Structural Rewiring of IL-7R Dimerization by an Oncogenic Transmembrane Mutation Can Be Reversed by Rational Design

Mutations in transmembrane domains (TMDs) of cytokine receptors often drive ligand-independent signaling in cancer, yet their mechanisms remain unclear. Here, we show that an oncogenic mutation in the IL-7 receptor rewires its dimerization mode to enable constitutive activation. Structure-guided transmembrane peptides selectively disrupt this aberrant signaling, providing a strategy to target disease-causing TMD mutations.

Glucose Hypometabolism and p-Tau Reveal a Synergistic Mechanism in Alzheimer’s Disease

This study elucidates the molecular mechanism by which reduced glucose metabolism and p-Tau synergistically drive AD progression through regulating the RIPK1-mediated necroptosis pathway.

From single-cell fate divergence to extracellular protease–mediated terminal events: redefining necrotic cell death

Long-Range Force Between Proteins Drives Dynamics of Transmembrane Signaling

Native NMDA Receptor Structures Reveal Conformational Diversity and Fully Opening Mechanism

Researchers Developed a Deep-Coverage, High-Throughput Method for Single-Cell Metabolomics

Alzheimer’s & Dementia | Kaiwen He's Research Team Identifies a Locus Coeruleus–Driven Mechanism Underlying Early Sleep Disturbances in Alzheimer’s Disease

This study not only identifies the locus coeruleus as a key brain region driving early sleep disturbances in AD but also elucidates the molecular and circuit mechanisms underlying these changes. Moreover, it highlights α2A adrenergic receptors and Kv7 potassium channels as promising therapeutic targets for early intervention, providing new insights for the development of precision treatments targeting prodromal sleep symptoms in AD.

Next steps in regulatory T cells: Biology and clinical application

The article highlights Tregs as “living drugs” that restore immune tolerance and promote tissue repair, outlines key clinical milestones, and discusses remaining challenges and future directions for precision Treg-based therapies.

Kai-Wen He’s lab revealed the neural mechanism of early cortico-striatal decoupling in a Parkinson's Disease-like mouse model

The authors first established a methodology based on fiber photometry to assess coupling between the primary motor cortex (M1) and the striatum. They demonstrated that this method offers cell-type-specific resolution and can distinguish between coupling patterns associated with different behavioral paradigms (Fig. 1 I).

Turbocharging the AAA+ ATPase Motor: Zairong Zhang’s Lab Identifies a Power-Boosting Module Essential for Ubiquitin-Mediated Protein Degradation

This study identifies a previously unrecognized ubiquitin-binding helix (UBH) in UBX-containing cofactors such as FAF2 and FAF1, revealing it as a conserved module that boosts the mechanical output of the p97-UFD1L-NPLOC4 unfoldase. By enhancing substrate engagement and doubling p97’s working ATPase and unfolding activities, the UBH-UBX module enables extraction of challenging ubiquitinated proteins from membranes and other large assemblies. These findings uncover a fundamental mechanism shared across organelle quality-control pathways and suggest new targets for modulating protein homeostasis in disease.