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関連する概念動画

Abnormal Proliferation02:23

Abnormal Proliferation

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 daughter...
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

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.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

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.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
Replicative Cell Senescence02:15

Replicative Cell Senescence

Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds the telomeric...
Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...

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Updated: May 12, 2026

Yeast As a Chassis for Developing Functional Assays to Study Human P53
14:57

Yeast As a Chassis for Developing Functional Assays to Study Human P53

Published on: August 4, 2019

p53による非細胞自律性腫瘍抑制

Amaia Lujambio1, Leila Akkari, Janelle Simon

  • 1Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA.

Cell
|April 9, 2013
PubMed
まとめ

p53腫瘍抑制タンパク質は,細胞衰老と抗腫瘍環境を促進することによって,肝がんを予防します. 肝細胞におけるp53機能の喪失は,線維症,肝硬変,肝細胞がんの発症を加速する.

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Purification of Ubiquitinated p53 Proteins from Mammalian Cells
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Purification of Ubiquitinated p53 Proteins from Mammalian Cells

Published on: March 21, 2022

関連する実験動画

Last Updated: May 12, 2026

Yeast As a Chassis for Developing Functional Assays to Study Human P53
14:57

Yeast As a Chassis for Developing Functional Assays to Study Human P53

Published on: August 4, 2019

Analysis of Human T Cell Activity in an Allogeneic Co-Culture Setting of Pre-Treated Tumor Cells
09:04

Analysis of Human T Cell Activity in an Allogeneic Co-Culture Setting of Pre-Treated Tumor Cells

Published on: March 7, 2025

Purification of Ubiquitinated p53 Proteins from Mammalian Cells
10:55

Purification of Ubiquitinated p53 Proteins from Mammalian Cells

Published on: March 21, 2022

科学分野:

  • 腫瘍学 腫瘍学
  • 細胞生物学 細胞生物学
  • 肝臓病理学 肝臓病理学

背景:

  • p53腫瘍抑制剤は,細胞サイクル停止,アポトーシス,老化を通して悪性変異を防ぐために重要である.
  • 細胞の老化は,安定した細胞サイクル停止であり,組織マイクロ環境に影響を与える分泌因子を含む.
  • 慢性肝損傷は,p53機能の障害によって悪化する可能性があります.

研究 の 目的:

  • 慢性肝損傷中の肝臓のステラ細胞におけるp53依存的衰老の役割を調査する.
  • 肝臓のステラト細胞におけるp53の状態が肝臓線維症,肝硬変,肝細胞性がんの発達にどのように影響するかを決定する.
  • 腫瘍微環境の形成におけるp53の非細胞自律的機能,特にマクロファージの極化を解明する.

主な方法:

  • 慢性肝損傷モデルにおける肝臓のステラ細胞におけるp53依存の衰老の消去.
  • 肝繊維症,肝硬変,および肝細胞癌の発生率の評価.
  • 衰老または増殖するp53欠乏星状細胞によって分泌される因子に反応するマクロファージの偏分 (M1対M2状態) の分析.
  • In vitro共同培養試験では,老化細胞に対するマクロファージ媒介の攻撃を評価する.

主要な成果:

  • 肝臓のステラ細胞におけるp53依存の衰老の除去により,肝臓線維症と肝硬変が著しく増加し,生存率が低下しました.
  • 肝臓のステラ細胞におけるp53機能の喪失は,隣接する上皮細胞の肝細胞がんへの変容を強めた.
  • p53を発現する老朽化した星状細胞は,M1マクロファージの極化を促進する因子を分泌し,これは腫瘍を阻害し,老朽化した細胞を攻撃することができる.
  • p53欠乏の増殖ステラート細胞は,M2マクロファージの偏分を誘発する因子を分泌し,腫瘍促進状態であり,悪性前細胞増殖を高めました.

結論:

  • p53は,抗腫瘍微環境を確立することによって,腫瘍形成を抑制する上で重要な非細胞自律的な役割を果たします.
  • p53衰老の肝臓のステラート細胞から分泌される因子は,マクロファージの機能を調節し,腫瘍抑制に向けてバランスを変化させます.
  • 肝臓の星状細胞におけるp53機能とp53依存の衰老を維持することは,肝臓線維症,肝硬変,肝細胞癌の予防に不可欠です.