関連する実験動画
Updated: May 5, 2026

12:19
Analysis of Cell Cycle Position in Mammalian Cells
Published on: January 21, 2012
60.4K
まとめ
c-mycやc-rasKiのような細胞腫瘍遺伝子は,がんと関連している. その発現は細胞の成長と分裂に結びついており,化学的変異により正常な細胞循環の調節が妨げられます.
科学分野:
- 分子生物学は分子生物学である.
- 細胞生物学 細胞生物学
- がん研究 がん研究
背景:
- 細胞腫瘍遺伝子は,がんの発症に関与するDNA配列である.
- 細胞の変容におけるそれらの正確な役割は不明である.
- プロトオンコゲンであるc-mycとc-rasKiは,これらのプロセスを理解するための重要な標的である.
研究 の 目的:
- プロトオンコゲン発現 (c-myc,c-rasKi) と細胞成長制御との関係を調査する.
- 微分化と化学変換が原発性腫瘍遺伝子の発現にどのように影響するか調べる.
- プロト・オンコゲン機能を,増殖制御とその破壊と結びつける.
主な方法:
- Balb/c 3T3細胞,化学的に変換された誘導体 (BPA31, DA31) およびF9テラトカルシノマ幹細胞のc-mycおよびc-rasKimRNAレベルを分析する.
- 静止細胞,成長細胞,分化細胞におけるmRNAの豊富さを比較する.
- 血清刺激および末端分化中の遺伝子発現変化の評価.
主要な成果:
- 血清刺激により,静止状態のBalb/c 3T3細胞におけるc-mycプロトオンコゲンの発現が上昇する.
- 化学的に変異した細胞 (BPA31,DA31) は,構成的なc-myc発現を示し,細胞サイクル依存性を失います.
- c-rasKiの発現は,変形細胞の細胞サイクルに依存し,G0/G1.0の半ばから後半に増加します.
- F9細胞の末端分化により,c-rasKi mRNAよりもc-myc mRNAが減少する.
結論:
- プロトオンコゲン発現 (myc, rasKi) は,細胞の成長状態に依存しています.
- 成長制御は,成長因子に依存し,細胞サイクルにタイミングを合わせた腫瘍遺伝子の発現を伴う.
- 化学的変換は,増幅または過剰表現なしに,c-mycのような腫瘍遺伝子の細胞サイクル調節の喪失につながる可能性があります.
関連する概念動画
Positive Regulator Molecules
100.8K
To consistently produce healthy cells, the cell cycle—the process that generates daughter cells—must be precisely regulated.
100.8K
Positive Regulator Molecules
5.3K
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.
5.3K
Inhibition of Cdk Activity
4.8K
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...
4.8K
Mitogens and the Cell Cycle
6.3K
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...
6.3K
Abnormal Proliferation
4.0K
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...
4.0K
The Ras Gene
5.7K
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...
Ras is a...
5.7K

