptor potential (TRP) cation channels, and the sulphated version of pregnenolone, 'mother' of all steroid hormones, has been identified.
The spindle assembly checkpoint is crucial for maintaining genome integrity in dividing cells by preventing premature chromosome segregation. Degradation of the APC/C activator Cdc20 seems to be an essential and conserved mechanism to maintain this checkpoint in the presence of chromosomes that are not attached to the mitotic spindle.
Studies in Drosophila melanogaster reveal a mechanism for regulating caspases, the key executioners of the apoptotic cell-death program. An initiator caspase and its activating partner promote degradation of each other, thereby limiting the levels of the active protease complex. This negative-feedback inhibition helps to explain how cells avoid unwanted caspase activation and apoptosis.
The tumour suppressor p53 triggers either cell-cycle arrest or apoptosis. Now, arginine methylation joins a panoply of other post-translational modifications that regulate p53. PRMT5 mediates p53 methylation, which disposes the cell to arrest rather than death.
Modelling intracellular force variations at cell protrusions suggests that cell adhesion is regulated at the interface between vinculin and integrin and reveals a putative feedback between increases in tension and F-actin assembly.
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.
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.
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 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 apoptotic inhibitor IAP1 regulates a feedback loop between the caspase Dronc1 and its apoptosome adaptor Apaf1 to maintain low caspase activity in cells that are not destined to die.
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.
The circadian clock is synchronized with the environment. In mammals, besides light input mediated by Per genes, little is known about resetting mechanisms. TGF-β and activin reset the clock by acting on the circadian gene Dec1.
Human glioblastoma cells release microvesicles containing a diverse set of proteins, miRNAs and mRNAs, which can be taken up by normal host cells that translate the mRNA. Glioma-derived microvesicles carrying the specific tumour markers EGFRvIII and miRNA-21 promote cell proliferation and may serve as a diagnostic tool.
Neurons and cancer cells metabolize glucose extensively. Intracellular gluthatione produced by this metabolic pathway reduces cytochrome c release from mitochondria to increase cell survival.
