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Cell Specific Gene Expression01:58

Cell Specific Gene Expression

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Multicellular organisms contain a variety of structurally and functionally distinct cell types, but the DNA in all the cells originated from the same parent cells. The differences in the cells can be attributed to the differential gene expression. Liver cells, whose functions include detoxification of blood, production of bile to metabolize fats, and synthesis of proteins essential for metabolism, must express a specific set of genes to perform their functions. Gene expression also varies with...
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Co-activators and Co-repressors02:04

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Gene transcription is regulated by the synergistic action of several proteins that form a complex at a gene regulatory site. This is observed in eukaryotes, where the regulation of gene expression is a complex process. Regulatory proteins in eukaryotes can broadly be classified into two types – regulators that bind directly to specific DNA sequences and co-regulators that associate with regulatory proteins but cannot directly bind to the DNA. These co-regulators are further divided into...
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Abnormal Proliferation02:23

Abnormal Proliferation

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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
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GPCRs Regulate Adenylyl Cylase Activity01:09

GPCRs Regulate Adenylyl Cylase Activity

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Some GPCRs transmit signals through adenylyl cyclase (AC), a transmembrane enzyme. AC helps synthesize second messenger cyclic adenosine monophosphate (cAMP). AC catalyzes cyclization reaction and converts ATP to cAMP by releasing a pyrophosphate. The pyrophosphate is further hydrolyzed to phosphate by the enzyme pyrophosphatase, which drives cAMP synthesis to completion. However, cAMP is rapidly degraded to 5′ AMP by the enzymes phosphodiesterase (PDE), preventing overstimulation of...
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cAMP-dependent Protein Kinase Pathways01:25

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Cyclic Adenosine Monophosphate (cAMP) is an essential second messenger that activates protein kinase A (PKA) and regulates various biological processes. A single epinephrine molecule binds to GPCR and activates several heterotrimeric G proteins, each stimulating multiple adenylyl cyclase, amplifying the signal, and synthesizing large numbers of cAMP molecules. Small changes in cAMP concentration affect PKA activity. The binding of four cAMP molecules induces a conformational change in PKA,...
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Transducer Mechanism: Nuclear Receptors01:31

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Nuclear receptors, or NRs, are unique transcription factors that regulate gene transcription and affect the cellular pathways involved in reproduction, development, or metabolism. Their ability to be stimulated by small lipophilic ligands and control vital cellular processes makes them ideal drug targets. Nearly 10-15% of currently prescribed drugs target these receptors.
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Isolation and Differentiation of Stromal Vascular Cells to Beige/Brite Cells
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PPARalpha活性化剤は,ヒト単細胞における組織因子の発現と活性を阻害する.

N Marx1, N Mackman, U Schönbeck

  • 1Department of Internal Medicine II-Cardiology, University of Ulm, Germany. nikolaus.marx@medizin.uni-ulm.de

Circulation
|February 24, 2001
PubMed
まとめ

ペロキシソーム増殖器活性化受容体アルファ (PPARalpha) アクティベータは,ヒト単細胞における組織因子 (TF) の発現と活性を低下させます. この発見は,動脈硬化性病変における血栓形成性を減らすための潜在的な治療戦略を示唆しています.

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科学分野:

  • 心血管生物学 心血管生物学
  • 分子医学は分子医学である.
  • 薬理学 薬理学とは

背景:

  • モノサイト/マクロファージの組織因子 (TF) は,急性冠動脈症候群において血栓形成を開始する.
  • ペロキシソーム増殖器活性化受容体アルファ (PPARalpha) は,遺伝子発現を調節する.
  • PPARalpha活性化剤は,患者のTF活動を低下させる可能性があります.

研究 の 目的:

  • PPARalpha活性化剤がヒト単細胞細胞におけるTF反応を制限できるかどうかを調査する.
  • PPARalpha活性化剤がTF発現に影響を与えるメカニズムを探求する.

主な方法:

  • 人間のモノサイトとマクロファージは,PPARalpha活性化剤 (WY14643,ETYA) で治療されました.
  • リポポリサッカリド (LPS) は,TFの活性と発現を誘導するために使用されました.
  • TF活性,タンパク質,mRNA,およびプロモーター活性が測定されました.
  • 核因子-kappaB (NF-κB) の結合と活性が評価されました.

主要な成果:

  • PPARalpha活性化剤は,LPS誘発のTF活動とモノサイト/マクロファージの発現を著しく低下させた.
  • PPARガンマ活性化剤は,同様の効果を示さなかった.
  • WY14643は,腫瘍死滅因子アルファタンパク質を減少させ,LPS誘発のTFプロモーター活性を抑制し,おそらくNF-κB抑制によるものであった.

結論:

  • PPARα活性化剤は,ヒトモノサイト/マクロファージにおけるTF発現と活性を効果的に低下させます.
  • これらの発見は,動脈硬化性病変の血栓性低下におけるPPARalpha活性化剤の潜在的な役割を示唆しています.
  • このデータは,PPARアルファ活性化化合物がアテロトロンボシスにどのように影響するかを洞察する情報を提供します.