A5024585149- Cancer-related molecular mechanisms research
- RNA Research and Splicing
- Bone Metabolism and Diseases
- Circular RNAs in diseases
- Connective Tissue Growth Factor Research
- Inflammatory mediators and NSAID effects
- Kruppel-like factors research
- Genetic factors in colorectal cancer
- Neuroscience and Neuropharmacology Research
- Cancer-related gene regulation
- RNA modifications and cancer
- Gastrointestinal motility and disorders
- Ion channel regulation and function
- Cancer, Hypoxia, and Metabolism
- Epilepsy research and treatment
- Osteoarthritis Treatment and Mechanisms
- Child Nutrition and Feeding Issues
- Congenital gastrointestinal and neural anomalies
- MicroRNA in disease regulation
Wenzhou Medical University
2025
First Affiliated Hospital of Wenzhou Medical University
2025
Hospital for Special Surgery
2023-2024
La Trobe University
2023-2024
Genomics (United Kingdom)
2024
Southern Medical University
2023-2024
Hokkaido University
2023-2024
Cornell University
2024
Paul Ehrlich Institut
2024
New York Hospital Queens
2024
The enteric nervous system (ENS) is recognized as a second brain because of its complexity and largely autonomic control bowel function. Recent progress in studying the interactions between ENS central (CNS) has implicated alterations gut/brain axis possible mechanism pathophysiology autism spectrum disorders (ASDs), Parkinson's disease (PD) other human CNS disorders, whereas underlying mechanisms are unknown lack good model systems. Human induced pluripotent stem cells (hiPSCs) have ability...
Human epiphyseal development has been mainly investigated through radiological and histological approaches, uncovering few details of cellular temporal genetic alternations. Using single-cell RNA sequencing, we the dynamic transcriptome changes during post-conception weeks (PCWs) 15-25 human distal femoral epiphysis cells. We find cells contain multiple subtypes distinguished by specific markers, gene signatures, Gene Ontology (GO) enrichment analysis, set variation analysis (GSVA). identify...
<title>Abstract</title> The IncRNA Malat1 was initially believed to be dispensable for physiology due the lack of observable phenotypes in knockout (KO) mice. However, our study challenges this conclusion. We found that both KO and conditional mice osteoblast lineage exhibit significant osteoporosis. Mechanistically, acts as an intrinsic regulator osteoblasts promote osteogenesis. Interestingly, does not directly affect osteoclastogenesis but inhibits a non-autonomous manner <italic>in...
The IncRNA Malat1 was initially believed to be dispensable for physiology due the lack of observable phenotypes in knockout (KO) mice. However, our study challenges this conclusion. We found that both KO and conditional mice osteoblast lineage exhibit significant osteoporosis. Mechanistically, acts as an intrinsic regulator osteoblasts promote osteogenesis. Interestingly, does not directly affect osteoclastogenesis but inhibits a non-autonomous manner vivo via integrating crosstalk between...
<title>Abstract</title> The IncRNA Malat1 was initially believed to be dispensable for physiology due the lack of observable phenotypes in knockout (KO) mice. However, our study challenges this conclusion. We found that both KO and conditional mice osteoblast lineage exhibit significant osteoporosis. Mechanistically, acts as an intrinsic regulator osteoblasts promote osteogenesis. Interestingly, does not directly affect osteoclastogenesis but inhibits a non-autonomous manner <italic>in...
The IncRNA Malat1 was initially believed to be dispensable for physiology due the lack of observable phenotypes in knockout (KO) mice. However, our study challenges this conclusion. We found that both KO and conditional mice osteoblast lineage exhibit significant osteoporosis. Mechanistically, acts as an intrinsic regulator osteoblasts promote osteogenesis. Interestingly, does not directly affect osteoclastogenesis but inhibits a non-autonomous manner vivo via integrating crosstalk between...
The IncRNA Malat1 was initially believed to be dispensable for physiology due the lack of observable phenotypes in knockout (KO) mice. However, our study challenges this conclusion. We found that both KO and conditional mice osteoblast lineage exhibit significant osteoporosis. Mechanistically, acts as an intrinsic regulator osteoblasts promote osteogenesis. Interestingly, does not directly affect osteoclastogenesis but inhibits a non-autonomous manner vivo via integrating crosstalk between...
The IncRNA Malat1 was initially believed to be dispensable for physiology due the lack of observable phenotypes in knockout (KO) mice. However, our study challenges this conclusion. We found that both KO and conditional mice osteoblast lineage exhibit significant osteoporosis. Mechanistically, acts as an intrinsic regulator osteoblasts promote osteogenesis. Interestingly, does not directly affect osteoclastogenesis but inhibits a non-autonomous manner vivo via integrating crosstalk between...
The IncRNA Malat1 was initially believed to be dispensable for physiology due the lack of observable phenotypes in knockout (KO) mice. However, our study challenges this conclusion. We found that both KO and conditional mice osteoblast lineage exhibit significant osteoporosis. Mechanistically, acts as an intrinsic regulator osteoblasts promote osteogenesis. Interestingly, does not directly affect osteoclastogenesis but inhibits a non-autonomous manner