MKP

• MAPキナーゼホスファターゼ

関

mitogen-activated protein kinase phosphatase

WordNet

1. the 13th letter of the Roman alphabet (同)m

PrepTutorEJDIC

1. Mach number / mark[s] / Monsieur

Wikipedia preview

出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2014/06/01 00:36:43」(JST)

wiki en

[Wiki en表示]

MKP or mkp may refer to:

Codes

• MKP, the NYSE ticker for the S&P 500 index
• mkp, the ISO 639-3 language code for Moikodi, spoken by small groups in the southeastern peninsula of New Guinea

Organizations

• The ManKind Project, a non-profit international educational organization
• Miles Kelly Publishing, an independent children’s publishing company based in Essex, UK

Political parties

• Party of the Hungarian Coalition (Hungarian: Magyar Koalíció Pártja), a political party in Slovakia, for the Magyar (i.e. ethnic Hungarian) minority
• Hungarian Communist Party (Hungarian: Magyar Kommunista Párt), a former Hungarian political party
• Maoist Communist Party (Turkish: Maoist Komünist Partisi), a clandestine communist organization in Turkey
• Maurin Kiribati Pati, a political party in Kiribati
• Mazdoor Kisan Party, a communist party in Pakistan

Science and technology

• MAP kinase phosphatase (with MAP standing for mitogen-activated protein), an enzyme (see also: MAP kinase)
• Metallized plastic polypropylene (German: Metallisierter Kunststoff Polypropylen), a type of plastic-film capacitor
• Monobasic potassium phosphate, another name for monopotassium phosphate (KH₂PO₄). The K comes from Latin kalium, which means potassium.
• Multidimensional knapsack problem, a problem in combinatorial optimization

People

• MKP is used to refer to Starcraft 2 progamer MarineKingPrime

UpToDate Contents

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• 1. 前立腺癌の分子生物学 molecular biology of prostate cancer
• 2. 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
• 3. 喘息におけるステロイド耐性のメカニズムおよび 臨床的意義 mechanisms and clinical implications of glucocorticoid resistance in asthma

English Journal

• Alveolar bone loss: mechanisms, potential therapeutic targets, and interventions.

• Intini G1, Katsuragi Y, Kirkwood KL, Yang S.Author information 1Department of Oral Medicine, Infection, and Immunity, Harvard School of Dental Medicine, 188 Longwood Avenue, REB 513, Boston, MA 02115, USA.AbstractThis article reviews recent research into mechanisms underlying bone resorption and highlights avenues of investigation that may generate new therapies to combat alveolar bone loss in periodontitis. Several proteins, signaling pathways, stem cells, and dietary supplements are discussed as they relate to periodontal bone loss and regeneration. RGS12 is a crucial protein that mediates osteoclastogenesis and bone destruction, and a potential therapeutic target. RGS12 likely regulates osteoclast differentiation through regulating calcium influx to control the calcium oscillation-NFATc1 pathway. A working model for RGS10 and RGS12 in the regulation of Ca(2+) oscillations during osteoclast differentiation is proposed. Initiation of inflammation depends on host cell-microbe interactions, including the p38 mitogen-activated protein kinase (MAPK) signaling pathway. Oral p38 inhibitors reduced lipopolysaccharide (LPS)-induced bone destruction in a rat periodontitis model but showed unsatisfactory safety profiles. The p38 substrate MK2 is a more specific therapeutic target with potentially superior tolerability. Furthermore, MKP-1 shows anti-inflammatory activity, reducing inflammatory cytokine biosynthesis and bone resorption. Multipotent skeletal stem cell (SSC) populations exist within the bone marrow and periosteum of long bones. These bone-marrow-derived SSCs and periosteum-derived SSCs have shown therapeutic potential in several applications, including bone and periodontal regeneration. The existence of craniofacial bone-specific SSCs is suggested based on existing studies. The effects of calcium, vitamin D, and soy isoflavone supplementation on alveolar and skeletal bone loss in post-menopausal women were investigated. Supplementation resulted in stabilization of forearm bone mass density and a reduced rate of alveolar bone loss over 1 yr, compared with placebo. Periodontal attachment levels were also well-maintained and alveolar bone loss suppressed during 24 wk of supplementation.
• Advances in dental research.Adv Dent Res.2014 May;26(1):38-46. doi: 10.1177/0022034514529305.
• This article reviews recent research into mechanisms underlying bone resorption and highlights avenues of investigation that may generate new therapies to combat alveolar bone loss in periodontitis. Several proteins, signaling pathways, stem cells, and dietary supplements are discussed as they relat
• PMID 24736703

• Mitogen-activated protein kinase phosphatase-1 promotes neovascularization and angiogenic gene expression.

• Boerckel JD1, Chandrasekharan UM, Waitkus MS, Tillmaand EG, Bartlett R, Dicorleto PE.Author information 1From the Department of Cellular and Molecular Medicine, Lerner Research Institute, Cleveland Clinic, OH (J.D.B., U.M.C., M.S.W., E.G.T., R.B., P.E.D.); and Department of Aerospace and Mechanical Engineering, University of Notre Dame, IN (J.D.B.).AbstractOBJECTIVE: Angiogenesis is the formation of new blood vessels through endothelial cell sprouting. This process requires the mitogen-activated protein kinases, signaling molecules that are negatively regulated by the mitogen-activated protein kinase phosphatase-1 (MKP-1). The purpose of this study was to evaluate the role of MKP-1 in neovascularization in vivo and identify associated mechanisms in endothelial cells.
• Arteriosclerosis, thrombosis, and vascular biology.Arterioscler Thromb Vasc Biol.2014 May;34(5):1020-31. doi: 10.1161/ATVBAHA.114.303403. Epub 2014 Feb 27.
• OBJECTIVE: Angiogenesis is the formation of new blood vessels through endothelial cell sprouting. This process requires the mitogen-activated protein kinases, signaling molecules that are negatively regulated by the mitogen-activated protein kinase phosphatase-1 (MKP-1). The purpose of this study wa
• PMID 24578378

• Macrophage Migration Inhibitory Factor inhibits the anti-inflammatory effects of glucocorticoids via glucocorticoid-induced leucine zipper.

• Fan H1, Kao W, Yang YH, Gu R, Harris J, Fingerle-Rowson G, Bucala R, Ngo D, Beaulieu E, Morand EF.Author information 1Centre for Inflammatory Diseases, Monash University, Melbourne, Australia.AbstractObjectives: Glucocorticoids remain a mainstay of the treatment of rheumatoid arthritis (RA). Dose-dependent adverse effects highlight the potential for therapies that regulate glucocorticoid sensitivity to enable glucocorticoid dose reduction. Macrophage migration inhibitory factor (MIF) is a pro-inflammatory protein implicated in the pathogenesis of RA, which also impairs glucocorticoid sensitivity via inhibition of the MAP kinase phosphatase, MKP-1. The intracellular protein glucocorticoid-induced leucine zipper (GILZ) mimics the effects of glucocorticoids in models of RA, but whether it represents a target for the modulation of glucocorticoid sensitivity remains unknown. We therefore investigated whether GILZ is implicated in regulation of glucocorticoid sensitivity by MIF. Methods: GILZ expression was studied in the presence and absence of MIF, and the role of GILZ in the MIF-dependent regulation of the glucocorticoid sensitivity mediator MAP kinase phosphatase-1 (MKP-1) studied at the level of expression and function. Results: GILZ expression was significantly inhibited by endogenous MIF, both basally and during responses to glucocorticoid treatment. The effects of MIF on GILZ were dependent on the expression and Akt-induced nuclear translocation of the transcription factor FoxO3a. GILZ was shown to regulate the expression of MKP-1, and consequent MAP kinase phosphorylation and cytokine release. Conclusions: MIF exerts its effects on MKP-1 expression and MAP kinase activity through inhibitory effects on GILZ. These findings suggest a previously unsuspected intersection between these two molecules and identify GILZ as a potential target for the therapeutic regulation of glucocorticoid sensitivity. © 2014 American College of Rheumatology.
• Arthritis & rheumatology (Hoboken, N.J.).Arthritis Rheumatol.2014 Apr 29. doi: 10.1002/art.38689. [Epub ahead of print]
• Objectives: Glucocorticoids remain a mainstay of the treatment of rheumatoid arthritis (RA). Dose-dependent adverse effects highlight the potential for therapies that regulate glucocorticoid sensitivity to enable glucocorticoid dose reduction. Macrophage migration inhibitory factor (MIF) is a pro-in
• PMID 24782327

Japanese Journal

• A New Artificial Fish Swarm Algorithm for the Multiple Knapsack Problem

• LIU Qing,ODAKA Tomohiro,KUROIWA Jousuke,SHIRAI Haruhiko,OGURA Hisakazu
• IEICE Transactions on Information and Systems E97.D(3), 455-468, 2014
• … A new artificial fish swarm algorithm (AFSA) for solving the multiple knapsack problem (MKP) is introduced in this paper. …
• NAID 130003394861

• アフラトキシン B1 誘導ラット肝細胞癌由来 K2 細胞の悪性化に secreted protein acidic and rich in cysteine（SPARC）のダウンレギュレーションが関与している

• 須田 三記也,鴨志田 光,林 朋子,小川 槙子,大塚 寛子,村上 重和,古宮 裕子,村上 康文,秋山 弘匡,田代 文夫
• マイコトキシン 63(2), 151-159, 2013
• … る．以前に私達は，アフラトキシン B1 誘発ラット肝細胞癌由来 K2 細胞において14-3-3β/fourteen-three-three-beta interactant1（FBI1）/specific protein 3（Sp3）転写因子/histone deacetylase 1（HDAC1）複合体は，MAP kinase phosphatase 1（MKP-1）の遺伝子発現を負に制御することで MAP キナーゼシグナル伝達経路を活性化し，転移や造腫瘍能を賦与していることを明らかにした．本研究においては，K2 細胞の悪性化メカニズムをさらに解明するために …
• NAID 130003384016

• Circadian clock-controlled diurnal oscillation of Ras/ERK signaling in mouse liver

• TSUCHIYA Yoshiki,MINAMI Itsunari,KADOTANI Hiroshi [他],TODO Takeshi,NISHIDA Eisuke
• Proceedings of the Japan Academy, Series B 89(1), 59-65, 2013
• … Furthermore, expression of MAP kinase phosphatase-1 (Mkp-1) shows diurnal changes in liver. …
• NAID 130003365106

Related Links

• 名鉄協商 MKPポイントカード

MKPポイントカードは、名鉄協商パーキング（時間貸し）のご利用でポイントがたまるカードです 名鉄協商パーキングで貯まる、使える。MKPポイントカード

• MKPギフトカード

MKPギフトカードはギフトにも使える、お支払いに便利なプリペイドカードです。名鉄協商パーキングで共通でご使用いただけます。 ... ※Webショップモール「MPNナゴヤ」内店舗「名鉄協商パーキング」からの お申込になります ...

Related Pictures

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★リンクテーブル★

リンク元	「MAPキナーゼホスファターゼ」「mitogen-activated protein kinase phosphatase」
関連記事	「M」「MK」

「MAPキナーゼホスファターゼ」

　　[★]

英

mitogen-activated protein kinase phosphatase、MKP

関

マイトジェン活性化プロテインキナーゼホスファターゼ、MAPキナーゼ脱リン酸化酵素

「mitogen-activated protein kinase phosphatase」

　　[★]

• マイトジェン活性化プロテインキナーゼホスファターゼ、MAPキナーゼホスファターゼ、MAPキナーゼ脱リン酸化酵素

関

MKP

「M」

　　[★] メチオニン methionine 　 　

「MK」

　　[★] メナキノン menaquinone