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The bromodomain and extraterminal (BET) inhibitor JQ1 synergizes with the histone deacetylase inhibitor SAHA to suppress tumor growth in mouse models of pancreatic cancer.
Upregulation of the ATP-dependent ACF chromatin-remodeling complex in the NAc is a necessary and causal component for susceptibility to stress-induced depressive behaviors in mice, and this complex is also shown to be upregulated in the NAc of depressed humans.
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.
MALDI mass spectrometry shows distinct patterns of drug distribution in tuberculosis lesions in human lungs that provide insight into treatment efficacy.
Kidney fibrosis is a main pathological component of chronic kidney disease. Two new studies pinpoint a partial epithelial-to-mesenchymal transition as a mechanism driving the development of kidney fibrosis, thus paving the way for novel treatments of fibrosis-associated diseases.
A new study identifies the RAS-MAPK pathway to be an Achilles' heel of EML4-ALK fusion-positive lung cancer and suggests that up-front combination therapy directed against both pathways can achieve sustained suppression of tumor growth.
As medical use of cannabis becomes more commonplace, scientists seek to conduct rigorous studies that can define its benefits and risks for various disease indications. But overly cumbersome government regulations continue to create logistical and funding burdens.
Seven years after the launch of the Human Microbiome Project, we still lack sufficient tools to visualize the microbiome in a living host. A new study provides experimental tools to label and track live anaerobic bacteria in the microbial communities in the mouse gut and beyond.
Disease models inform our understanding of central nervous system disorder pathogenesis and enable testing of novel therapeutics. A frank discussion of the rationale for using particular disease models, as well as their limitations, may enable comparisons between studies and facilitate drug development.
In this Perspective, the authors discuss the currently available models for psychiatric disease modeling. They present a framework for translating new knowledge by placing more emphasis on identifying neurophysiological defects.