WordNet
- be a contributing factor; "make things factor into a companys profitability"
- any of the numbers (or symbols) that form a product when multiplied together
- an independent variable in statistics
- anything that contributes causally to a result; "a number of factors determined the outcome"
- consider as relevant when making a decision; "You must factor in the recent developments" (同)factor in, factor out
- resolve into factors; "a quantum computer can factor the number 15" (同)factor in, factor out
- an event known to have happened or something known to have existed; "your fears have no basis in fact"; "how much of the story is fact and how much fiction is hard to tell"
- a concept whose truth can be proved; "scientific hypotheses are not facts"
- a piece of information about circumstances that exist or events that have occurred; "first you must collect all the facts of the case"
- a statement or assertion of verified information about something that is the case or has happened; "he supported his argument with an impressive array of facts"
- the mathematical process of obtaining the derivative of a function
- a discrimination between things as different and distinct; "it is necessary to make a distinction between love and infatuation" (同)distinction
- cell that functions in the breakdown and resorption of bone tissue
PrepTutorEJDIC
- (…の)『要因』,(…を生み出す)要素《+『in』+『名』(do『ing』)》 / 囲数,約数 / 代理人,《おもに英》仲買人 / =factorize
- 〈C〉『事実』,実際にある(あった)事 / 〈U〉真相,真実(truth) / 《the~》(法律用語で)犯行
UpToDate Contents
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- 1. 骨粗鬆症に対するデノスマブ denosumab for osteoporosis
- 2. 骨格の正常な発達および骨形成ならびに骨吸収の調節 normal skeletal development and regulation of bone formation and resorption
- 3. IL - 1、IL - 6、およびRANKLを抑制する生物学的製剤の関節リウマチ
におけるランダム化臨床試験 randomized clinical trials in rheumatoid arthritis of biologic agents that inhibit il 1 il 6 and rankl - 4. 転移性癌患者におけるビスホスホネートおよびデノスマブ bisphosphonates and denosumab in patients with metastatic cancer
- 5. 骨転移の機序 mechanisms of bone metastases
English Journal
- Dominant Negative MCP-1 Blocks Human Osteoclast Differentiation.
- Morrison NA, Day CJ, Nicholson GC.Author information School of Medical Science, Griffith University Gold Coast Campus, Parklands Drive, Southport, Queensland, 4215, Australia.AbstractHuman osteoclasts were differentiated using receptor activator of NFκB ligand (RANKL) and macrophage colony stimulating factor (M-CSF) from colony forming unit-granulocyte macrophage (CFU-GM) precursors of the myeloid lineage grown from umbilical cord blood. Gene expression profiling using quantitative polymerase chain reaction (Q-PCR) showed more than 1,000-fold induction of chemokine MCP-1 within 24 h of RANKL treatment. MCP-1 mRNA content exceeds that of other assayed chemokines (CCL1, 3, 4, and 5) at all time points up to day 14 of treatment. MCP-1 induction preceded peak induction of calcium signaling activator calmodulin 1 (CALM1) and transcription factors JUN and FOS, which were at 3 days. Key osteoclast related transcription factors NFATc1 and NFATc2 showed peak induction at 7 days, while marker genes for osteoclast function cathepsin K and tartrate resistance acid phosphatase (TRAP) were maximally induced at 14 days, corresponding with mature osteoclast function. To test whether the early and substantial peak in MCP-1 expression is part of human osteoclast differentiation events, a dominant negative inhibitor of MCP-1 (7ND) was added simultaneously with RANKL and M-CSF, resulting in blockade of CALM1, JUN and NFATc2 induction and strong inhibition of human osteoclast differentiation. These data show that a cascade of gene expression leading to osteoclast differentiation depends on intact early MCP-1 induction and signaling in human osteoclasts. J. Cell. Biochem. 115: 303-312, 2014. © 2013 Wiley Periodicals, Inc.
- Journal of cellular biochemistry.J Cell Biochem.2014 Feb;115(2):303-12. doi: 10.1002/jcb.24663.
- Human osteoclasts were differentiated using receptor activator of NFκB ligand (RANKL) and macrophage colony stimulating factor (M-CSF) from colony forming unit-granulocyte macrophage (CFU-GM) precursors of the myeloid lineage grown from umbilical cord blood. Gene expression profiling using quantita
- PMID 23996571
- The transcription factor T-box3 regulates Colony Stimulating Factor 1-dependent Jun Dimerization Protein 2 expression and plays an important role in osteoclastogenesis.
- Yao C, Yao GQ, Sun BH, Zhang C, Tommasini SM, Insogna K.Author information Yale University School of Medicine, United States;AbstractColony Stimulating Factor 1(CSF1) is known to promote osteoclast progenitor survival but its role in osteoclast differentiation and mature osteoclast function are less well understood. In a microarray screen, Jun dimerization protein 2 (JDP2) was identified as significantly induced by CSF1. Recent reports indicate that JDP2 is required for normal osteoclastogenesis and skeletal metabolism. As there are no reports on the transcriptional regulation of this gene, the DNA sequence from -2612 to +682 bp (relative to the transcription start site) of the JDP2 gene was cloned and promoter activity analyzed. The T box-binding element (TBE) between -191 and -141 bp was identified as the cis-element responsible for CSF1-dependent JDP2 expression. Using degenerate PCR, Tbx3 was identified as the major isoform binding the TBE. Overexpression of Tbx3 induced JDP2 promoter activity while suppressing Tbx3 expression substantially attenuated CSF1-induced transcription. Suppressing Tbx3 in osteoclast precursors reduced JDP2 expression and significantly impaired RANKL/CSF1-induced osteoclastogenesis. A MEK1/2-specific inhibitor was found to block CSF1-induced JDP2 expression. Consistent with these data, JDP2-/- mice were found to have increased bone mass. In summary, CSF1 upregulates JDP2 expression by inducing Tbx3 binding to the JDP2 promoter. The downstream signaling cascade from activated c-fms involves the MEK1/2-ERK1/2 pathway. Tbx3 plays an important role in osteoclastogenesis at least in part by regulating CSF1-dependent expression of JDP2.
- The Journal of biological chemistry.J Biol Chem.2014 Jan 6. [Epub ahead of print]
- Colony Stimulating Factor 1(CSF1) is known to promote osteoclast progenitor survival but its role in osteoclast differentiation and mature osteoclast function are less well understood. In a microarray screen, Jun dimerization protein 2 (JDP2) was identified as significantly induced by CSF1. Recent r
- PMID 24394418
- Novel RANK Antagonists for the Treatment of Bone Resorptive Disease: Theoretical Predictions and Experimental Validation.
- Téletchéa S, Stresing V, Hervouet S, Baud'huin M, Heymann MF, Bertho G, Charrier C, Ando K, Heymann D.Author information INSERM, UMR 957, Equipe labellisée LIGUE 2012, Université de Nantes, LPRO (Laboratory of the Physiopathology of Bone Resorption and Therapy of Primary Bone Tumors), Nantes, France.AbstractReceptor activator of nuclear factor-κB (RANK) and RANK ligand play a pivotal role in bone metabolism, and selective targeting of RANK signaling has become a promising therapeutic strategy in the management of resorptive bone diseases. Existing antibody-based therapies and novel inhibitors currently in development were designed to target the ligand, rather than the membrane receptor expressed on osteoclast precursors. We describe here an alternative approach to designing small peptides able to specifically bind to the hinge region of membrane RANK responsible for the conformational change upon RANKL association. A nonapeptide generated by this method was validated for its biological activity in vitro and in vivo and served as a lead compound for the generation of a series of peptide RANK antagonists derived from the original sequence. Our study presents a structure- and knowledge based strategy for the design of novel effective and affordable small peptide inhibitors specifically targeting the receptor RANK and opens a new therapeutic opportunity for the treatment of resorptive bone-disease. © 2014 American Society for Bone and Mineral Research.
- Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research.J Bone Miner Res.2014 Jan 6. doi: 10.1002/jbmr.2170. [Epub ahead of print]
- Receptor activator of nuclear factor-κB (RANK) and RANK ligand play a pivotal role in bone metabolism, and selective targeting of RANK signaling has become a promising therapeutic strategy in the management of resorptive bone diseases. Existing antibody-based therapies and novel inhibitors currentl
- PMID 24390798
Japanese Journal
- (2S)-2′-Methoxykurarinone Inhibits Osteoclastogenesis and Bone Resorption through Down-Regulation of RANKL Signaling
- Kim Ju-Young,Kim Jung Young,Kim Jeong Joong,Oh Jaemin,Kim Youn-Chul,Lee Myeung Su
- Biological and Pharmaceutical Bulletin 37(2), 255-261, 2014
- … Therefore, we examined the effect and mechanism of action of MK on receptor activator of nuclear factor-κB ligand (RANKL)-induced osteoclast differentiation and bone resorption. … MK inhibited osteoclast differentiation in bone marrow cell–osteoblast cocultures but did not affect the RANKL-to-osteoprotegerin ratio induced by osteoclastogenic factors in osteoblasts. …
- NAID 130003390926
- 6,4'-Dihydroxy-7-methoxyflavanone Inhibits Osteoclast Differentiation and Function
- Im Nam-Kyung,Choi Je-Yong,Oh Hyuncheol [他]
- Biological & pharmaceutical bulletin 36(5), 796-801, 2013-05
- NAID 40019637471
- ヒト間葉系幹細胞による破骨細胞の分化抑制作用と関節リウマチ治療への応用
- 尾下 浩一,山岡 邦宏,田中 良哉
- 産業医科大学雑誌 35(1), 33-37, 2013-03-01
- … MSC)を利用した新しいRA治療法の確立を目指した研究が盛んに行われている.我々はヒト骨髄由来MSCが破骨細胞分化阻害因子であるosteoprotegerin (OPG)を恒常的に産生する細胞であり,receptor activator of nuclear factor kappa-B ligand(RANKL)の刺激で誘導される破骨細胞分化を抑制する作用を有することを明らかにした.したがって, MSCはRAにおける骨破壊進行を抑制できる可能性があるだけでなく,関節構造維持に重要な細胞であることが示唆 …
- NAID 110009593199
Related Links
- 1. Nature. 2010 Nov 4;468(7320):98-102. doi: 10.1038/nature09387. Epub 2010 Sep 29. Osteoclast differentiation factor RANKL controls development of progestin-driven mammary cancer. Schramek D(1), Leibbrandt A, Sigl V, Kenner ...
- Osteoclast Differentiation Factor explanation free. What is Osteoclast Differentiation Factor? Meaning of Osteoclast Differentiation Factor medical term. What does Osteoclast Differentiation Factor mean? Osteoclast Differentiation ...
Related Pictures
★リンクテーブル★
| リンク元 | 「破骨細胞分化因子」「RANKL」「receptor activator of NF-kappaB ligand」 |
| 関連記事 | 「fact」「factor」「differentiation」 |
「破骨細胞分化因子」
- 英
- osteoclast differentiation factor、receptor activator of NF-kappaB ligand、RANKL
- 関
- 破骨細胞分化抑制因子リガンド、NFκB活性化受容体リガンド、ランクリガンド
-RANKL
- 同
- receptor activator for nuclear factor kB ligand
「RANKL」
- 同
- receptor activator for nuclear factor kB ligand
「receptor activator of NF-kappaB ligand」
「fact」
- n.
「factor」
- n.
「differentiation」
- n.