Unravelling the volcanic history of the enigmatic lunar farside is essential for understanding the hemispheric dichotomy of the Moon1-3. Cratering chronology established for the lunar nearside has been used to suggest long-lived volcanism on the farside of the Moon3,4, but without sample verification. Here we report two newly recognized episodes of basaltic volcanism with Pb-Pb dating for basalt fragments

Despite recent advances in mammalian synthetic biology, there remains a lack of modular synthetic receptors that can robustly respond to soluble ligands and in turn activate bespoke cellular functions. Such receptors would have extensive clinical potential to regulate the activity of engineered therapeutic cells, but to date only receptors against cell surface targets have approached clinical translation1

Thiazoles and isothiazoles are privileged motifs in drug and agrochemical discovery.1,2 The synthesis of these derivatives is generally approached, designed and developed on a case-by-case basis. Sometimes, the lack of robust synthetic methods to a given target can pose significant difficulties or even thwart the preparation of specific derivatives for further study.3,4 Here, we report a conceptually

The continuous evolution of SARS-CoV-2, particularly the emergence of BA.2.86/JN.1 lineage replacing XBB, necessitates re-evaluation of vaccine compositions 1–3. Here, we provide a comprehensive analysis of the humoral immune response to XBB and JN.1 human exposure. We demonstrate the antigenic distinctiveness of XBB and JN.1 lineages in SARS-CoV-2-naive individuals, and JN.1 infection elicits superior

Lytic cell death culminates in plasma membrane rupture (PMR), which releases large intracellular molecules to augment the inflammatory response. PMR is mediated by the effector membrane protein ninjurin-1 (NINJ1)1, which polymerises and ruptures the membrane via its hydrophilic face1–4. How NINJ1 is restrained under steady-state conditions to ensure cell survival remains a mystery. Here we describe

Approximately 3.4 million patients worldwide are diagnosed each year with cancers that harbor pathogenic mutations in one of three RAS proto-oncogenes (KRAS, NRAS and HRAS)1,2. These mutations impair the GTPase activity of RAS, leading to activation of downstream signaling and proliferation3-6. Long-standing efforts to restore the hydrolase activity of RAS mutants have been unsuccessful, extinguishing

The central nervous system (CNS), despite the presence of strategically positioned anatomical barriers designed to protect it, is not entirely isolated from the immune system1,2. In fact, it remains physically connected to and can be influenced by the peripheral immune system1. How the CNS retains such responsiveness while maintaining an immunologically unique status remains an outstanding conundrum