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Protein Networks02:26

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An organism can have thousands of different proteins, and these proteins must cooperate to ensure the health of an organism. Proteins bind to other proteins and form complexes to carry out their functions. Many proteins interact with multiple other proteins creating a complex network of protein interactions.
These interactions can be represented through maps depicting protein-protein interaction networks, represented as nodes and edges. Nodes are circles that are representative of a protein,...
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Inositol-requiring kinase one or IRE1 is the most conserved eukaryotic unfolded protein response (UPR) receptor. It is a type I transmembrane protein kinase receptor with a distinctive site-specific RNase activity. As the binding mechanics of the misfolded proteins with the N-terminal domain of IRE-1 are unclear, three binding models — direct, indirect, and allosteric -- are proposed for receptor activation. Nevertheless, it is known that once a misfolded protein associates with IRE1, it...
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Cell death is an essential process where the body gets rid of old or damaged cells. Cell proliferation and death need to be balanced, as an imbalance between the two may lead to cancer or autoimmune diseases.
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Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
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Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
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Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...
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デザイナーのタンパク質が細胞死を誘発する.

Wayne J Fairbrother1, Avi Ashkenazi2

  • 1Department of Early Discovery Biochemistry, Genentech, Inc., 1 DNA Way, South San Francisco, CA 94080, USA.

Cell
|June 21, 2014
PubMed
まとめ
この要約は機械生成です。

研究者は,コンピューティング方法とターゲティング進化を使用して,新しいポリペプチド阻害剤を設計しました. この阻害剤は,ウイルスのBcl-2-のようなタンパク質を効果的に標的とし,感染した細胞にアポトーシスを誘導します.

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科学分野:

  • バイオケミストリー バイオケミストリー
  • コンピュータ生物学 コンピュータ生物学
  • 分子生物学は分子生物学である.

背景:

  • デノボのタンパク質設計は,歴史的に,既存のタンパク質の構造を修正することに限定されてきた.
  • ウイルス感染症に対する新しい治療薬の開発は,依然として重要な課題です.

研究 の 目的:

  • ウイルスのBcl-2-のようなタンパク質を標的としたデノボポリペプチド阻害剤を計算的に設計し,実験的に検証する.
  • ウイルスに感染した細胞のアポトーシスを誘発するこの阻害剤の可能性を調査する.

主な方法:

  • 革新的な計算設計戦略を使用して,新しいタンパク質構造を作成しました.
  • 阻害剤の効能と特異性を最適化するために,試験管標的進化で採用されます.
  • ウイルスに感染した細胞でアポトーシスを誘発する阻害剤の有効性を評価した.

主要な成果:

  • 強力なポリペプチド阻害剤をデ・ノボ・コンピューティング・デザインとターゲティング・エボリューションで成功裏に生成した.
  • 設計された阻害剤は,ウイルス性Bcl-2-のようなタンパク質に対して有意な活性を示した.
  • 抑制剤はウイルスに感染した細胞でアポトーシスを効果的に誘導し,その治療的可能性を強調しました.

結論:

  • De novo計算設計は,標的型進化と組み合わせると,非常に効果的なタンパク質ベースの治療法を得ることができます.
  • 開発されたポリペプチド阻害剤は,標的細胞死を誘発することによって,ウイルス感染症と戦うための有望な新しい戦略を表しています.