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関連する概念動画

The Ras Gene02:38

The Ras Gene

6.1K
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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Small GTPases - Ras and Rho01:24

Small GTPases - Ras and Rho

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Ras and Rho are small monomeric GTPases that act downstream of receptor tyrosine kinase (RTK) and regulate various cellular processes. These GTPases switch between active and inactive states by binding to guanine nucleotides.
Three regulatory proteins control their activity:
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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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mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

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The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
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Targeted Cancer Therapies02:57

Targeted Cancer Therapies

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The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against...
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The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

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Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
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関連する実験動画

Updated: May 21, 2025

Assessing Cellular Target Engagement by SHP2 PTPN11 Phosphatase Inhibitors
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Assessing Cellular Target Engagement by SHP2 PTPN11 Phosphatase Inhibitors

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RAS変異がんにおけるSHOC2RAS相互作用を標的とする

Zachary J Hauseman1, Frédéric Stauffer2, Kim S Beyer2

  • 1Novartis BioMedical Research, Cambridge, MA, USA.

Nature
|May 7, 2025
PubMed
まとめ

研究者らは,SHOC2をRAS ((Q61*) がんの依存性として特定し,新しい標的治療法の開発を可能にしました. SHOC2-RASの相互作用を標的とする小さな分子は癌細胞の成長を阻害し,がん治療のための有望な新しい道を提供します.

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Initiation of Metastatic Breast Carcinoma by Targeting of the Ductal Epithelium with Adenovirus-Cre: A Novel Transgenic Mouse Model of Breast Cancer
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Initiation of Metastatic Breast Carcinoma by Targeting of the Ductal Epithelium with Adenovirus-Cre: A Novel Transgenic Mouse Model of Breast Cancer

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Characterize Disease-related Mutants of RAF Family Kinases by Using a Set of Practical and Feasible Methods
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Characterize Disease-related Mutants of RAF Family Kinases by Using a Set of Practical and Feasible Methods

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関連する実験動画

Last Updated: May 21, 2025

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Initiation of Metastatic Breast Carcinoma by Targeting of the Ductal Epithelium with Adenovirus-Cre: A Novel Transgenic Mouse Model of Breast Cancer
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Characterize Disease-related Mutants of RAF Family Kinases by Using a Set of Practical and Feasible Methods
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科学分野:

  • 腫瘍学
  • 分子生物学
  • 薬物の発見

背景:

  • ラット・サーコマ (RAS) 遺伝子の活性化変異は,ヒトのがんに共通する腫瘍発生因子である.
  • KRAS阻害剤が新興している一方で,メラノーマで流行しているNRAS ((Q61) *) 変異体に対する効果的な治療法は依然として必要である.

研究 の 目的:

  • RAS (Q61*) 腫瘍における依存性を特定する.
  • SHOC2RASの相互作用を標的とした新しい治療薬の発見と開発

主な方法:

  • RAS ((Q61*) 腫瘍における依存性としてSHOC2を特定した.
  • NRAS ((Q61R)) - SHOC2の相互作用を明らかにするために,X線共結結晶構造を使用した.
  • SHOC2を標的にする小分子を見つけるために,高通量スクリーニングを in vitroで行いました.
  • ツールコンパウンドを開発するために構造ベースの最適化を行いました.

主要な成果:

  • SHOC2は,ヌクレオチド状態依存性およびイソフォームアグノスティックな方法で依存性として識別されました.
  • 腫瘍性NRAS (Q61R) とSHOC2の間の直接的な相互作用は,X線結晶学で確認された.
  • SHOC2-NRAS ((Q61*) 相互作用を阻害する小分子が見つかりました.
  • RAS変異がんのモデル,特にNRAS ((Q61) *) でMAPKシグナル伝達と増殖を抑制することが実証された.

結論:

  • SHOC2-RASタンパク質の相互作用は,がん治療の薬剤対象である.
  • この研究は,RASシグナル伝達経路を標的とした新しい治療法の開発のための基盤を提供します.
  • SHOC2を標的にすることは,NRAS変異がんの治療に有望な戦略です.