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"
(genetics) the organic process whereby the DNA sequence in a gene is copied into mRNA; the process whereby a base sequence of messenger RNA is synthesized on a template of complementary DNA
a sound or television recording (e.g., from a broadcast to a tape recording)
something written, especially copied from one medium to another, as a typewritten version of dictation (同)written text

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
〈U〉(…を)書き写す(書き直す)こと,(…の)転写,謄写《+of+名》 / 〈C〉写し(書き直し)[たもの] / 〈U〉〈C〉編曲[されたもの] / 〈U〉〈C〉(ラジオ・テレビの)録音(録画)

UpToDate Contents

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1. 巨核球の生物学と血小板の産生 megakaryocyte biology and the production of platelets
2. 赤血球産生調節 regulation of erythropoiesis
3. 骨髄造血の制御 regulation of myelopoiesis
4. 慢性関節リウマチにおける滑膜異常 synovial pathology in rheumatoid arthritis
5. 喘息における吸入ステロイドの分子学的影響 molecular effects of inhaled glucocorticoid therapy in asthma

English Journal

Nuclear presence of nuclear factor of activated T cells (NFAT) c3 and c4 is required for Toll-like receptor-activated innate inflammatory response of monocytes/macrophages.

Minematsu H, Shin MJ, Celil Aydemir AB, Kim KO, Nizami SA, Chung GJ, Lee FY.AbstractNuclear factor of activated T cells (NFATs) are crucial transcription factors that tightly control proinflammatory cytokine expression for adaptive immunity in T and B lymphocytes. However, little is known about the role of NFATs for innate immunity in macrophages. In this study, we report that NFAT is required for Toll-like receptor (TLR)-initiated innate immune responses in bone marrow-derived macrophages (BMMs). All TLR ligand stimulation including LPS, a TLR4 ligand, and Pam(3)CSK(4), a TLR1/2 ligand, induced expression of TNF which was inhibited by VIVIT, an NFAT-specific inhibitor peptide. BMMs from NFATc4 knock-out mouse expressed less TNF than wild type. Despite apparent association between NFAT and TNF, LPS did not directly activate NFAT based on NFAT-luciferase reporter assay, whereas NF-κB was inducibly activated by LPS. Instead, macrophage exhibited constitutive NFAT activity which was not increased by LPS and was decreased by VIVIT. Immunocytochemical examination of NFATc1-4 of BMMs exhibited nuclear localization of NFATc3/c4 regardless of LPS stimulation. LPS stimulation did not cause nuclear translocation of NFATc1/c2. Treatment with VIVIT resulted in nuclear export of NFATc3/c4 and inhibited TLR-activated TNF expression, suggesting that nuclear residence of NFATc is required for TLR-related innate immune response. Chromatin immunoprecipitation (ChIP) assay using anti-RNA polymerase II (PolII) antibody suggested that VIVIT decreased PolII binding to TNF gene locus, consistent with VIVIT inhibition of LPS-induced TNF mRNA expression. This study identifies a novel paradigm of innate immune regulation rendered by NFAT which is a well known family of adaptive immune regulatory proteins.
Cellular signalling.Cell Signal.2011 Nov;23(11):1785-93. Epub 2011 Jun 25.
Nuclear factor of activated T cells (NFATs) are crucial transcription factors that tightly control proinflammatory cytokine expression for adaptive immunity in T and B lymphocytes. However, little is known about the role of NFATs for innate immunity in macrophages. In this study, we report that NFAT
PMID 21726630

Nickel differentially regulates NFAT and NF-κB activation in T cell signaling.

Saito R, Hirakawa S, Ohara H, Yasuda M, Yamazaki T, Nishii S, Aiba S.SourceDepartment of Dermatology, Tohoku University Graduate School of Medicine, Sendai 980-8574, Japan.
Toxicology and applied pharmacology.Toxicol Appl Pharmacol.2011 Aug 1;254(3):245-55. Epub 2011 May 4.
Nickel is a potent hapten that induces contact hypersensitivity in human skin. While nickel induces the maturation of dendritic cells via NF-κB and p38 MAPK activation, it also exerts immunosuppressive effects on T cells through an unknown mechanism. To elucidate the molecular mechanisms of its eff
PMID 21569788

Japanese Journal

炎症性骨破壊における免疫系と骨軟骨細胞のクロストーク

末松綾子,高柳広
日本臨床免疫学会会誌 = Japanese journal of clinical immunology 30(1), 22-28, 2007-02-28
… た研究からRA骨破壊のメカニズムの解明や骨免疫疾患の新しい治療戦略にますます重要になっている．ここでは，免疫系と骨軟骨細胞のクロストークについて概説し，T細胞が産生する制御因子による破骨細胞分化制御，破骨細胞分化マスター転写因子NFATc1の同定，免疫グロブリン様受容体群を介したRANKL共刺激の発見やカルモジュリンキナーゼ（CaMK）による破骨細胞分化および機能の制御などの最新の知見を紹介する． …
NAID 10018858006

Interaction between the immune system and bone metabolism: an emerging field of osteoimmunology

TAKAYANAGI Hiroshi
Proceedings of the Japan Academy, Series B 83(5), 136-143, 2007
… In rheumatoid arthritis, IL-17-producing helper T cells (TH17) induces receptor activator of NF-κB ligand (RANKL), which stimulates osteoclast differentiation through nuclear factor of activated T cells (NFAT)c1. … Accumulating evidence suggests that the immune and skeletal systems share cytokines, signaling molecules, transcription factors and membrane receptors. …
NAID 130000093902