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Transcription Factors02:16

Transcription Factors

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Tissue-specific transcription factors contribute to diverse cellular functions in mammals. For example, the gene for beta globin, a major component of hemoglobin, is present in all cells of the body. However, it is only expressed in red blood cells because the transcription factors that can bind to the promoter sequences of the beta globin gene are only expressed in these cells. Tissue-specific transcription factors also ensure that mutations in these factors may impair only the function of...
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Regulation of Expression Occurs at Multiple Steps02:24

Regulation of Expression Occurs at Multiple Steps

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Gene expression can be regulated at almost every step from gene to protein. Transcription is the step that is most commonly regulated. This involves the binding of proteins to short regulatory sequences on the DNA. This association can either promote or inhibit the transcription of a gene associated with the respective sequence.
Transcription results in the generation of precursor (pre-mRNA) that consists of both exons and introns, which needs further processing before being translated to a...
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Master Transcription Regulators02:23

Master Transcription Regulators

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Master transcription regulators are regulatory proteins that are predominantly responsible for regulating the expression of multiple genes. Often these genes work in concert to drive a  complex process. Activation of a master transcription regulator can lead to a cascade of transcriptional activation necessary for that outcome. These regulators can directly bind to the regulatory sequences of the various genes involved, or they can indirectly regulate transcription by binding to regulatory...
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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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General Transcription Factors01:30

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Tissue-specific transcription factors contribute to diverse cellular functions in mammals. For example, the gene for beta globin, a major component of hemoglobin, is present in all cells of the body. However, it is only expressed in red blood cells because the transcription factors that can bind to the promoter sequences of the beta globin gene are only expressed in these cells. Tissue-specific transcription factors also ensure that mutations in these factors may impair only the function of...
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When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
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In Vitro Differentiation of Human CD4+FOXP3+ Induced Regulatory T Cells (iTregs) from Na&#239;ve CD4+ T Cells Using a TGF-&#946;-containing Protocol
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Foxp3は,AML1/Runx1と相互作用することで,T細胞の調節機能を制御する.

Masahiro Ono1, Hiroko Yaguchi, Naganari Ohkura

  • 1Department of Experimental Pathology, Institute for Frontier Medical Sciences, Graduate School of Medicine, Kyoto University, Kyoto 606-8507, Japan.

Nature
|March 23, 2007
PubMed
まとめ

調節性T細胞 (T・R細胞) は免疫のバランスを維持する. 転写因子Foxp3はAML1と相互作用してIL-2とIFN-ガンマを抑制し,T(R) 細胞機能と免疫反応を制御する.

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科学分野:

  • 免疫学 免疫学とは
  • 分子生物学は分子生物学である.
  • トランスクリプション・ファクターの機能

背景:

  • 自然に発生するCD25+CD4+調節性T細胞 (T・R細胞) は,免疫的自己耐性および免疫ホメオスタシスの維持に不可欠です.
  • T (R) 細胞は異常な免疫反応を抑制し,自己免疫疾患やアレルギーを予防します.
  • 転写因子Foxp3はT(R) 細胞の発達と機能の重要な調節因子であり,子宮外の発現は抑制活性を与える.

研究 の 目的:

  • Foxp3がT(R) 細胞の機能を制御する分子機構を明らかにし,その中には,サイトカインの産生とT(R) 細胞に関連した分子の発現を含む.
  • 転写因子AML1 (急性骨髄性白血病1) /Runx1がT(R) 細胞関連遺伝子発現を調節する役割を調査する.
  • T細胞媒介免疫応答を制御するためにFoxp3-AML1相互作用を標的とする可能性を調査する.

主な方法:

  • 天然T (R) 細胞におけるFoxp3とAML1の相互作用を調査した.
  • この相互作用がIL-2とIFN-ガンマの遺伝子発現に与える影響を分析した.
  • T(R) 細胞関連分子と全体的な抑制活性に対する上昇調節への影響を評価した.

主要な成果:

  • AML1/Runx1が,従来のCD4+T細胞におけるIL-2およびIFN-ガンマ遺伝子発現を活性化することを示した.
  • Foxp3が自然T (R) 細胞におけるAML1と物理的に相互作用することを示した.
  • このFoxp3-AML1相互作用がIL-2およびIFN-ガンマ生成を抑制し,T(R) 細胞分子を上調し,抑制活性を与えるという証拠を提供した.

結論:

  • Foxp3とAML1の相互作用は,T(R) 細胞の機能と抑制活動を制御する重要なメカニズムです.
  • Foxp3とAML1によるこの転写制御は,免疫ホメオスタシスの維持に不可欠である.
  • Foxp3-AML1相互作用を標的にすることは,生理学的および病理学的条件下でT細胞媒介免疫反応を調節するための潜在的な戦略を提供します.