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AML cells carrying R882 mutations in DNMT3A fail to sense and repair DNA damage induced by standard-dose chemotherapy as a result of impaired chromatin remodeling
Selective pharmacological blockade of forebrain excitatory AMPA receptors that express the TARP γ-8 subunit enables antiepileptic therapy in rodent models of epilepsy without inducing motor impairments associated with currently used antiepileptic drugs.
Antibodies elicited by vaccination with influenza vaccine produced in eggs bind more strongly to the egg-adapted vaccine strain than to wild-type circulating strains.
Analysis of T cells isolated from patients with and without type 1 diabetes reveals reactivity to a range of native as well as post-translationally modified self-antigens only in individuals with T1D.
In triple-negative breast cancer, the PIM1 kinase is highly expressed, acts to promote tumor cell survival and growth, and increases MYC transcriptional activity.
Whole-genome sequencing identified recurrent fusions involving the MET oncogene, and MET inhibitors suppressed tumor growth in mouse models and in a human patient.
Dietary zinc supplements are in common use, but their effect on infection is unclear. New findings now show that excess dietary zinc reduces the diversity of the gut microbiota and increases the susceptibility of antibiotic-treated mice to Clostridium difficile infection.
In a mouse model of traumatic brain injury, treatment with a carbon-monoxide-releasing molecule is shown to reduce pericyte cell death and promote neurogenesis, leading to an amelioration of neurological deficits.
Differences in the composition of the gut microbiota of infants associate with relative risk of atopy in childhood, and metabolites linked with these distinct microbial states alter T cell differentiation ex vivo.
The ubiquitin-specific protease HAUSP deubiquitinates and stabilizes N-Myc, and small-molecule inhibitors of HAUSP suppress the growth of MYCN-amplified human neuroblastoma cell lines implanted in mice.
The ability of transplanted neural stem cells to ameliorate neuropathological and behavioral phenotypes after experimental stroke in mice is enhanced by co-treatment with 3K3A-APC, which acts to stimulate neuronal differentiation and functional integration within the host circuitry.
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.