WordNet

complicated in structure; consisting of interconnected parts; "a complex set of variations based on a simple folk melody"; "a complex mass of diverse laws and customs"
a compound described in terms of the central atom to which other atoms are bound or coordinated (同)coordination_compound
a conceptual whole made up of complicated and related parts; "the complex of shopping malls, houses, and roads created a new town" (同)composite
(psychoanalysis) a combination of emotions and impulses that have been rejected from awareness but still influence a persons behavior

PrepTutorEJDIC

『いくつかの部分から成る』,複合の,合成の / 『複雑な』,入りくんだ,こみいった(complicated) / 複合体,合成物 / コンプレックス,複合(抑圧されて心に残った複雑なしこり)

UpToDate Contents

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1. T細胞受容体シグナル伝達 t cell receptor signaling
2. 体液性免疫応答 the humoral immune response
3. 関節リウマチの病因 pathogenesis of rheumatoid arthritis
4. 補体系の後天性疾患 acquired disorders of the complement system
5. 補体系の制御因子および受容体 regulators and receptors of the complement system

English Journal

Mammalian target of rapamycin signaling in cardiac physiology and disease.

Sciarretta S, Volpe M, Sadoshima J.Author information From the Cardiovascular Research Institute, Department of Cell Biology and Molecular Medicine, Rutgers New Jersey Medical School, Newark, NJ (S.S., J.S.); IRCCS Neuromed, Pozzilli, Italy (S.S., M.V.); and Division of Cardiology, Department of Clinical and Molecular Medicine, Faculty of Medicine and Psychology, University Sapienza, Rome, Italy (M.V.).AbstractThe protein kinase mammalian or mechanistic target of rapamycin (mTOR) is an atypical serine/threonine kinase that exerts its main cellular functions by interacting with specific adaptor proteins to form 2 different multiprotein complexes, mTOR complex 1 (mTORC1) and mTOR complex 2 (mTORC2). mTORC1 regulates protein synthesis, cell growth and proliferation, autophagy, cell metabolism, and stress responses, whereas mTORC2 seems to regulate cell survival and polarity. The mTOR pathway plays a key regulatory function in cardiovascular physiology and pathology. However, the majority of information available about mTOR function in the cardiovascular system is related to the role of mTORC1 in the unstressed and stressed heart. mTORC1 is required for embryonic cardiovascular development and for postnatal maintenance of cardiac structure and function. In addition, mTORC1 is necessary for cardiac adaptation to pressure overload and development of compensatory hypertrophy. However, partial and selective pharmacological and genetic inhibition of mTORC1 was shown to extend life span in mammals, reduce pathological hypertrophy and heart failure caused by increased load or genetic cardiomyopathies, reduce myocardial damage after acute and chronic myocardial infarction, and reduce cardiac derangements caused by metabolic disorders. The optimal therapeutic strategy to target mTORC1 and increase cardioprotection is under intense investigation. This article reviews the information available regarding the effects exerted by mTOR signaling in cardiovascular physiology and pathological states.
Circulation research.Circ Res.2014 Jan 31;114(3):549-64. doi: 10.1161/CIRCRESAHA.114.302022.
The protein kinase mammalian or mechanistic target of rapamycin (mTOR) is an atypical serine/threonine kinase that exerts its main cellular functions by interacting with specific adaptor proteins to form 2 different multiprotein complexes, mTOR complex 1 (mTORC1) and mTOR complex 2 (mTORC2). mTORC1
PMID 24481845

Genetic and Pharmacologic Evidence That mTOR Targeting Outweighs mTORC1 Inhibition as an Antimyeloma Strategy.

Chen X, Díaz-Rodríguez E, Ocio EM, Paiva B, Mortensen DS, Lopez-Girona A, Chopra R, Miguel JS, Pandiella A.Author information Authors' Affiliations: 1Instituto de Biología Molecular y Celular del Cáncer, CSIC-Universidad de Salamanca; 2Hospital Universitario de Salamanca, Salamanca, Spain; Departments of 3Medicinal Chemistry and 4Translational Development, Celgene, Summit, New Jersey.AbstractThe mammalian target of rapamycin (mTOR) is a serine/threonine kinase that regulates cell growth, proliferation, metabolism, and cell survival, and plays those roles by forming two functionally distinct multiprotein complexes: mTOR complex 1 (mTORC1) and mTOR complex 2 (mTORC2). Deregulation of the mTOR pathway has been found in different cancers, including multiple myeloma. Agents acting on mTORC1, such as rapamycin and derivatives, are being explored as antitumoral strategies. However, whether targeting mTOR would be a more effective antimyeloma strategy than exclusively acting on the mTORC1 branch remains to be established. In this report, we explored the activation status of mTOR routes in malignant plasma cells, and analyzed the contribution of mTOR and its two signaling branches to the proliferation of myeloma cells. Gene expression profiling demonstrated deregulation of mTOR pathway-related genes in myeloma plasma cells from patients. Activation of the mTOR pathway in myelomatous plasma cells was corroborated by flow cytometric analyses. RNA interference (RNAi) experiments indicated that mTORC1 predominated over mTORC2 in the control of myeloma cell proliferation. However, mTOR knockdown had a superior antiproliferative effect than acting only on mTORC1 or mTORC2. Pharmacologic studies corroborated that the neutralization of mTOR has a stronger antimyeloma effect than the individual inhibition of mTORC1 or mTORC2. Together, our data support the clinical development of agents that widely target mTOR, instead of agents, such as rapamycin or its derivatives, that solely act on mTORC1. Mol Cancer Ther; 13(2); 1-13. ©2014 AACR.
Molecular cancer therapeutics.Mol Cancer Ther.2014 Jan 28. [Epub ahead of print]
The mammalian target of rapamycin (mTOR) is a serine/threonine kinase that regulates cell growth, proliferation, metabolism, and cell survival, and plays those roles by forming two functionally distinct multiprotein complexes: mTOR complex 1 (mTORC1) and mTOR complex 2 (mTORC2). Deregulation of the
PMID 24431075

Lysine Deacetylase (KDAC) Regulatory Pathways: an Alternative Approach to Selective Modulation.

Van Dyke MW.Author information Department of Chemistry & Biochemistry, Kennesaw State University, 1000 Chastain Road, MD# 1203, Kennesaw, GA 30144 (USA). mvandyk2@kennesaw.edu.AbstractProtein lysine deacetylases (KDACs), including the classic Zn2+ -dependent histone deacetylases (HDACs) and the nicotinamide adenine dinucleotide (NAD+ )-requiring sirtuins, are enzymes that play critical roles in numerous biological processes, particularly the epigenetic regulation of global gene expression programs in response to internal and external cues. Dysregulation of KDACs is characteristic of several human diseases, including chronic metabolic, neurodegenerative, and cardiovascular diseases and many cancers. This has led to the development of KDAC modulators, two of which (HDAC inhibitors vorinostat and romidepsin) have been approved for the treatment of cutaneous T cell lymphoma. By their nature, existing KDAC modulators are relatively nonspecific, leading to pan-KDAC changes and undesired side effects. Given that KDACs are regulated at many levels, including transcriptional, post-translational, subcellular localization, and through their complexation with other proteins, it should be possible to affect specific KDAC activity through manipulation of endogenous signaling pathways. In this Minireview, we discuss our present knowledge of the cellular controls of KDAC activity and examples of their pharmacologic regulation.
ChemMedChem.ChemMedChem.2014 Jan 21. doi: 10.1002/cmdc.201300444. [Epub ahead of print]
Protein lysine deacetylases (KDACs), including the classic Zn2+ -dependent histone deacetylases (HDACs) and the nicotinamide adenine dinucleotide (NAD+ )-requiring sirtuins, are enzymes that play critical roles in numerous biological processes, particularly the epigenetic regulation of global gene e
PMID 24449617

Japanese Journal

核内レセプターを介した情報伝達機構

加藤茂明
日本薬理学雑誌 116(3), 133-140, 2000-09-01
… DNA-bound nuclear receptors control transcription in a ligand-binding dependent way in cooperation with a multiprotein complex containing RNA polymerase II and a series of auxillary factors, TFILA, B, D, E, F and H. … Several transcriptional co-activators and co-repressors forming coactivator complexes have been recently identified, and their function is discussed. …
NAID 10008180830