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Hongyi Gao

Publications and source records attributed to Hongyi Gao.

3 recordsLinked to original sources

Engineering local nitrogen coordination environments of Palladium subnanometric clusters in metal-organic frameworks for efficient hydrogenation.

Subnanometric clusters (SCs) bridge the gap between single-atom catalysts and nanoparticles by combining high atomic utilization with cooperative multi-atom effects. However, stabilizing low-coordinated SCs while maintaining accessible active sites remains challenging. Here, we introduce pyrazole-3,5-dicarboxylic acid (PZDC), pyridine-3,5-dicarboxylic acid (PDC), and pyrrole-3,5-dicarboxylic acid (PPy) as secondary ligands in metal-organic frameworks to regulate the local nitrogen (N) coordination environment of Pd SCs (∼0.6 nm). Specifically, PZDC provides a chemically differentiated pyrazolic dual-N environment containing formally pyridinic-like and pyrrolic-like N sites. Aberration-corrected high-angle annular dark-field scanning transmission electron microscopy (AC HAADF-STEM) and X-ray absorption spectroscopy (XAS) confirm the formation of low-coordinated Pd clusters containing PdN and PdPd interactions, while CO diffuse reflectance infrared Fourier transform spectroscopy (CO-DRIFTS) reveals a distinctive adsorption environment characterized by geminal dicarbonyl species and strongly suppressed bridge-bonded CO adsorption. Within this catalyst series, the PZDC-functionalized material exhibits the highest activity and tetrahydrocyclopentadiene (THDCPD) selectivity in dicyclopentadiene (DCPD) hydrogenation. These results demonstrate that modification of the local N environment can regulate the average coordination structure, adsorption behavior, and catalytic properties of MOF-supported Pd SCs.

Hydrogenation catalysis

Controlled framework nickel exsolution in metal-organic frameworks creates confined active sites for chemoselective citral hydrogenation.

Selective hydrogenation of citral to citronellal over non-noble-metal catalysts remains challenging because highly active metallic Ni simultaneously promotes efficient substrate activation and undesired over‑hydrogenation of the desired product. Herein, we develop a controlled exsolution strategy in waste polyethylene terephthalate (PET)-derived nickel metal-organic frameworks (Ni-MOFs) to transform framework Ni into confined metallic active sites while preserving the porous framework architecture. During reductive treatment, framework Ni2+ species undergo gradual node-to-metal evolution, generating highly dispersed Ni0 sites confined within the partially retained MOF framework. More importantly, the degree of framework Ni exsolution governs the balance between citral activation and citronellal over‑hydrogenation, thereby establishing a distinct chemoselective window. Within the optimal exsolution regime, the framework-confined Ni0 sites enable efficient H2 activation and selective hydrogenation of the CC bond while suppressing the subsequent hydrogenation of citronellal. Consequently, the optimized catalyst achieves ∼99% citral conversion and 100% citronellal selectivity at 90 °C and 2 MPa H2, together with excellent catalytic stability and recyclability. Beyond the sustainable valorization of waste PET, this work establishes controlled framework exsolution as an effective strategy for engineering confined active sites and regulating chemoselectivity in non-noble-metal hydrogenation catalysts.

Chemoselective hydrogenation

NOTCH3 Internal Tandem Duplication Defines a Novel Oncogenic Activation Mechanism of NOTCH Signaling.

NOTCH signaling is activated in tumors through multiple mechanisms, including mutations, gene rearrangements, and gene amplification. We report a novel activation mechanism, an internal tandem duplication (ITD) near the NOTCH3 negative regulatory region (NRR), found in a myogenic mesenchymal neoplasm. This 17-amino acid residue duplication disrupts the tightly autoinhibited structure surrounding the S2 cleavage site, resulting in ligand-independent S2 cleavage and constitutive pathway activation, as demonstrated by increased expression of the NOTCH3 target gene HES1. Cells expressing NOTCH3-ITD showed increased nuclear localization of the receptor and exhibited malignant phenotypes, including enhanced proliferation and migration. Together, these findings support the oncogenic role of NOTCH3-ITD.

Receptor, Notch3