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  5. 医療科学
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  11. Mettl13 Eef1aのメチル化は,腫瘍発生を促進するトランスレーション出力を増加させる
  1. ホーム
  3. 研究分野
  5. 医療科学
  7. 流行病学について
  9. 疫学的な方法
  11. Mettl13 Eef1aのメチル化は,腫瘍発生を促進するトランスレーション出力を増加させる

関連する実験動画

Targeted DNA Methylation Analysis by Next-generation Sequencing
08:38

Targeted DNA Methylation Analysis by Next-generation Sequencing

Published on: February 24, 2015

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METTL13 eEF1Aのメチル化は,腫瘍発生を促進するトランスレーション出力を増加させる

Shuo Liu1, Simone Hausmann2, Scott Moore Carlson1

  • 1Department of Biology, Stanford University, Stanford, CA 94305, USA.

Cell
|January 8, 2019

PubMed で要約を見る

まとめ
この要約は機械生成です。

ユカリオット延長因子1AのMETTL13タンパク質の改変が癌の成長を促進する. METTL13とeEF1AK55me2を阻害すると,Ras誘発がんの腫瘍発症が減り,薬剤感受性が増加する.

科学分野:

  • 分子生物学
  • 腫瘍学
  • 生物化学

背景:

  • タンパク質合成の増加は 癌の発生に不可欠です
  • Ras駆動の癌は,腫瘍形成のトランスレーション出力の強化に依存しています.

研究 の 目的:

  • Ras誘発がんにおけるMETTL13媒介のeEF1Aメチル化の役割を調査する.
  • METTL13-eEF1AK55me2を 治療対象として検討する.

主な方法:

  • GTPaseの活性を測定する in vitro 測定法
  • タンパク質の生産を評価する細胞検査
  • マウスモデルと患者からの異種移植 (PDX) を用いたin vivo研究.

主要な成果:

  • リンシン55 (eEF1AK55me2) でのeEF1AのMETTL13二メチル化により,タンパク質合成が増加し,腫瘍の成長が促進されます.
  • METTL13とeEF1AK55me2の値上昇は,臓がんと肺がんの患者の生存率の低下と相関しています.
  • METTL13の消去またはeEF1AK55me2の喪失はRas誘導腫瘍の生体内での成長を有意に抑制する.
  • METTL13の減少は 標的治療に腫瘍を敏感にします
キーワード:
METTL13 についてRAS についてeEF1A肺がんリジンメチル化臓がんタンパク質メチル化翻訳トランスレーションの延長

さらに関連する動画

Methylated DNA Immunoprecipitation
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Methylated DNA Immunoprecipitation

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In vitro Methylation Assay to Study Protein Arginine Methylation
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In vitro Methylation Assay to Study Protein Arginine Methylation

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Targeted DNA Methylation Analysis by Next-generation Sequencing
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Targeted DNA Methylation Analysis by Next-generation Sequencing

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Methylated DNA Immunoprecipitation
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Methylated DNA Immunoprecipitation

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In vitro Methylation Assay to Study Protein Arginine Methylation
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In vitro Methylation Assay to Study Protein Arginine Methylation

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結論:

  • METTL13-eEF1AK55me2軸は,Ras駆動がんの高いタンパク質合成要求を満たすのに不可欠です.
  • METTL13を標的にすることは,異常なRasシグナル伝達を持つがんに対する潜在的な治療戦略です.