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Search Results to Jae-Hyuck Shim PhD

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One or more keywords matched the following properties of Shim, Jae-Hyuck

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keywords Bone can Cartilage
overview

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, Paget's disease of bone, and heterotopic ossification. 

Osteoporosis affects approximately ten million people in the US over the age of 50, with around 1.5 million suffering from osteoporosis-related fractures each year. Unfortunately, the prognosis for patients who suffer these kinds of fractures can be poor; approximately 20% of patients with osteoporosis who suffer a hip fracture will die within a year. Similarly, patients with inflammatory arthritis develop focal articular erosions and systemic bone loss, resulting in osteopenia/osteoporosis. New approaches are needed to address the bone manifestations of inflammatory arthritis for approximately 1.3 million Americans with rheumatoid arthritis because disease modifying agents are inadequate to fully prevent systemic bone loss. Whilst there are some therapeutic options already available, it is crucial that further novel therapeutic strategies are developed. Some existing options focus on inhibiting bone resorption, however many are associated with a variety of undesirable side effects. For example, some therapies that increase bone formation, such as teriparatide, also increase bone resorption and a risk in bone tumor, and treatments that block bone resorption, such as bisphosphonates, arrest new bone formation along with atypical fractures and osteonecrosis of the jaw. 

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 and activation in skeletal biology. 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 systems. In these systems, nanoparticles or adeno-associated virus are modified to home to the bone surface and deliver RNA interference 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 could be used as a therapeutic approach for patients suffering with low bone density disorders.

 


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 Bone Marrow Transplantation
Concept Bone Regeneration
Concept Bone Marrow Cells
Concept Bone Morphogenetic Proteins
Concept Bone Morphogenetic Protein Receptors
Concept Bone Morphogenetic Protein 2
Academic Article p38a MAPK is required for tooth morphogenesis and enamel secretion.
Academic Article MEKK2 mediates an alternative ß-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.

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