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関連する概念動画

Positive Regulator Molecules01:45

Positive Regulator Molecules

To consistently produce healthy cells, the cell cycle—the process that generates daughter cells—must be precisely regulated.
Negative Regulator Molecules01:23

Negative Regulator Molecules

Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
Positive Regulator Molecules02:39

Positive Regulator Molecules

Mitotic cell division results in daughter cells that exactly resemble the parent cell. However, errors in the DNA replication or distribution of genetic material may lead to genetic mutations that may be passed down to every new cell formed from the resulting abnormal cell. Propagation of such mutant cells is restricted through checkpoint mechanisms present at different stages of the cell cycle. These checkpoints involve regulator molecules that either promote or demote cell cycle events.
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
M-Cdk Drives Transition Into Mitosis02:15

M-Cdk Drives Transition Into Mitosis

Checkpoints throughout the cell cycle serve as safeguards and gatekeepers, allowing the cell cycle to progress in favorable conditions and slow or halt it in problematic ones. This regulation is known as the cell cycle control system.
Cyclin-dependent kinases, or Cdks, work in concert with cyclins to control cell cycle transitions. M-Cdk, a complex of Cdk1 bound to M cyclin, is a well-known example of this coordinated control that drives the transition from the G2 to the M phase.
M cyclin...
Inhibition of CDK Activity02:34

Inhibition of CDK Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...

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関連する実験動画

Updated: May 13, 2026

Analysis of Cell Cycle Position in Mammalian Cells
12:19

Analysis of Cell Cycle Position in Mammalian Cells

Published on: January 21, 2012

サイクリンC/cdk3はRb依存のG0出口を促進する.

Shengjun Ren1, Barrett J Rollins

  • 1Department of Medical Oncology, Dana-Farber Cancer Institute, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.

Cell
|April 16, 2004
PubMed
まとめ

細胞のG0脱出には,サイクリンCとcdk3が関与し,それらはpRbをリン酸化して,細胞サイクルへの再侵入を可能にします. この独特のサイクリン/cdkの組み合わせは,G1/S相調節と同様に,G0/G1移行を調節する.

科学分野:

  • 細胞生物学 細胞生物学
  • 分子生物学は分子生物学である.
  • バイオケミストリー バイオケミストリー

背景:

  • 細胞サイクルは,G0 (休息状態) とG1 (DNA合成の準備) を含む明確な段階を含んでいます.
  • G1/S移行はよく知られているが,G0/G1移行の規制はほとんど不明である.
  • 網膜芽細胞腫タンパク質 (pRb) の不活性化は,G0.0.から細胞サイクル再入力に不可欠です.

研究 の 目的:

  • G0/G1移行を調節する分子メカニズムを調査する.
  • G0終了時にpRbのリン酸化に関与する主要なタンパク質を特定する.
  • G0/G1の調節におけるサイクリンCとその関連キナーゼの役割を明らかにする.

主な方法:

  • G0終了時のサイクリンC mRNAレベルの分析.
  • サイクリンCとサイクリン依存キナーゼ (cdks) の相互作用を調査する.
  • シクリンC/cdk3複合体の特定の部位でのpRbリン酸化に対する効果の評価 (S807/811)

主要な成果:

  • サイクリンCのレベルは,G0の脱出時にピークに達し,このプロセスにおける役割を示唆しています.
  • cdk8に関連していないサイクリンCのプールは,cdk3と複合体を形成する.

さらに関連する動画

Development of Inhibitors of Protein-protein Interactions through REPLACE: Application to the Design and Development Non-ATP Competitive CDK Inhibitors
10:33

Development of Inhibitors of Protein-protein Interactions through REPLACE: Application to the Design and Development Non-ATP Competitive CDK Inhibitors

Published on: October 26, 2015

Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols
12:02

Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols

Published on: June 6, 2017

関連する実験動画

Last Updated: May 13, 2026

Analysis of Cell Cycle Position in Mammalian Cells
12:19

Analysis of Cell Cycle Position in Mammalian Cells

Published on: January 21, 2012

Development of Inhibitors of Protein-protein Interactions through REPLACE: Application to the Design and Development Non-ATP Competitive CDK Inhibitors
10:33

Development of Inhibitors of Protein-protein Interactions through REPLACE: Application to the Design and Development Non-ATP Competitive CDK Inhibitors

Published on: October 26, 2015

Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols
12:02

Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols

Published on: June 6, 2017

  • このサイクリンC/cdk3複合体は,S807/811でpRbをリン酸化し,効率的なG0出口に不可欠である.

    • 結論:

    • G0/G1の移行は,特定のサイクリン/cdkの組み合わせ,特にサイクリンC/cdk3.3によって制御されます.
    • サイクリンC/cdk3によるS807/811のpRbのリン酸化は,細胞がG0.0から脱出するための重要なステップです.
    • この発見は,G1/S移行に類似する規制メカニズムを明らかにしているが,サイクリン/cdkペアが異なる.