TNF-family member Receptor Activator of NF-κB (RANK) and RANK-Ligand (RANKL) in bone remodelling
| Publication Date: |
2018-08-31
|
|---|---|
| Publisher: |
Institute of Physics (IOP)
|
| Print ISSN: |
1755-1307
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| Electronic ISSN: |
1755-1315
|
| Topics: |
Geography
Geosciences
Physics
|
| Published by: |
| _version_ | 1836399040440303617 |
|---|---|
| autor | W J Quax, A H G van Assen and Y Z Wang |
| beschreibung | Receptor Activator of NF-κB (RANK) and RANK-Ligand (RANKL) are members of the Tumour Necrosis Factor (TNF)-superfamily involved in bone homeostasis. In a tightly controlled interplay of this receptor and ligand, bone is continuously being remodelled. Several pathological conditions resulting from a misbalance between bone resorption and bone formation have been documented. Most frequently resorption gets the overhand resulting in a lower Bone Mineral Density (BMD), increased fracture risk and reduced mobility of patients. RANKL is expressed on bone producing osteoblasts whereas RANK is expressed on preosteoclasts, which can develop in bone resorbing osteoclasts. The binding of RANKL to RANK functions as a trigger for the formation of these bone resorbing osteoclasts. With the development of a monoclonal antibody directed against RANKL a new therapeutic strategy to interfere with bone remodelling has become available some years ago. In this manuscript we discuss the prospective o... |
| citation_standardnr | 6326048 |
| datenlieferant | ipn_articles |
| feed_id | 108844 |
| feed_publisher | Institute of Physics (IOP) |
| feed_publisher_url | http://www.iop.org/ |
| insertion_date | 2018-08-31 |
| journaleissn | 1755-1315 |
| journalissn | 1755-1307 |
| publikationsjahr_anzeige | 2018 |
| publikationsjahr_facette | 2018 |
| publikationsjahr_intervall | 7984:2015-2019 |
| publikationsjahr_sort | 2018 |
| publisher | Institute of Physics (IOP) |
| quelle | IOP Conference Series: Earth and Environmental Science |
| relation | http://iopscience.iop.org/1755-1315/185/1/012001 |
| search_space | articles |
| shingle_author_1 | W J Quax, A H G van Assen and Y Z Wang |
| shingle_author_2 | W J Quax, A H G van Assen and Y Z Wang |
| shingle_author_3 | W J Quax, A H G van Assen and Y Z Wang |
| shingle_author_4 | W J Quax, A H G van Assen and Y Z Wang |
| shingle_catch_all_1 | TNF-family member Receptor Activator of NF-κB (RANK) and RANK-Ligand (RANKL) in bone remodelling Receptor Activator of NF-κB (RANK) and RANK-Ligand (RANKL) are members of the Tumour Necrosis Factor (TNF)-superfamily involved in bone homeostasis. In a tightly controlled interplay of this receptor and ligand, bone is continuously being remodelled. Several pathological conditions resulting from a misbalance between bone resorption and bone formation have been documented. Most frequently resorption gets the overhand resulting in a lower Bone Mineral Density (BMD), increased fracture risk and reduced mobility of patients. RANKL is expressed on bone producing osteoblasts whereas RANK is expressed on preosteoclasts, which can develop in bone resorbing osteoclasts. The binding of RANKL to RANK functions as a trigger for the formation of these bone resorbing osteoclasts. With the development of a monoclonal antibody directed against RANKL a new therapeutic strategy to interfere with bone remodelling has become available some years ago. In this manuscript we discuss the prospective o... W J Quax, A H G van Assen and Y Z Wang Institute of Physics (IOP) 1755-1307 17551307 1755-1315 17551315 |
| shingle_catch_all_2 | TNF-family member Receptor Activator of NF-κB (RANK) and RANK-Ligand (RANKL) in bone remodelling Receptor Activator of NF-κB (RANK) and RANK-Ligand (RANKL) are members of the Tumour Necrosis Factor (TNF)-superfamily involved in bone homeostasis. In a tightly controlled interplay of this receptor and ligand, bone is continuously being remodelled. Several pathological conditions resulting from a misbalance between bone resorption and bone formation have been documented. Most frequently resorption gets the overhand resulting in a lower Bone Mineral Density (BMD), increased fracture risk and reduced mobility of patients. RANKL is expressed on bone producing osteoblasts whereas RANK is expressed on preosteoclasts, which can develop in bone resorbing osteoclasts. The binding of RANKL to RANK functions as a trigger for the formation of these bone resorbing osteoclasts. With the development of a monoclonal antibody directed against RANKL a new therapeutic strategy to interfere with bone remodelling has become available some years ago. In this manuscript we discuss the prospective o... W J Quax, A H G van Assen and Y Z Wang Institute of Physics (IOP) 1755-1307 17551307 1755-1315 17551315 |
| shingle_catch_all_3 | TNF-family member Receptor Activator of NF-κB (RANK) and RANK-Ligand (RANKL) in bone remodelling Receptor Activator of NF-κB (RANK) and RANK-Ligand (RANKL) are members of the Tumour Necrosis Factor (TNF)-superfamily involved in bone homeostasis. In a tightly controlled interplay of this receptor and ligand, bone is continuously being remodelled. Several pathological conditions resulting from a misbalance between bone resorption and bone formation have been documented. Most frequently resorption gets the overhand resulting in a lower Bone Mineral Density (BMD), increased fracture risk and reduced mobility of patients. RANKL is expressed on bone producing osteoblasts whereas RANK is expressed on preosteoclasts, which can develop in bone resorbing osteoclasts. The binding of RANKL to RANK functions as a trigger for the formation of these bone resorbing osteoclasts. With the development of a monoclonal antibody directed against RANKL a new therapeutic strategy to interfere with bone remodelling has become available some years ago. In this manuscript we discuss the prospective o... W J Quax, A H G van Assen and Y Z Wang Institute of Physics (IOP) 1755-1307 17551307 1755-1315 17551315 |
| shingle_catch_all_4 | TNF-family member Receptor Activator of NF-κB (RANK) and RANK-Ligand (RANKL) in bone remodelling Receptor Activator of NF-κB (RANK) and RANK-Ligand (RANKL) are members of the Tumour Necrosis Factor (TNF)-superfamily involved in bone homeostasis. In a tightly controlled interplay of this receptor and ligand, bone is continuously being remodelled. Several pathological conditions resulting from a misbalance between bone resorption and bone formation have been documented. Most frequently resorption gets the overhand resulting in a lower Bone Mineral Density (BMD), increased fracture risk and reduced mobility of patients. RANKL is expressed on bone producing osteoblasts whereas RANK is expressed on preosteoclasts, which can develop in bone resorbing osteoclasts. The binding of RANKL to RANK functions as a trigger for the formation of these bone resorbing osteoclasts. With the development of a monoclonal antibody directed against RANKL a new therapeutic strategy to interfere with bone remodelling has become available some years ago. In this manuscript we discuss the prospective o... W J Quax, A H G van Assen and Y Z Wang Institute of Physics (IOP) 1755-1307 17551307 1755-1315 17551315 |
| shingle_title_1 | TNF-family member Receptor Activator of NF-κB (RANK) and RANK-Ligand (RANKL) in bone remodelling |
| shingle_title_2 | TNF-family member Receptor Activator of NF-κB (RANK) and RANK-Ligand (RANKL) in bone remodelling |
| shingle_title_3 | TNF-family member Receptor Activator of NF-κB (RANK) and RANK-Ligand (RANKL) in bone remodelling |
| shingle_title_4 | TNF-family member Receptor Activator of NF-κB (RANK) and RANK-Ligand (RANKL) in bone remodelling |
| timestamp | 2025-06-30T23:36:39.531Z |
| titel | TNF-family member Receptor Activator of NF-κB (RANK) and RANK-Ligand (RANKL) in bone remodelling |
| titel_suche | TNF-family member Receptor Activator of NF-κB (RANK) and RANK-Ligand (RANKL) in bone remodelling |
| topic | R TE-TZ U |
| uid | ipn_articles_6326048 |