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Acetylation of tau at K174 is identified in Alzheimer's disease (AD) brain tissue and exacerbates tau-mediated neurodegeneration and memory impairments in mice. Pharmacological inhibition of tau acetylation ameliorates these phenotypes in a mouse model of AD.
In NOTCH-induced T cell acute lymphoblastic leukemia, the resistance to anti-NOTCH therapy conferred by loss of the Pten tumor suppressor is linked to reversal of the effects of NOTCH inhibition on leukemic cell metabolism.
Two studies demonstrate that the methyltransferase KMT2D, which is recurrently mutated in several types of human B cell lymphoma, suppresses tumorigenesis by altering the epigenetic landscape of B cells; Kmt2d deletion in mice perturbs normal B cell development.
Two studies demonstrate that the methyltransferase KMT2D, which is recurrently mutated in several types of human B cell lymphoma, suppresses tumorigenesis by altering the epigenetic landscape of B cells; Kmt2d deletion in mice perturbs normal B cell development.
Minimal reduction of PU.1 in mice is sufficient to elicit a preleukemic state that, when combined with a DNA mismatch repair defect, results in progression to myelodysplastic syndrome and acute myeloid leukemia.
Although previous work indicated that the antitumor effects of anti-CD47 require macrophage phagocytosis of tumor cells, new work done in immunocompetent mice bearing syngeneic tumors reveals a key role for dendritic cell cross-priming of CD8+ T cells.
The membrane protein Nogo-B, resident in the endoplasmic reticulum, acts in endothelial cells to inhibit the rate-limiting enzyme of the de novo pathway of sphingolipid biosynthesis, thereby regulating vascular function and blood pressure.
The gut and oral microbiomes are altered in individuals with rheumatoid arthritis, and these changes can be used to stratify individuals for diagnostic and prognostic purposes.
Carl June and colleagues report the results of a phase I/II trial of adoptively transferred engineered T cells in patients with advanced multiple myeloma.
Nicotinamide N-methyltransferase acts through its product, N1-methylnicotinamide, to stabilize Sirt1 and thus regulate hepatic glucose and lipid metabolism.
Whole-genome and targeted sequencing of multiple sections of each of 50 tumors reveals varying degrees of subclonal diversification and genomic heterogeneity.
BMP9 activates signaling through the BMPR-II receptor in endothelial cells and reverses established disease in three animal models of pulmonary hypertension, thus pointing to a potential new treatment for this disease.