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Mitogens and the Cell Cycle02:38

Mitogens and the Cell Cycle

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Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
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The Ras Gene02:38

The Ras Gene

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The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
Ras is a...
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The Retinoblastoma Gene01:20

The Retinoblastoma Gene

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Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
The first-ever tumor suppressor gene called Rb was identified in retinoblastoma - a rare eye tumor in children. In inherited forms of the disease, a child inherits one defective copy of the Rb gene, which predisposes them to retinoblastoma. However,...
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Receptor Downregulation in MVBs01:15

Receptor Downregulation in MVBs

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Multivesicular bodies (MVBs) are mature endosomes that sort ubiquitinated proteins and then fuse with lysosomes to degrade the sorted proteins. Epidermal growth factor (EGF) and its receptor (EGFR) form a complex that can be internalized through endocytosis, sorted into an MVB, and later degraded.
The EGFR can initiate signaling pathways that  lead to cell proliferation, migration, and differentiation. Overexpression of EGFR  stimulates cells to proliferate. Excessive  EGFR...
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Regulation of Angiogenesis and Blood Supply01:24

Regulation of Angiogenesis and Blood Supply

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Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl...
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Role of Ephrin-Eph Signalling in Intestinal Stem Cell Renewal

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Erythropoietin-producing hepatocellular carcinoma receptor (Eph) and its ligand, Eph receptor-interacting protein (Ephrin) were first discovered in the human carcinoma cell line, hence the name. Ephrin-Eph interaction guides cells to reach their appropriate location in adult tissues. They also play an essential role in the immune system by helping in immune cell migration, adhesion, and activation. Based on their structure and function, Eph is divided into two classes — EphA and EphB.
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Updated: May 5, 2026

A Combined 3D Tissue Engineered In Vitro/In Silico Lung Tumor Model for Predicting Drug Effectiveness in Specific Mutational Backgrounds
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EGFRは不確定状態にある.

Michael J Eck1, William C Hahn

  • 1Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA 02215, USA. eck@red.dfci.harvard.edu

Cell
|May 15, 2012
PubMed
まとめ
この要約は機械生成です。

エピデルマ・成長因子受容体 (EGFR) の腫瘍性変異は,乱れたキナーゼ状態を安定させ,異常な活性化につながるので,癌を促進します. この研究は,EGFR変異が構造的不安定性を通して癌を駆動する方法を明らかにしています.

さらに関連する動画

Establishing Dual Resistance to EGFR-TKI and MET-TKI in Lung Adenocarcinoma Cells In Vitro with a 2-step Dose-escalation Procedure
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Deciphering the Structural Effects of Activating EGFR Somatic Mutations with Molecular Dynamics Simulation
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A Combined 3D Tissue Engineered In Vitro/In Silico Lung Tumor Model for Predicting Drug Effectiveness in Specific Mutational Backgrounds
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Establishing Dual Resistance to EGFR-TKI and MET-TKI in Lung Adenocarcinoma Cells In Vitro with a 2-step Dose-escalation Procedure
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Deciphering the Structural Effects of Activating EGFR Somatic Mutations with Molecular Dynamics Simulation
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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
  • 分子生物学は分子生物学である.
  • がん研究 がん研究

背景:

  • 皮膚表皮成長因子受容体 (EGFR) のシグナル伝達は,正常な細胞機能にとって極めて重要です.
  • EGFRの活性化には通常,リガンド結合が求められ,受容体の二分化が起こります.
  • 変異によって引き起こされる異常なEGFRシグナリングは,多くのがんの特徴です.

研究 の 目的:

  • 腫瘍性EGFR活性化の構造的基礎を調査する.
  • EGFRの突然変異が正常な規制メカニズムを克服する方法を理解する.

主な方法:

  • EGFRキナーゼドメインの構造分析.
  • ダイメリゼーションとアクティベーション状態を評価するための生化学的測定法.

主要な成果:

  • EGFRキナーゼは部分的に乱れた状態に存在します.
  • 発がん性突然変異は,この乱れた状態を安定させ,二分化を促進します.
  • 乱れた状態の安定化は,リガンド独立のEGFR活性化につながります.

結論:

  • EGFRキナーゼの部分的に乱れた状態は本質的に不安定である.
  • 腫瘍性突然変異は,この不安定性を相殺し,異常なEGFRシグナリングを誘導する.
  • この構造的不安定性をターゲットにすることで,EGFR変異がんに対する新しい治療戦略を提供することができる.