Browse Articles

Synthesis of Bicyclo[2.1.0]pentanes and Vinylcyclopropanes Using Palladium Carbenes: Ligand-Controlled Carbene Reactivity

Enantioselective Assembly of (Hetero)aryl Alkyl Sulfilimines via Copper-Catalyzed <i>S</i>-Arylation of <i>S</i>-Alkyl Sulfenamides with (Hetero)aryl Iodides

Ubiquitous Chiral Symmetry Breaking of Conjugated Polymers via Liquid–Liquid Phase Separation

Flexibility-Induced Robustness in Molecular Catalysts for Electrocatalytic CO₂ Reduction

Anharmonic Phonon Scattering Triggering Multi-ion Migration in Oxide-Based Superionic Conductors

Unveiling the Origin of Morphological Instability in Topologically Complex Electrocatalytic Nanostructures

Cofactor-independent photo-enzymatic reductions with water mediated by reductive graphene quantum dots

Cation-Controlled Assembly, Activity, and Organization of Biomimetic DNA Receptors in Synthetic Cell Membranes

GALNTL5 binds GalNAc and is required for migration through the uterotubal junction and sperm-zona pellucida binding

Abstract More than 20 genes expressed in the male reproductive tract have been identified as essential factors for sperm migration to and through the utero-tubal junction (UTJ), and they are divided into ADAM3-dependent and ADAM3-independent pathways. In parallel, sperm having UTJ migration defects also show impaired binding to the zona pellucida (ZP). Herein, we demonstrate that knockout of Galntl5, encoding a sperm surface protein, causes impaired sperm binding with the UTJ and ZP, and null males have severe infertility. GALNTL5 appreciably disappears in sperm lacking Adam3 or Lypd4, required for ADAM3-dependent and ADAM3-independent pathways, and GALNTL5 binds to N-acetylgalactosamine (GalNAc) distributed on the UTJ and ZP. Blockage of GalNAc decreases the number of sperm binding to the UTJ and ZP. Thus, we unveil that GALNTL5 is a responsible factor for UTJ migration and sperm-ZP binding, and that sperm bind to the UTJ and ZP through interaction of GALNTL5 and GalNAc.

Naiavirus: an enveloped giant virus with a pleomorphic, flexible tail

Oxidatively Induced Reductive N₂ Binding: A Dinickel-Bridging Bent N₂ Radical Anion and Its Redox-Triggered N₂ Release

NR3C1 limits the imprinting of astrocyte epigenetic inflammatory memory early in life

Water as an Electron Donor for Cross-Electrophile Coupling Reactions

Efficient and dynamic neural geometry of value and modality encoding in the primate putamen for value-guided behavior

<i>Aspergillus fumigatus</i> Metallothionein CmtA Binds and Receives a [2Fe-2S] Cluster from Monothiol Glutaredoxin GrxD

Southern Ocean CO2 outgassing and nutrient load reduced by a well-ventilated glacial North Pacific

Abstract Southern Ocean biogeochemistry impacts global nutrient distributions, carbon cycling, and climate, motivating study of its underlying controls across different climate states. Today, poorly-ventilated North Pacific waters supply the majority of carbon and nutrients upwelling in the Southern Ocean, outpacing biological carbon uptake and fueling CO 2 outgassing. Reducing this supply is both central to glacial CO 2 theories involving reduced outgassing and well-supported by paleo-proxy reconstructions. While past studies emphasize physical processes (reduced upwelling, enhanced stratification), we propose a complementary mechanism where the carbon/nutrient load of waters feeding the Southern Ocean surface is reduced remotely, prior to being upwelled. Comparing glacial North Pacific and Southern Ocean proxy records, alongside Earth System Model simulations, we show that ventilating the glacial North Pacific reduces the carbon/nutrient content of waters supplying the Southern Ocean surface and Subantarctic CO 2 outgassing. This highlights an interhemispheric influence on Southern Ocean biogeochemical conditions that could modulate glacial-interglacial CO 2 variability.

Pillar-like Macrocycle Reversibly Self-Assembled from a Molecular Thermally Activated Delayed Fluorescence Emitter Based on B ← N Dative Bonds with Intriguing Fluorescence

Deep microbial colonization during impact-generated hydrothermal circulation at the Lappajärvi impact structure, Finland

Abstract Deeply fractured rocks of meteorite impact structures have been hypothesized as hot spots for microbial colonization on Earth and other planetary bodies. Biosignatures of such colonization are rare, however, and most importantly, direct geochronological evidence linking the colonization to the impact-generated hydrothermal systems are completely lacking. Here we provide timing constraints to microbial colonization of the 77.85 ± 0.78 Ma old Lappajärvi impact structure, Finland, by using coupled microscale stable isotope biosignature detection and radioisotopic dating of vug- and fracture-filling assemblages in impactites. The first detected mineral precipitation at habitable temperatures for life (47.0 ± 7.1 °C) occurred at 73.6 ± 2.2 Ma and featured substantially 34S-depleted pyrite consistent with microbial sulfate reduction. Later stages of vug-mineral precipitation occurred more than 10 Myr later, at gradually lower temperatures, and featured δ13Ccalcite values diagnostic for both anaerobic microbial consumption and production of methane. These insights confirm the capacity of medium-sized (and large) meteorite impacts to generate long-lasting hydrothermal systems, enabling microbial colonization as the crater cools to ambient conditions, an effect that may have important implications for the emergence of life on Earth and beyond.

CO Adsorbates Induced Framework-Associated Low-Valence Co^δ+ Sites in Co-ZSM-5 for Ethane Dehydrogenation

RBM39 degrader invigorates innate immunity to eradicate neuroblastoma despite cancer cell plasticity

Abstract The cellular plasticity of neuroblastoma is defined by a mixture of two major cell states, adrenergic and mesenchymal, which may contribute to therapy resistance. However, how neuroblastoma cells switch cellular states during therapy remains largely unknown, and how to eradicate neuroblastoma regardless of its cell state is a clinical challenge. To better understand the cellular plasticity of neuroblastoma in chemoresistance, we define the transcriptomic and epigenetic map of adrenergic and mesenchymal types of neuroblastomas using human and murine models treated with indisulam, a selective RBM39 degrader. We show that cancer cells not only undergo a bidirectional switch between adrenergic and mesenchymal states, but also acquire additional cellular states, reminiscent of the developmental pliancy of neural crest cells. These cell state alterations are coupled with epigenetic reprogramming and dependency switching of cell state–specific transcription factors, epigenetic modifiers, and targetable kinases. Through targeting RNA splicing, indisulam induces an inflammatory tumor microenvironment and enhances the anticancer activity of natural killer cells. The combination of indisulam with anti-GD2 immunotherapy results in a durable, complete response in high-risk transgenic neuroblastoma models, providing an innovative, rational therapeutic approach to eradicate tumor cells regardless of their potential to switch cell states.