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The transcription factor Twist1 interacts with the Bmi1 polycomb group protein. This complex is proposed to regulate the epithelial–mesenchymal transition and the tumour-initiating capability of head-and-neck squamous cell carcinoma cells.
Keratin 8 and 18 protect hepatocytes from apoptosis. Inhibiting keratin 18 glycosylation is shown to sensitize cells to liver and pancreatic injury and apoptosis, through a pathway involving Akt and PKCθ.
Mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) lead to accumulation of proteins aggregates in airways. Mutated CFTR promotes transglutaminases-mediated crosslinking of beclin 1, a positive regulator of autophagy, to induce accumulation of LC3-binding protein p62 and prevent autophagic degradation of aggregates.
The role of different histone H3 variants following mouse fertilization has not been addressed. The histone H3.3, and its Lys 27 are involved in the establishment of paternal heterochromatin in the pericentric region of the mouse early embryo, through a mechanism involving dsRNA.
The metabolic enzyme CTP synthase (CtpS) of Caulobacter crescentus can polymerize into cytoskeletal filaments. It functions together with the intermediate filament protein crescentin to control cell shape.
Both endoplasmic reticulum and mitochondrial membranes are thought to contribute to the formation of autophagosomes during autophagy induction. We now learn that plasma membrane is also involved, and is partly targeted to the growing autophagosome through clathrin-mediated endocytosis.
The significance of autophagy for signal transduction has been unclear. Autophagy negatively regulates Wnt signalling by promoting Dishevelled (Dvl) degradation. The von Hippel-Lindau protein ubiquitylates Dvl to faciliatate its recruitment to autophagosomes through p62.
The shelterin complex binds and protects mammalian telomeres. The shelterin component, Rap1, binds to non-telomeric regions and has extra-telomeric functions in transcriptional gene regulation.
Mammalian Rap1 protein is found to have a non-telomeric function in regulating the substrate specificity of IKKs towards the p65 subunit of NF-κB, leading to NF-κB transcriptional activity.
The stress-activated kinase, JNK, is regulated by the anaphase promoting complex (APC) ubiquitin ligase. Conversely, JNK also negatively controls the APC by directly phosphorylating the Cdh1 component of the APC and decreasing its affinity for the APC core subunits.
The non-processive motor, myosin II, is shown to be an effector of the Golgi-associated Rab6 GTPase. The acto-myosin machinery is involved in the fission of transport carriers from Golgi membranes.
Autophagy is involved in tumour suppression. Cytoplasmic FoxO1 is acetylated in response to stress and binds the autophagy regulator Atg7 to promote autophagy, cell death and tumour suppression, independently of its transcriptional activity.
During wound healing, the matricellular protein, CCN1, through its adhesion receptors α6β1 and heparan sulphate proteoglycans, activates senescence in fibroblasts by activation of p53. Senescence induced by CCN1 prevents fibrosis during tissue repair.
Recognition of apoptotic cells by phagocytes is not fully understood. In C. elegans, the transthyretin-like protein, TTR-52, is secreted by the endoderm and clusters around apoptotic cells, inducing their engulfment through the CED-1/6/7 pathway.
Hair follicle stem cells have increased resistance to DNA damage-induced cell death. This is due to higher expression of Bcl2 and to a faster non-homologous end-joining (NHEJ) DNA repair activity, which attenuates p53 activation.
Cyclin-dependent kinase 5 phosphorylates Ape1, a regulator of base excision repair, to reduce its endonuclease activity and increase neuronal death following treatment with neurotoxins. Interestingly, increase in Ape1 phosphorylation is also observed in patients with neurodegenerative diseases.
α-Catenin can respond to myosinII-mediated forces in cell–cell junctions through a force-dependent interaction with vinculin that regulates adherens junction development.
Real-time visualization of single mRNA-protein complexes reveals messenger ribonucleotide protein transport dynamics in the nucleoplasm and determines the translocation time through the pore to be 500 ms. The presence of introns does not affect movement through the nucleoplasm but increases export efficiency.
BH3-only protein tBID induces mitochondrial outer membrane permeabilization in response to death receptor activation. The mitochondrial carrier homologue 2 (MTCH2) protein acts as the tBID receptor on the mitochondria and is required for fas-induced cell death in mouse liver.
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.