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Joyal et al. (p 439) show that dysregulated lipid and glucose metabolism within photoreceptors can lead to retinal neovascularization, as occurs in age-related macular degeneration. The cover shows a 3D scanning electron microscopy image of pseudo-colored photoreceptor mitochondria in wild-type mice. Image credit: Michael Powner and Marcus Fruttiger. Artwork by Erin Dewalt.
Ablation of the tumor suppressor phosophatase and tensin homlog (PTEN) unexpectedly suppresses the development of pre-B acute lymphoblastic leukemia (ALL).
Human T cells that target tumor-specific mutations are attractive for cancer immunotherapy, but obtaining these T cells is challenging. A new study shows that tumor mutation–specific T cells can be isolated from the peripheral blood of patients with melanoma.
Current dogma suggests that high-energy–consuming photoreceptors depend on glucose. A new study reveals that the retina also uses fatty acid b-oxidation for energy, and that dysregulated lipid and glucose photoreceptor energy metabolism may drive neovascular age-related macular degeneration (AMD).
A new study with patient stem cell–based modeling of Smith-Lemli-Opitz syndrome (SLOS) shows that the accumulation of a specific cholesterol precursor dysregulates the Wnt/b-catenin pathway, which in turn leads to precocious neural differentiation.
Hessell et al. report that post-exposure treatment with HIV-1–specific neutralizing antibodies clears SHIV infection from the blood and tissues of infant rhesus macaques.
Genomic analysis of a single metastasis informs about the oncogenic—and potentially druggable—genomic alterations present in other tumors within the same man with metastatic prostate cancer.
Analysis of SLOS patient-derived iPSCs reveals that cellular accumulation of the cholesterol precursor 7DHC, rather than cholesterol deficiency, causes dysregulation of Wnt/β-catenin signaling and aberrant neural differentiation.
In a rat model of spinal cord injury, calpain-dependent cleavage of motoneuron sodium channels can be pharmacologically targeted to achieve long-lasting amelioration of spasticity.
As beta cells age their levels of p16 rise, and the cells become senescent; rather than leading to dysfunction, this results in an increased capacity of the beta cells for glucose-stimulated insulin secretion.
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.
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.
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.