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One or more keywords matched the following properties of Shim, Jae-Hyuck
keywords Bone fracture, large bone defect

Bone mass reflects the coupled balance of activity of osteoblasts to synthesize and osteoclasts to degrade bone matrix.  Coupling of the activity between these two lineages is required for balance in bone remodeling, and dysregulation of this process is a major mechanism in the pathogenesis of many of human skeletal disorders, such as osteoporosis, inflammation-induced bone loss, and periodontitis. Additionally, osteoblast differentiation capacity of skeletal stem cells must be tightly controlled, as inadequate bone formation results in low bone mass, skeletal fragility, and bone healing defect, while over-exuberant osteogenesis results in extra-bone formation in the soft connective tissues, such as trauma-induced heterotopic ossification and fibrodysplasia ossificans progressiva by a genetic mutation.

Understanding the molecular mechanisms that regulate these activities is a key to developing improved therapeutics to treat human skeletal disorders. To this end, we took advantage of an unbiased high-throughput screens to identify new proteins that control osteoblast and osteoclast commitment, differentiation, and activation under pathological conditions. Alternatively, using the premise that tissues emerging from similar points during vertebrate evolution may share common intracellular signaling networks to guide their activity, we have sought to leverage our extensive knowledge obtained from the immune system to understand the mechanism in which bone cells are regulated. 

For the above proteins that we identified, we have developed sophisticated in vivo gene transfer technologies. In these technologies, nanoparticles, liposomes, exosomes, or adeno-associated virus (AAV) are modified to home to the bone surface and deliver RNA interference and/or healthy gene to osteoblasts and osteoclasts, thus affecting their activity. The impact of this work could have far reaching effects. If the molecular pathways regulating osteoclast/osteoblast coupling can be better understood, then targeted approaches to promote osteoblast activity via systemic infusion or local implantation could be used as a therapeutic approach for patients suffering with low bone density disorders, such as osteoporosis, bone fracture healing defect, or critical-sized bone defect. Furthermore, these technologies can be used to directly correct a genetic mutation in the body in order to treat and/or cure skeletal rare diseases with monogenic mutations, such as fibrodysplasia ossificans progressiva or osteogenesis imperfecta.


One or more keywords matched the following items that are connected to Shim, Jae-Hyuck
Item TypeName
Academic Article MLK3 regulates bone development downstream of the faciogenital dysplasia protein FGD1 in mice.
Concept Bone Resorption
Concept Bone Development
Concept Bone Diseases, Developmental
Concept Bone Morphogenetic Protein 7
Concept Bone and Bones
Concept Fractures, Bone
Concept Bone Marrow Transplantation
Concept Bone Regeneration
Concept Bone Remodeling
Concept Heart Defects, Congenital
Concept Bone Marrow Cells
Concept Bone Morphogenetic Proteins
Concept Bone Morphogenetic Protein Receptors
Concept Bone Diseases, Metabolic
Concept Bone Morphogenetic Protein 2
Academic Article p38a MAPK is required for tooth morphogenesis and enamel secretion.
Academic Article MEKK2 mediates an alternative ?-catenin pathway that promotes bone formation.
Academic Article Distinctive Capillary Action by Micro-channels in Bone-like Templates can Enhance Recruitment of Cells for Restoration of Large Bony Defect.
Academic Article CHMP5 controls bone turnover rates by dampening NF-?B activity in osteoclasts.
Academic Article Zinc inhibits osteoclast differentiation by suppression of Ca2+-Calcineurin-NFATc1 signaling pathway.
Academic Article Schnurri-3 regulates ERK downstream of WNT signaling in osteoblasts.
Academic Article Control of bone resorption in mice by Schnurri-3.
Academic Article Administration of BMP2/7 in utero partially reverses Rubinstein-Taybi syndrome-like skeletal defects induced by Pdk1 or Cbp mutations in mice.
Academic Article The p38 MAPK pathway is essential for skeletogenesis and bone homeostasis in mice.
Academic Article TAK1 mediates BMP signaling in cartilage.
Academic Article TAK1 is an essential regulator of BMP signalling in cartilage.
Academic Article Ecsit is required for Bmp signaling and mesoderm formation during mouse embryogenesis.
Academic Article c-Jun N-Terminal Kinases (JNKs) Are Critical Mediators of Osteoblast Activity In Vivo.
Academic Article Bone Loss in Rheumatoid Arthritis: Basic Mechanisms and Clinical Implications.
Academic Article A cell surface clicked navigation system to direct specific bone targeting.
Academic Article Bone-targeting AAV-mediated silencing of Schnurri-3 prevents bone loss in osteoporosis.
Academic Article The ERK MAPK Pathway Is Essential for Skeletal Development and Homeostasis.
Academic Article Bone-Targeting AAV-Mediated Gene Silencing in Osteoclasts for Osteoporosis Therapy.
Academic Article Osteoblast-Osteoclast Communication and Bone Homeostasis.
Academic Article A RUNX2 stabilization pathway mediates physiologic and pathologic bone formation.
Academic Article Targeting skeletal endothelium to ameliorate bone loss.
Academic Article Trabecular bone organoid model for studying the regulation of localized bone remodeling.
Academic Article Discovery of a periosteal stem cell mediating intramembranous bone formation.
Grant A novel bone-targeting AAV-mediated gene therapy to promote bone formation in osteoporosis
Grant Development of novel gene therapeutics for bone fracture and graft defect
Grant Novel approaches to promote healing of bone loss in inflammatory arthritis
Concept Cancellous Bone
Academic Article The Extracellular Signal-Regulated Kinase Mitogen-Activated Protein Kinase Pathway in Osteoblasts.
Academic Article WNT-modulating gene silencers as a gene therapy for osteoporosis, bone fracture, and critical-sized bone defects.
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  • Bone fracture
  • large
  • bone
  • defect