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Bruner et al. report that defective HIV-1 proviruses predominate in early infection, even when antiretroviral therapy is initiated in the first months after infection. The results highlight challenges in estimating the reservoir of intact, replication-competent virus that may influence cure strategies.
Mutation or downregulation of cohesin components confer ERK reactivation and resistance to BRAF or MEK inhibitors in melanoma cells expressing BRAF or NRAS activating mutations.
Damaged erythrocytes accumulate in various pathological conditions, such as hemolytic anemia, anemia of inflammation, and sickle cell disease. In mice challenged with damaged erythorcytes, a monocyte subset migrates to the liver (but not to the spleen), and this subset differentiates into a transient macrophage population that removes the damaged erythrocytes, thus preventing organ damage.
Chemogenetic activation of central nervous system reward circuitry in the mouse VTA is shown to strengthen immunological host defenses against subsequent bacterial exposure and infection.
A new study by Jane Visvader, Geoff Lindeman and colleagues reports on the potential role of RANK signaling in pre-neoplastic breast tissue from BRCA1-mutation carriers and in a mouse model of Brca1-deficient mammary cancer, suggesting that targeting RANK could be explored as an approach to prevent growth of tumors harboring mutated BRCA1.
Li et al. show that the retinoic acid derivative acitretin activates HIV-1 transcription in latently infected T cells and induces RIG-I signaling, which leads to cell death and suggests an approach to reduce the HIV reservoir.
A single injection of FGF1 into the hypothalamic region of the brain in rodents with diabetes achieves sustained normalization of blood glucose levels in these animals.
Cachexia-inducing tumors release complex factors that promote the increased uptake and burning of fats by muscle, resulting in muscle atrophy—a process that can be blocked if fatty acid oxidation is pharmacologically inhibited.
Leukemias bearing heterozygous mutations in the SRSF2 splicing-factor-encoding gene can be therapeutically targeted by pharmacologic inhibition of residual spliceosome function.
Choi et al. identify a Bacteroides fragilis–encoded protease that activates the bacterial enterotoxin and is important for bloodstream infection in mice.
The chemotherapeutic agent doxorubicin causes cardiac injury in a subset of cancer patients. This variable clinical response to doxorubicin treatment can be recapitulated in vitro by using cardiomyocytes derived from patient-specific induced pluripotent cells.
Mark Kay and colleagues report that liver toxicity due to high doses of shRNAs is triggered by a decrease in an isoform of the abundant liver microRNA, miR-122.
Retinal neovascularization, as occurs in age-related macular degeneration, may result from an increase in VEGFA levels due to dysregulated lipid and glucose metabolism within photoreceptors.
In the triple-negative subtype of breast cancer, for which treatment options are limited, overexpression of the MYC oncoprotein is associated with increased sensitivity to growth inhibition by fatty acid oxidation inhibitors, thus pointing to a new therapeutic strategy.
Fatty acid transport from blood vessels to skeletal muscle, across endothelial cells, is regulated by the branched chain amino acid metabolite 3-hydroxy-isobutyrate. This finding provides a mechanistic explanation for the link between high levels of branched chain amino acids and diabetes.
Inhibition of ROR-γt impairs TH17 responses, but not innate lymphoid cells, and is therapeutically effective in mouse models of intestinal inflammation.
Genome-wide DNA methylation analysis of metastatic biopsies from patients with castration-resistant prostate cancer reveals marked epigenetic differences between samples with adenocarcinoma and neuroendocrine histologies.
When encapsulated with alginate derivatives that resist the foreign-body response, human embryonic stem cell–derived beta cells restore long-term normoglycemia in immunocompetent mice without the need for immunosuppression.