Browse Articles

Buried-interface stabilization for efficient and bright blue perovskite LEDs

Distinguishing intrinsic and interfacial pyroelectric effects by polarization reversal measurements

Biomass-based thermally tunable dual afterglow with room temperature daylight visibility

Observation of tunable chiral spin textures with nonlinear optics

Abstract Chiral spin textures, such as spin spirals and skyrmions, are key to advancing spintronics by enabling ultrathin, energy-efficient memory, and high-density data storage and processing. However, their realization remains hindered by the scarcity of suitable host materials and the formidable experimental challenges associated with the characterization of these intricate chiral magnetic states. Here, we report the observation of tunable chiral magnetic textures in van der Waals magnet CrPS 4 with nonlinear optics. These tunable textures exhibit strong chiral third-order nonlinear optical responses, driven by interlayer and intralayer spin couplings under varying magnetic fields and temperatures. These pronounced chiral nonlinear optical responses highlight the potency and high sensitivity of the nonlinear optical readout for probing non-collinear magnetic orders. Moreover, our findings position van der Waals magnets and their heterostructures as an exceptional platform for reconfigurable spin-photonics and spintronics, unifying optical, electrical, and magnetic properties through unique intralayer and interlayer spin coupling properties and effective spin interaction between photons and electrons.

Regulation of H+ transfer pathways promotes C-C coupling in acidic CO2 electroreduction

DNA methylation reprogramming in marsupial embryos is restricted to the extraembryonic lineage

Spatial and network principles behind neural generation of locomotion

Multimodal multitask deep learning for grading management system in non-small cell lung cancer

Nesting behaviour predicts heat tolerance evolution and climate vulnerability in bees

Constraining near-term projections of the South Asian high and Afro-Asian summer monsoon rainfall

HER2∆16 directs luminal cell identity and estrogen receptor signaling in HER2+ breast cancer

Abstract Co-expression of the estrogen receptor (ER) and human epidermal growth factor receptor 2 (HER2) contributes to breast cancer heterogeneity and therapeutic resistance. However, the molecular mechanisms promoting ER positivity within HER2+ cancers remains largely unknown. Here we show, across HER2+ transgenic mouse models the oncogenic HER2 splice variant lacking exon 16 (HER2∆16) promotes the development of aggressive luminal tumors by facilitating an ER-mediated transcriptional program which is sensitive to endocrine therapies. HER2∆16 is detected across human HER2+ breast tumors and cell lines with higher levels correlating with increased expression of ER and downstream transcriptional targets. Notably, in human cell lines HER2∆16 expression is elevated upon acquired resistance to HER2-targeted therapy and can sensitize cells to the ER-antagonist tamoxifen. Overall, these findings offer valuable insights into the role of HER2∆16 in promoting luminal cell identity and estrogen receptor positivity in breast cancer, providing a useful platform to model HER2+/ER+ disease.

Deep learning completes US flood hazard maps revealing millions exposed to previously unrecognized risk

In situ iodine generation enables solution-phase polymerization of organic pollutants for continuous resource recovery from water

Systematic discovery of UFM1 receptors reveals a regulatory module in DNA repair directing non-homologous end-joining

Abstract Posttranslational modifications with ubiquitin-like modifiers (UBLs) are critical for genome maintenance, yet many remain mechanistically uncharacterised. Here, we identify UFM1 as a key regulator of non-homologous end-joining (NHEJ), a major DNA double-strand break repair pathway. Using a structure-guided chemical biology approach, we develop a photo-crosslinkable UFM1 probe and, in combination with NMR, map non-canonical UFM1-binding interfaces in core NHEJ factors, including the disordered XRCC4 tail. Mechanistically, proximity-dependent proteomics and functional assays identify Ku70 as a crucial UFMylation substrate and reveal a UFM1-dependent axis in which XRCC4 engages UFMylated Ku70 to stabilise NHEJ complex assembly on chromatin. Disruption of this molecular mechanism via UFSP2 depletion or a hypomorphic UBA5 variant in patient-derived cells impairs NHEJ function, linking UFMylation defects to compromised genome integrity processes. Our findings define a complete UFM1 signalling module in DNA repair and establish a generalisable framework for dissecting low-affinity UBL networks with broad functional and disease relevance.

Graphdiyne confined-membrane with intrinsic in-plane-pores for angstrom-scale gas sieving

Machine-learning-guided inverse design of lead-free relaxors enabled by multimodal literature mining

SMARCA4 loss reprograms p300 chromatin occupancy to subvert p53-mediated transcriptional repression in ovarian small cell carcinoma

Tumor suppressor genotype influences the extent and mode of immunosurveillance in lung cancer

Abstract The impact of cancer driving mutations on immunosurveillance throughout tumor development remains poorly understood. To better understand the contribution of tumor genotype to immunosurveillance, we generated and validated lentiviral-based vectors that create increasingly immunogenic neoantigens. This vector system is compatible with autochthonous Cre-regulated cancer models, CRISPR/Cas9-mediated somatic genome editing, and tumor barcoding. Here, we show that in the context of oncogenic KRAS-driven lung cancer and strong neoantigen expression, tumor suppressor genotype dictates the degree of immune cell recruitment, positive selection of tumors with neoantigen silencing, and tumor outgrowth. By quantifying the impact of 11 commonly inactivated tumor suppressor genes on tumor growth across neoantigenic contexts, we show that the growth-promoting effects of tumor suppressor gene inactivation correlate with increasing sensitivity to immunosurveillance. Importantly, some genotypes also dramatically changed sensitivity to immunosurveillance independently of their growth-promoting effects. We propose a model of immunoediting in which tumor suppressor gene inactivation works in tandem with neoantigen expression to shape tumor immunosurveillance and immunoediting such that the same neoantigens uniquely modulate tumor immunoediting depending on the genetic context.

A minimal chemo-mechanical Markov model for rotary catalysis of F1-ATPase

Abstract F 1 -ATPase, the catalytic domain of ATP synthase, is pivotal for mechano-chemical energy conversion in mitochondria. Aiming at a minimal yet quantitative and thermodynamically consistent model for its rotary catalysis mechanism, here we developed a chemo-mechanical Markov model incorporating essential conformational and chemical degrees of freedom. By systematically evaluating over 14,000 model variants via Bayesian inference and cross-validation, we find that a fully functional minimal model requires four functionally distinct $${\beta}$$ β -subunit conformations. Our model reconciles the decade-long bi-site versus tri-site controversy, showing that both pathways contribute depending on ATP concentration. Furthermore, our model suggests a Brownian-ratchet-like mechanism that explains the observation that one ATP hydrolysis event can trigger larger than 120º rotations, thereby explaining seemingly over 100% efficiency. Beyond this prototypic example of a complex biomolecular machine, our approach should enable one to study other enzymatic mechanisms that implement close coupling between conformational motions, substrate binding, and chemical reactions.

TASP1-mediated cleavage of REV3L enhances the activity of DNA polymerase ζ in mammalian cells