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"
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
全文を閲覧するには購読必要です。 To read the full text you will need to subscribe.
- 1. Toll様受容体：疾患および治療における役割 toll like receptors roles in disease and therapy
- 2. 複合免疫不全 combined immunodeficiencies
- 3. リードスタンバーグ細胞およびホジキンリンパ腫の病因 the reed sternberg cell and the pathogenesis of hodgkin lymphoma
- 4. 頭頸部の扁平上皮癌化：分子学的および遺伝学的変化 head and neck squamous cell carcinogenesis molecular and genetic alterations
- 5. 血友病患者における第VIIIおよび第IX因子阻害物質 factor viii and factor ix inhibitors in patients with hemophilia
English Journal
- Smad6 suppresses the growth and self-renewal of hepatic progenitor cells.
- Ding ZY, Liang HF, Jin GN, Chen WX, Wang W, Datta PK, Zhang MZ, Zhang B, Chen XP.Author information Hepatic Surgery Centre, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.AbstractActivation of hepatic progenitor cells (HPCs) is commonly observed in chronic liver disease and Wnt/β-catenin signaling plays a crucial role in the expansion of HPCs. However, the molecular mechanisms that regulate the activation of Wnt/β-catenin signaling in the liver, especially in HPCs, remain largely elusive. Here, we reported that ectopic expression of Smad6 suppressed the proliferation and self-renewal of WB-F344 cells, a HPC cell line. Mechanistically, we found that Smad6 inhibited Wnt/β-catenin signaling through promoting the interaction of C-terminal binding protein (CtBP) with β-catenin/T-cell factor (TCF) complex to inhibit β-catenin mediated transcriptional activation in WB-F344 cells. We used siRNA targeting β-catenin to demonstrate that Wnt/β-catenin signaling was required for the proliferation and self-renewal of HPCs. Taken together, these results suggest that Smad6 is a regulatory molecule which regulates the proliferation, self-renewal and Wnt/β-catenin signaling in HPCs. J. Cell. Physiol. 229: 651-660, 2014. © 2013 Wiley Periodicals, Inc.
- Journal of cellular physiology.J Cell Physiol.2014 May;229(5):651-60. doi: 10.1002/jcp.24488.
- Activation of hepatic progenitor cells (HPCs) is commonly observed in chronic liver disease and Wnt/β-catenin signaling plays a crucial role in the expansion of HPCs. However, the molecular mechanisms that regulate the activation of Wnt/β-catenin signaling in the liver, especially in HPCs, remain
- PMID 24446200
- TNF-α Upregulates Sclerostin Expression in Obese Mice Fed a High-Fat Diet.
- Baek K, Hwang HR, Park HJ, Kwon A, Qadir AS, Ko SH, Woo KM, Ryoo HM, Kim GS, Baek JH.Author information Department of Molecular Genetics, School of Dentistry and Dental Research Institute, Seoul National University, Seoul, Korea; Department of Pharmacology, College of Dentistry and Research Institute of Oral Science, Gangneung-Wonju National University, Gangwondo, Korea.AbstractSclerostin decreases bone mass by antagonizing the Wnt signaling pathway. We examined whether obesity-induced bone loss is associated with the expression of sclerostin. Five-week-old male mice were assigned to one of two groups (n = 10 each) and fed either a control diet (10% kcal from fat; CON) or a high-fat diet (60% kcal from fat; HF) for 12 weeks. Thex final body weight and whole body fat mass of the HF mice were higher than those of the CON mice. The distal femur cancellous bone mineral density and bone formation rate was lower in HF mice than in CON mice. The percent erosion surface was higher in the HF mice than the CON mice. The serum levels and femoral osteocytic protein expression levels of tumor necrosis factor-α (TNF-α) were significantly higher in HF mice than in CON mice. Sclerostin mRNA levels and osteocytic sclerostin protein levels in femoral cortex were also higher in HF mice than in CON mice. Sclerostin expression in MLO-Y4 osteocytes increased with TNF-α treatment, and TNF-α-induced sclerostin expression was blocked by the inhibition of NF-κB activation. Chromatin immunoprecipitation and a luciferase reporter assay demonstrated that NF-κB directly binds to the NF-κB binding elements on the mouse sost promoter and stimulates sclerostin expression. These results support a model in which, in the context of obesity or other inflammatory diseases that increase the production of TNF-α, TNF-α upregulates the expression of sclerostin through NF-κB signaling pathway, thus contributing to bone loss. J. Cell. Physiol. 229: 640-650, 2014. © 2013 Wiley Periodicals, Inc.
- Journal of cellular physiology.J Cell Physiol.2014 May;229(5):640-50. doi: 10.1002/jcp.24487.
- Sclerostin decreases bone mass by antagonizing the Wnt signaling pathway. We examined whether obesity-induced bone loss is associated with the expression of sclerostin. Five-week-old male mice were assigned to one of two groups (n = 10 each) and fed either a control diet (10% kcal from fat; CON)
- PMID 24446199
- Connective Tissue Growth Factor (CTGF/CCN2) Negatively Regulates BMP-2 Induced Osteoblast Differentiation and Signaling.
- Mundy C, Gannon M, Popoff SN.Author information Department of Anatomy and Cell Biology, Temple University School of Medicine, Philadelphia, Pennsylvania.AbstractConnective tissue growth factor (CTGF/CCN2) and bone morphogenetic protein (BMP)-2 are both produced and secreted by osteoblasts. Both proteins have been shown to have independent effects in regulating osteoblast proliferation, maturation and mineralization. However, how these two proteins interact during osteoblast differentiation remains unknown. In this study, we utilized two cell culture model systems, osteoblasts derived from CTGF knockout (KO) mice and osteoblasts infected with an adenovirus which over-expresses CTGF (Ad-CTGF), to investigate the effects of CTGF and BMP-2 on osteoblast development and function in vitro. Contrary to a previously published report, osteoblast maturation and mineralization were similar in osteogenic cultures derived from KO and WT calvaria in the absence of BMP-2 stimulation. Interestingly, in KO and WT osteoblast cultures stimulated with BMP-2, the KO osteoblasts exhibited enhanced osteoblast differentiation. This increase in osteoblast differentiation was accompanied by increased protein levels of phosphorylated Smad 1/5/8 and mRNA expression levels of bone morphogenetic protein receptor Ib. We also examined osteoblast differentiation in cultures that were infected with an adenoviral-CTGF vector (Ad-CTGF) and in controls. Continuous over-expression of CTGF resulted in decreased osteoblast maturation and mineralization in both unstimulated and BMP-2 stimulated cultures. Impaired osteoblast differentiation in cultures over-expressing CTGF was accompanied by decreased protein levels of phosphorylated Smad 1/5/8. Collectively, the data from these studies demonstrate that CTGF acts to negatively regulate BMP-2 induced signaling and osteoblast differentiation, and warrant additional studies to determine the precise mechanism(s) responsible for this effect. J. Cell. Physiol. 229: 672-681, 2014. © 2013 Wiley Periodicals, Inc.
- Journal of cellular physiology.J Cell Physiol.2014 May;229(5):672-81. doi: 10.1002/jcp.24491.
- Connective tissue growth factor (CTGF/CCN2) and bone morphogenetic protein (BMP)-2 are both produced and secreted by osteoblasts. Both proteins have been shown to have independent effects in regulating osteoblast proliferation, maturation and mineralization. However, how these two proteins interact
- PMID 24127409
Japanese Journal
- Antiinflammatory Activities of Crebanine by Inhibition of NF-κB and AP-1 Activation through Suppressing MAPKs and Akt Signaling in LPS-Induced RAW 264.7 Macrophages
- Biological and Pharmaceutical Bulletin advpub(0), 2016
- NAID 130005104414
- Hepatic stellate cells relay inflammation signaling from sinusoids to parenchyma in mouse models of immune-mediated hepatitis.
- Hepatology, 2015-09-30
- NAID 120005663256
- Induction of hypothalamic neurons from pluripotent stem cells (Special issue : proceedings of parvo- and magnocellular symposium in Sendai : creating a new stream of neuroendocrinology)
- Interdisciplinary Information Sciences 21(3), 261-266, 2015-09
- NAID 110009966535
Related Links
- Impact Factor: 4.315 ℹ Impact Factor: 2014: 4.315 The Impact Factor measures the average number of citations received in a particular year by papers published in the journal during the two preceding years. ...
- Science Signaling (SCI SIGNAL) impact factors: 6.279(2014), 6.337(2013), 7.648(2012), 7.499(2011), 6.12(2010). ISSN: 1945-0877. ... Year Impact Factor (IF) Total Articles Total Cites 2014/2015 6.279 170 7211 2013 6.337 187 6207
Related Pictures
★リンクテーブル★
| リンク元 | 「シグナル因子」「シグナル伝達因子」 |
| 関連記事 | 「fact」「factor」「signaling」 |
「シグナル因子」
「シグナル伝達因子」
「fact」
- n.
「factor」
- n.
「signaling」
- n.