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 1st letter of the Roman alphabet (同)a
the blood group whose red cells carry the A antigen (同)type_A, group A

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
answer / ampere
antipersonnel / (またA.P.)Associated Press

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. ステロイド抵抗性喘息 glucocorticoid resistant asthma
2. 特発性肺線維症の病因 pathogenesis of idiopathic pulmonary fibrosis
3. T細胞受容体シグナル伝達 t cell receptor signaling
4. 光による老化 photoaging
5. リポ蛋白の分類、代謝、およびアテローム性動脈硬化症における役割 lipoprotein classification metabolism and role in atherosclerosis

English Journal

The mechanisms by which pardaxin, a natural cationic antimicrobial peptide, targets the endoplasmic reticulum and induces c-FOS.

Ting CH1, Huang HN2, Huang TC3, Wu CJ2, Chen JY4.Author information 1Marine Research Station, Institute of Cellular and Organismic Biology, Academia Sinica, 23-10 Dahuen Road, Jiaushi, Ilan 262, Taiwan.2Department of Food Science, National Taiwan Ocean University, 2, Pei-Ning Road, Keelung 202, Taiwan.3Ph.D. Program for Cancer Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University and Academia Sinica, Taiwan.4Marine Research Station, Institute of Cellular and Organismic Biology, Academia Sinica, 23-10 Dahuen Road, Jiaushi, Ilan 262, Taiwan. Electronic address: zoocjy@gate.sinica.edu.tw.AbstractPardaxin is a cationic antimicrobial peptide derived from Red Sea Moses sole. Previous studies have shown that pardaxin selectively triggers the death of cancer cells, initiating the development of a pardaxin-based cancer vaccine; however, the underlying mechanism by which pardaxin kills cancer cells has not yet been elucidated. Here, we demonstrate that this mechanism involves endoplasmic reticulum (ER) targeting and c-FOS induction. Transcriptiome analysis of pardaxin-treated HT-1080 cells revealed induction of the gene encoding c-FOS, an AP-1 transcription factor. Pardaxin mediates cell death by activating c-FOS, but not other AP-1 transcription factors. Overexpression of c-FOS caused a dramatic increase in cell death, while knockdown of c-FOS induced pardaxin resistance; such effects were observed in both an in vitro cell model and an in vivo xenograft tumor model. Treatment with pardaxin also increased the level of calcium, and blockage of cellular calcium signaling disrupted pardaxin-induced cell death. Immunocytochemistry was used to demonstrate targeting of pardaxin to the endoplasmic reticulum, but not to the Golgi apparatus or mitochondria. Importantly, pardaxin treatment or c-FOS overexpression induced cell death in diverse cancer cell lines, indicating that pardaxin and c-FOS may possess therapeutic potential for use in cancer treatment.
Biomaterials.Biomaterials.2014 Apr;35(11):3627-40. doi: 10.1016/j.biomaterials.2014.01.032. Epub 2014 Jan 26.
Pardaxin is a cationic antimicrobial peptide derived from Red Sea Moses sole. Previous studies have shown that pardaxin selectively triggers the death of cancer cells, initiating the development of a pardaxin-based cancer vaccine; however, the underlying mechanism by which pardaxin kills cancer cell
PMID 24477193

Stability of sulforaphane for topical formulation.

Franklin SJ1, Dickinson SE, Karlage KL, Bowden GT, Myrdal PB.Author information 1College of Pharmacy, University of Arizona , Tucson, AZ , USA .AbstractAbstract Context: Sulforaphane (SFN) is a natural compound that has been investigated as a chemopreventive agent. SFN has been shown to inhibit the activator-protein-1 (AP-1) transcription factor and may be effective for inhibition of ultraviolet (UV) induced skin carcinogenesis. This study was designed to investigate the stability of SFN as a function of pH, temperature and in various solvents and formulations. Materials and methods: Stability was analyzed using high-performance liquid chromatography. A potential lead formulation was identified and evaluated in vivo. Results: SFN was determined to undergo apparent first-order degradation kinetics for the conditions explored. It was observed that SFN undergoes base catalyzed degradation. Buffer species and solvent type impacts stability as well. SFN was found to be very sensitive to temperature with degradation rate changing by a factor of nearly 3.1 for every 10 °C change in temperature (at pH 4.0). SFN completely degraded after 30 days in a conventional pharmaceutical cream formulation. Improved stability was observed in organic formulation components. Stability studies were conducted on two nonaqueous topical formulations: a polyethylene glycol (PEG) ointment base and an organic oleaginous base. Conclusion: Topically applied SFN in the PEG base formulation significantly reduced AP-1 activation after UV stimulation in the skin of a transgenic mouse model, indicating that SFN in this formulation retains efficacy in vivo.
Drug development and industrial pharmacy.Drug Dev Ind Pharm.2014 Apr;40(4):494-502. doi: 10.3109/03639045.2013.768634. Epub 2013 Apr 23.
Abstract Context: Sulforaphane (SFN) is a natural compound that has been investigated as a chemopreventive agent. SFN has been shown to inhibit the activator-protein-1 (AP-1) transcription factor and may be effective for inhibition of ultraviolet (UV) induced skin carcinogenesis. This study was desi
PMID 23611476

Novel anti-inflammatory function of NSC95397 by the suppression of multiple kinases.

Yang Y1, Yang WS1, Yu T1, Yi YS1, Park JG1, Jeong D1, Kim JH1, Oh JS1, Yoon K1, Kim JH2, Cho JY3.Author information 1Department of Genetic Engineering, Sungkyunkwan University, Suwon 440-746, Republic of Korea.2Department of Veterinary Physiology, College of Veterinary Medicine, Biosafety Research Institute, Chonbuk National University, Jeonju 561-756, Republic of Korea. Electronic address: jhkim1@chonbuk.ac.kr.3Department of Genetic Engineering, Sungkyunkwan University, Suwon 440-746, Republic of Korea. Electronic address: jaecho@skku.edu.AbstractNSC95397 (2,3-bis-[(2-hydroxyethyl)thio]-1,4-naphthoquinone) is a CDC25 inhibitor with anti-cancer properties. Since the anti-inflammatory activity of this compound has not yet been explored, the aim of this study was to examine whether this compound is able to modulate the inflammatory process. Toll like receptor (TLR)-mediated inflammatory responses were induced by lipopolysaccharide (LPS), a TLR4 ligand, and pam3CSK, a TLR2 ligand, in peritoneal macrophages and RAW264.7. The molecular mechanism of NSC95397's anti-inflammatory activity was studied using immunoblotting analysis, nuclear fractionation, immunoprecipitation, overexpression strategies, luciferase reporter gene assays, and kinase assays. NSC95397 dose-dependently suppressed the production of nitric oxide (NO), tumor necrosis factor (TNF)-α, and prostaglandin (PG)E2, and diminished the mRNA expression of inflammatory genes such as inducible NO synthase (iNOS), cyclooxygenase (COX)-2, interferon (IFN)-β, and TNF-α in peritoneal macrophages and RAW264.7 cells that were stimulated by LPS and pam3CSK. This compound also clearly blocked the activation of NF-κB (p65), AP-1 (c-Fos/c-Jun), and IRF-3 in LPS-treated RAW264.7 cells and TRIF- and MyD88-overexpressing HEK293 cells. In addition, biochemical and molecular approaches revealed that this compound targeted AKT, IKKα/β, MKK7, and TBK1. Therefore, these results suggest that the anti-inflammatory function of NSC95397 can be attributed to its inhibition of multiple targets such as AKT, IKKα/β, MKK7, and TBK1.
Biochemical pharmacology.Biochem Pharmacol.2014 Mar 15;88(2):201-15. doi: 10.1016/j.bcp.2014.01.022. Epub 2014 Jan 25.
NSC95397 (2,3-bis-[(2-hydroxyethyl)thio]-1,4-naphthoquinone) is a CDC25 inhibitor with anti-cancer properties. Since the anti-inflammatory activity of this compound has not yet been explored, the aim of this study was to examine whether this compound is able to modulate the inflammatory process. Tol
PMID 24468133

Japanese Journal

Anti-Wrinkle Effect of Magnesium Lithospermate B from Salvia miltiorrhiza BUNGE: Inhibition of MMPs via NF-kB Signaling

Jung Yu Ri,Kim Dae Hyun,Kim So Ra,An Hye Jin,Lee Eun Kyeong,Tanaka Takashi,Kim Nam Deuk,Yokozawa Takako,Park Jin Nam,Chung Hae Young
PLoS ONE 9(8), e102689, 2014-08-06
… In fibroblasts, MLB suppressed the transactivation of nuclear factor-kB (NF-kB) and activator protein 1(AP-1), which are the two transcription factors responsible for MMP expression, by suppressing oxidative stress and the mitogen activated protein kinase (MAPK) pathway. …
NAID 120005477030

Factor Xa in Mouse Fibroblasts May Induce Fibrosis More Than Thrombin

, , , , , , ,
International Heart Journal 55(4), 357-361, 2014
… Protease-activated receptor 1 (PAR1), activated by thrombin or factor (F) Xa, and PAR2, activated by FXa, have recently been reported to play roles not only in the coagulation system, but also in cardiac fibrosis. …
NAID 130004941269

AP-1-Mediated Expression of Brain-Specific Class IVa β-Tubulin in P19 Embryonal Carcinoma Cells

, , [他],
Journal of Veterinary Medical Science 76(12), 1609-1615, 2014
… Transient transfection assays employing a reporter construct found that ATRA-mediated regulatory region of the TUBB4a gene lay in the region from −83 nt to +137 nt relative to the +1 transcription start site. … Site-directed mutagenesis in the AP-1 binding site at −29/−17 suggested that the AP-1 binding site was a critical region for ATRA-mediated TUBB4a expression. …
NAID 130004780982