Nature Medicine is the premier journal for biomedical research. Respected internationally for the quality of its papers on areas ranging from infectious disease to cancer and neurodegeneration, Nature Medicine aims to bridge the gap between basic research and medical advances and is consistently ranked the number one journal by the Institute of Scientific Investigation in the Medicine, Research and Experimental category.
Malaria is thought to have shaped the worldwide distribution of human ABO blood but the underlying molecular details of this process have only recently started to be revealed. A new study provides insights on how malaria parasites interact with ABO blood group sugars, mediating rosetting events that cause severe disease.
Developing therapeutics for cancers targeting driver mutations in epigenetic regulators is a challenging frontier in cancer therapy. A new study identifies a pathway that, when activated, inhibits the actions of the histone methyltransferase DOT1L in MLL fusion leukemia.
Type 2 diabetes occurs when the pancreatic beta cells fail to meet the increased insulin requirement in insulin-resistant individuals. A new therapeutic approach targeting glutamate receptors on beta cells improves insulin secretion and preserves beta cell mass.
A study involving a mouse model of Down syndrome and analysis of human postmortem brain samples indicates that hippocampal GABAA receptor signaling in Down syndrome may be excitatory. This advance promises new clinical applications in Down syndrome.
Both chronic and acute treatment of adult Ts65Dn mice with the FDA-approved NKCC1 inhibitor bumetanide suppressed aberrant excitatory GABAAR signaling and rescued synaptic plasticity deficits and cognitive disabilities in this mouse model of Down syndrome.
The authors uncover the mechanism by which DOTL1 exerts its role as an epigenetic regulator required for leukemic progression by counteracting the effects of the chromatin regulators SIRT1 and SUV39H1.
A high-throughput chemical screen reveals that harmine and its analogs promote improved human pancreatic beta cell replication and function, thus identifying these molecules as a potential new class of antidiabetic agents.
William Bishai and colleagues report that cyclic-di-adenosine monophosphate produced during infection with Mycobacterium tuberculosis induces IFN-β and contributes to the innate sensing of tuberculosis.