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.
A recent paper in Nature shows that tumor exosomes expressing unique integrins can determine organotropic metastasis by preparing pre-metastatic niche through their integrins-mediated fusion with and fertilization of organ-specific resident cells.
Classical inflammatory monocytes and their derivative macrophages promote tumor metastasis whereas CD8+ T and NK cells restrict tumor growth. In a recent paper published in Science, Hanna and colleagues demonstrate that another monocyte population, nonclassical patrolling monocytes, is enriched in the microvasculature of tumor-challenged lung and reduces tumor metastasis by recruiting NK cells.
Liquid biopsy is ideal for early diagnosis of cancer and for prognosis upon treatment. Wen et al. describe a methylated CpG tandems amplification and sequencing method to profile hypermethylated CpG islands genome-widely in cell-free DNA, and further identify high performance markers in blood for potential detection of early stage hepatocellular carcinoma.
Adding to the Histone Code at DNA double-strand breaks, Mailand and colleagues now uncover non-degradative ubiquitin marks on linker histone H1 as key signaling intermediates in the DNA damage signal transduction cascade.
A paper recently published in Science reports that adenosine deaminase acting on RNA 1-dependent adenosine-to-inosine editing marks endogenous double strand RNA as self and prevents their immune recognition by cytosolic RNA sensor MDA5.
Inflammasomes control host cell death and inflammation in response to sterile or infectious stimuli. Two recent reports published in Science reveal the structural basis for the assembly of NAIP-NLRC4 inflammasomes.
The mammalian target of rapamycin (mTOR), a protein kinase, is the centre of huge attention due to its importance in intracellular signaling and in health and disease. In their recent study, Yin et al. show that mTOR can regulate signaling through the insulin-like growth factor 1 receptor and that it possesses a new enzymatic activity — the ability to phosphorylate proteins on tyrosine residues.
Chimeric antigen receptors (CARs) are synthetic receptors capable of directing potent antigen-specific anti-tumor T cell responses. A recent report by Wu et al. extends a series of strategies aiming to curb excessive T cell activity, utilizing in this instance a chemical dimerizer to aggregate antigen-binding, T cell-activating and costimulatory domains.
BET inhibition has emerged as a promising epigenetic therapy for malignancies in the last five years, but little consensus has developed regarding what may mediate the axis between sensitivity and resistance. Two recent papers published in Nature attempt to address this question in acute myeloid leukemia (AML) and independently identify the Wnt signaling pathway as a driver and biomarker of therapeutic resistance.
In a surprising twist, a hitherto unrecognized cleavage of the amyloid precursor protein (APP) by η-secretase, followed by α- or β-secretase cleavage releases a novel APP proteolytic fragment, Aη, which causes synaptic injury.
Inflammatory caspases drive a lytic form of cell death called pyroptosis in response to microbial infection and endogenous damage-associated signals. Two studies now demonstrate that cleavage of the substrate gasdermin D by inflammatory caspases necessitates eventual pyroptotic demise of a cell.
To maintain homeostasis, organs replace cells lost through normal cellular turnover, often through the straightforward replication of existing cells. A recent paper in Nature shows that cells in the liver are not equivalent when it comes to their replicative capacity; rather, a subset of hepatocytes defined by the maintenance of active Wnt signaling bears the brunt of responsibility for maintaining liver mass.
Anticancer therapeutics aimed at the inhibition of mTORC1 activity shift metabolism to favor the degradation of extracellular proteins. Recently Thompson and colleagues demonstrated a novel regulatory mechanism whereby mTORC1 plays a distinct role as a key regulator of metabolism depending on the environmental nutrient status.
Two proteolytic enzymes, β- and γ-secretases, work together to produce the amyloid β-peptide of Alzheimer's disease. New evidence suggests that these proteases directly interact and compounds that disrupt this interaction reduce amyloid β-peptide levels without directly blocking either enzyme's solo activity.
Cytosines in genomic DNA come in different flavors. A recent paper published in Nature reveals that an oxidized variety, 5-carboxylcytosine, is recognized by the elongating RNA polymerase, shedding light on the role of DNA oxidation in transcription regulation.
A recently paper published in Cell reports that dendritic cells (DCs) are dysfunctional in the tumor environment. Tumor impairs DC function through induction of endoplasmic reticulum stress response and subsequent disruption of lipid metabolic homeostasis.
High sodium consumption has been raising interest as a putative environmental factor linking Western lifestyle to the growing epidemic of autoimmune and inflammatory diseases. Now Zhang and colleagues show that high sodium drives macrophage to acquire a new proinflammatory effector phenotype with a distinct signature, paving the path to assess the role of salt-activated macrophages in human disease.
Neuronal activity-induced gene expression is crucial for the development and plasticity of the brain and for learning and memory. In a recent study published in Cell, Madabhushi et al. report that neuronal activity triggers the formation of DNA double-strand breaks on promoters of early response genes, which in turn controls their expression in neurons.
Culturing intestinal stem cells into 3D organoids results in heterogeneous cell populations, reflecting the in vivo cell type diversity. In a recent paper published in Nature, Wang et al. established a culture condition for a highly homogeneous population of intestinal stem cells.
