WordNet
- limit, block, or decrease the action or function of; "inhibit the action of the enzyme"; "inhibit the rate of a chemical reaction"
- control and refrain from showing; of emotions, desires, impulses, or behavior (同)bottle up, suppress
- limit the range or extent of; "Contact between the young was inhibited by strict social customs"
- any of a large group of nitrogenous organic compounds that are essential constituents of living cells; consist of polymers of amino acids; essential in the diet of animals for growth and for repair of tissues; can be obtained from meat and eggs and milk and legumes; "a diet high in protein"
- 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
- a substance that retards or stops an activity
PrepTutorEJDIC
- 《所有・所属》…『の』,…のものである,…に属する・《材料・要素》…『でできた』,から成る・《部分》…『の』[『中の』] ・《数量・単位・種類を表す名詞に付いて》…の・《原因・動機》…『で』,のために(because of) ・《主格関係》…『の』,による,によって・《目的格関係》…『を』,の・《同格関係》…『という』・《関係・関連》…『についての』[『の』],の点で・《抽象名詞などと共に》…の[性質をもつ] ・《『It is』+『形』+『of』+『名』+『to』 doの形で,ofの後の名詞を意味上の主語として》・《分離》…『から』・《起原・出所》…『から』[『の』](out of) ・《『名』+『of』+『a』(『an』)+『名』の形で》…のような・《『名』+『of』+『mine』(『yours, his』など独立所有格)の形で》…の…・《時》(1)《副詞句を作って》…に《形容詞句を作って》…の・《時刻》《米》…前(to,《米》before)
- 〈感情・欲望・行動・作用など〉‘を'抑制する / (…しないように)〈人〉‘を'抑制する,妨げる《+『名』+『from』+『名』(do『ing』)》
- 蛋白(たんばく)質
- 抑制する人(物) / 化学反応抑制剤
UpToDate Contents
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- 1. ヘルパーT細胞サブセット：疾患における分化および役割 t helper subsets differentiation and role in disease
- 2. 骨転移の機序 mechanisms of bone metastases
- 3. 関節リウマチの診断および評価における生物学的マーカー biologic markers in the diagnosis and assessment of rheumatoid arthritis
- 4. 研究用生物学的マーカーによる関節リウマチの診断および評価ま investigational biologic markers in the diagnosis and assessment of rheumatoid arthritis
- 5. 子癇前症：病因 preeclampsia pathogenesis
English Journal
- Conserved inhibitory role of teleost SOCS-1s in IFN signaling pathways.
- Nie L1, Xiong R1, Zhang YS1, Zhu LY1, Shao JZ2, Xiang LX3.Author information 1College of Life Sciences, Zhejiang University, Hangzhou 310058, People's Republic of China; Key Laboratory for Cell and Gene Engineering of Zhejiang Province, Hangzhou 310058, People's Republic of China; Key Laboratory of Animal Virology of Ministry of Agriculture, Hangzhou 310058, People's Republic of China.2College of Life Sciences, Zhejiang University, Hangzhou 310058, People's Republic of China; Key Laboratory for Cell and Gene Engineering of Zhejiang Province, Hangzhou 310058, People's Republic of China; Key Laboratory of Animal Virology of Ministry of Agriculture, Hangzhou 310058, People's Republic of China. Electronic address: shaojz@zju.edu.cn.3College of Life Sciences, Zhejiang University, Hangzhou 310058, People's Republic of China; Key Laboratory for Cell and Gene Engineering of Zhejiang Province, Hangzhou 310058, People's Republic of China; Key Laboratory of Animal Virology of Ministry of Agriculture, Hangzhou 310058, People's Republic of China. Electronic address: xianglx@zju.edu.cn.AbstractThe suppressor of cytokine signaling 1 (SOCS-1) protein is a critical regulator in the immune systems of humans and mammals, which functions classically as an inhibitor of the IFN signaling pathways. However, data on functional characterisation of SOCS-1 in ancient vertebrates are limited. In this study, we report the function of teleost SOCS-1s in IFN signaling in fish models (zebrafish and Tetraodon) and human cells. Structurally, teleost SOCS-1s share conserved functional domains with their mammalian counterparts. Functionally, teleost SOCS-1s could be significantly induced upon stimulation with IFN stimulants and zebrafish IFNφ1. Overexpression of teleost SOCS-1s could dramatically suppress IFNφ1-induced Mx, Viperin and PKZ activation in zebrafish, and IFN-induced ISG15 activation in HeLa cells. Furthermore, a SOCS-1 variant that lacks the KIR domain was also characterised. This study demonstrates the conserved negative regulatory role of teleost SOCS-1s in IFN signaling pathways, providing perspective into the functional conservation of SOCS-1 proteins during evolution.
- Developmental and comparative immunology.Dev Comp Immunol.2014 Mar;43(1):23-9. doi: 10.1016/j.dci.2013.10.007. Epub 2013 Oct 29.
- The suppressor of cytokine signaling 1 (SOCS-1) protein is a critical regulator in the immune systems of humans and mammals, which functions classically as an inhibitor of the IFN signaling pathways. However, data on functional characterisation of SOCS-1 in ancient vertebrates are limited. In this s
- PMID 24183820
- Methylglyoxal induces oxidative stress and mitochondrial dysfunction in osteoblastic MC3T3-E1 cells.
- Suh KS, Choi EM, Rhee SY, Kim YS.Author information Research Institute of Endocrinology, Kyung Hee University Hospital , Seoul , Republic of Korea.AbstractAbstract Methylglyoxal is a reactive dicarbonyl compound produced by glycolytic processing and identified as a precursor of advanced glycation end products. The elevated methylglyoxal levels in patients with diabetes are believed to contribute to diabetic complications, including bone defects. The objective of this study was to evaluate the effect of methylglyoxal on the function of osteoblastic MC3T3-E1 cells. The data indicated that methylglyoxal decreased osteoblast differentiation and induced osteoblast cytotoxicity. Pretreatment of MC3T3-E1 cells with aminoguanidine (a carbonyl scavenger), Trolox (an antioxidant), and cyclosporin A (a blocker of the mitochondrial permeability transition pore) prevented methylglyoxal-induced cytotoxicity in MC3T3-E1 cells. However, BAPTA/AM (an intracellular Ca(2+) chelator) and dantrolene (an inhibitor of endoplasmic reticulum Ca(2+) release) did not reverse the cytotoxic effect of methylglyoxal. Methylglyoxal increased the formation of intracellular reactive oxygen species, mitochondrial superoxide, and cardiolipin peroxidation in osteoblastic MC3T3-E1 cells. Methylglyoxal also decreased the mitochondrial membrane potential and intracellular ATP and nitric oxide levels, suggesting that carbonyl stress-induced loss of mitochondrial integrity contributes to the cytotoxicity of methylglyoxal. Furthermore, the results demonstrated that methylglyoxal induced protein adduct formation, inactivation of glyoxalase I, and activation of glyoxalase II. Aminoguanidine reversed all aforementioned effects of methylglyoxal. Taken together, these data support the notion that high methylglyoxal concentrations have detrimental effects on osteoblasts through a mechanism involving oxidative stress and mitochondrial dysfunction.
- Free radical research.Free Radic Res.2014 Feb;48(2):206-17. doi: 10.3109/10715762.2013.859387. Epub 2013 Nov 18.
- Abstract Methylglyoxal is a reactive dicarbonyl compound produced by glycolytic processing and identified as a precursor of advanced glycation end products. The elevated methylglyoxal levels in patients with diabetes are believed to contribute to diabetic complications, including bone defects. The o
- PMID 24164256
- miR-24 and miR-205 expression is dependent on HPV onco-protein expression in keratinocytes.
- McKenna DJ, Patel D, McCance DJ.Author information Biomedical Sciences Research Institute, University of Ulster, Coleraine, Co. Derry BT52 1SA, UK; Centre for Cancer Research and Cell Biology, School of Medicine, Dentistry and Biomedical Science, Queen's University Belfast, Belfast BT9 7BL, UK. Electronic address: dj.mckenna@ulster.ac.uk.AbstractA screen of microRNA (miRNA) expression following differentiation in human foreskin keratinocytes (HFKs) identified changes in several miRNAs, including miR-24 and miR-205. We investigated how expression of Human Papilloma Virus Type-16 (HPV16) onco-proteins E6 and E7 affected expression of miR-24 and miR-205 during proliferation and differentiation of HFKs. We show that the induction of both miR-24 and miR-205 observed during differentiation of HFKs is lost in HFKs expressing E6 and E7. We demonstrate that the effect on miR-205 is due to E7 activity, as miR-205 expression is dependent on pRb expression. Finally, we provide evidence that miR-24 effects in the cell may be due to targeting of cyclin dependent kinase inhibitor p27. In summary, these results indicate that expression of both miR-24 and miR-205 are impacted by E6 and/or E7 expression, which may be one mechanism by which HPV onco-proteins can disrupt the balance between proliferation and differentiation in keratinocytes.
- Virology.Virology.2014 Jan 5;448:210-6. doi: 10.1016/j.virol.2013.10.014. Epub 2013 Oct 29.
- A screen of microRNA (miRNA) expression following differentiation in human foreskin keratinocytes (HFKs) identified changes in several miRNAs, including miR-24 and miR-205. We investigated how expression of Human Papilloma Virus Type-16 (HPV16) onco-proteins E6 and E7 affected expression of miR-24 a
- PMID 24314651
Japanese Journal
- The small G protein Arf6 expressed in keratinocytes by HGF stimulation is a regulator for skin wound healing
- Scientific reports 7, 46649, 2017-04
- NAID 120006224678
- Imatinib ameliorates bronchiolitis obliterans via inhibition of fibrocyte migration and differentiation
- Journal of
- NAID 120005983030
- Ethanol extracts of <i>Aster yomena</i> (Kitam.) Honda inhibit adipogenesis through the activation of the AMPK signaling pathway in 3T3-L1 preadipocytes
- Drug Discoveries & Therapeutics, 2017
- NAID 130006168807
Related Links
- 1. Prostate. 2013 May;73(6):624-33. doi: 10.1002/pros.22603. Epub 2012 Oct 11. Inhibitor of differentiation 1 (Id1) and Id3 proteins play different roles in TGFβ effects on cell proliferation and migration in prostate cancer cells. Strong N ...
- Inhibitor of differentiation 4 (ID4): From development to cancer Divya Patel a, Derrick J. Morton a, Jason Carey b, Mathew C. Havrda c, Jaideep Chaudhary a, , a Department of Biological Sciences, Center for Cancer Research and ...
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★リンクテーブル★
| リンク元 | 「Id protein」「分化抑制タンパク質」 |
| 拡張検索 | 「inhibitor of differentiation protein 1」「inhibitor of differentiation protein 2」「inhibitor of differentiation protein 3」 |
| 関連記事 | 「inhibit」「inhibitor」「differentiation」 |
「Id protein」
「分化抑制タンパク質」
「inhibitor of differentiation protein 1」
- 関
- Id-1
「inhibitor of differentiation protein 2」
- 関
- Id-2
「inhibitor of differentiation protein 3」
- 関
- Id-3
「inhibit」
- v.
- 抑制する、阻害する、阻止する
- 関
- abrogate、block、depress、depression、deter、inhibition、interdict、prevent、prevention、repress、repression、restrain、restraint、suppress、suppression
「inhibitor」
- n.
「differentiation」
- n.