A5027422935- Endoplasmic Reticulum Stress and Disease
- Fibroblast Growth Factor Research
- Ubiquitin and proteasome pathways
- Heat shock proteins research
- RNA Research and Splicing
- RNA modifications and cancer
- Alkaline Phosphatase Research Studies
- Chromatin Remodeling and Cancer
- Muscle Physiology and Disorders
- Cell Adhesion Molecules Research
- Proteoglycans and glycosaminoglycans research
- Epigenetics and DNA Methylation
- Orthopaedic implants and arthroplasty
- Hedgehog Signaling Pathway Studies
- Tumors and Oncological Cases
- Tendon Structure and Treatment
- Cancer, Hypoxia, and Metabolism
- Bone Tumor Diagnosis and Treatments
- Bone fractures and treatments
- MicroRNA in disease regulation
- Cellular Mechanics and Interactions
- Connective tissue disorders research
- Osteoarthritis Treatment and Mechanisms
- Bone Metabolism and Diseases
University of Hong Kong
2007-2024
Chinese University of Hong Kong
2024
University of Hong Kong - Shenzhen Hospital
2020-2021
City University of Hong Kong, Shenzhen Research Institute
2017-2020
In protein folding and secretion disorders, activation of endoplasmic reticulum (ER) stress signaling (ERSS) protects cells, alleviating that would otherwise trigger apoptosis. Whether the stress-surviving cells resume normal function is not known. We studied in vivo impact ER terminally differentiating hypertrophic chondrocytes (HCs) during endochondral bone formation. transgenic mice expressing mutant collagen X as a consequence 13-base pair deletion Col10a1 (13del), misfolded α1(X) chains...
The integrated stress response (ISR) is activated by diverse forms of cellular stress, including endoplasmic reticulum (ER) and associated with diseases. However, the molecular mechanism(s) whereby ISR impacts on differentiation incompletely understood. Here, we exploited a mouse model Metaphyseal Chondrodysplasia type Schmid (MCDS) to provide insight into impact cell fate. We show protein kinase RNA-like ER (PERK) pathway that mediates preferential synthesis ATF4 CHOP, dominates in causing...
The synovial joint forms from a pool of progenitor cells in the future region joint, interzone. Expression Gdf5 and Wnt9a has been used to mark earliest cellular processes formation interzone cells. However, lineage specification progression toward different tissues are not well understood. Here, by lineage-tracing studies we identify population Lgr5+ that contribute cruciate ligaments, membrane, articular chondrocytes joint. This finding is supported single-cell transcriptome analyses. We...
Bone remodeling is a balanced process between bone synthesis and degradation, maintaining homeostasis constant mass in adult life. Imbalance will lead to conditions such as osteoporosis or hyperostosis. Osteoblasts build bone, becoming embedded matrix mature osteocytes. Osteocytes have role sensing translating mechanical loads into biochemical signals, regulating the differentiation activity of osteoblasts residing at surface through secretion Sclerostin (SOST), an inhibitor WNT signaling....
Apoptosis occurs during development when a separation of tissues is needed. Synovial joint formation initiated at the presumptive site (interzone) within cartilage anlagen, with changes in cellular differentiation leading to cavitation and tissue separation. has been detected phalangeal joints development, but its role regulation have not defined. Here, we use mouse model brachydactyly type A1 (BDA1) an Ihh
Abstract Multiple osteochondromas (MO) is an autosomal‐dominant disorder and mutations in EXT1 EXT2 account up to 78% of the cases studied, including missense, nonsense, frameshift, splice‐site mutations. encode glycosyltransferases required for synthesis heparan sulfate (HS) chains. The molecular pathogenesis underlying these still largely unknown. A heterozygous c.1173 + 1G > T ( ) mutation was identified a three‐generation 34‐member MO family present all 19 affected members....