Cell Death, Stem Cell and Immunology
A web focus from Cell Death & Differentiation, Cell Death & Disease and Nature Communications. Recent progress in cell death, stem cell biology and cancer research has created a new paradigm of research direction, shifting from pure analytical approaches toward a more translational one with animals and patients. The purpose of this focus is to cover a variety of important topics in cancer and immunology research under the main theme: "Cell Death, Stem Cell and Immunology."
From Cell Death & Differentiation
From Cell Death & Disease
From Nature Communications
Cytotoxicity of botulinum neurotoxins reveals a direct role of syntaxin 1 and SNAP-25 in neuron survival
Botulinum toxins can cause substantial neurodegeneration. Peng et al. study cultured rat hippocampal neurons and find that botulinum toxin-induced cytotoxicity occurs only when there is effective cleavage of the SNARE proteins, syntaxin 1 or SNAP-25, by type C and type E botulinum toxins.
Multifunctional S100 proteins are upregulated in brain injury, but their role in neurodegeneration is not clear. Dmytriyeva and colleagues study in vivomodels of brain trauma and find that the S100A4 protein and its peptide mimetics protect neurons via the interleukin-10 receptor and the Janus kinase (JAK)/STAT pathway.
Irradiation treatment for cancer therapy often causes irreparable damage to adult organs. Knox and colleagues study irradiated mouse submandibular salivary glands and find that restoring parasympathetic nerve function with the neurotrophic factor neurturin improves regeneration.
Ubiquitination and degradation of the FADD adaptor protein regulate death receptor-mediated apoptosis and necroptosis
Fas-associated protein with death domain (FADD) is part of a signalling complex that controls some forms of programmed cell death. Lee and colleagues demonstrate that FADD ubiquitination by the E3 ubiquitin ligase MKRN1 regulates FADD protein stability and thereby cell death.
Ectopic expression of the histone methyltransferase Ezh2 in haematopoietic stem cells causes myeloproliferative disease
The histone methyltransferase Ezh2 is thought to have a dual function both as a tumour suppressor and an oncogene. Using mouse models with Ezh2 gain-of-function, Herrera-Merchanet al. show that Ezh2 expression in HSCs severely compromises hematopoietic function, leading to myeloproliferative disease.
Damaged mitochondria are eliminated from the cell by a form of autophagy called mitophagy. Here the authors show that during mitophagy, specific proteins are rescued from degradation by evacuation from the mitochondria to the endoplasmic reticulum.
Extracellular Ca2+ is a danger signal activating the NLRP3 inflammasome through G protein-coupled calcium sensing receptors
Levels of extracellular calcium can increase at sites of infection and inflammation; however, the physiological significance of this has been unclear. This work shows that extracellular calcium acts as a danger signal, triggering the NLRP3 inflammasome via two G protein-coupled receptors.