ネズミの細胞におけるv-srcと鶏のc-srcの発現は,pp60v-srcとpp60c-srcの間の質的な違いを示しています
Cell
|May 1, 1984
まとめ
細胞内のsrcタンパク質 (pp60c-src) のレベルが上昇すると,癌は発生しません. しかし,ウイルス src タンパク質 (pp60v-src) は腫瘍の成長を誘発することができ,これらの関連腫瘍遺伝子の違いを強調します.
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
- 腫瘍生成 (オンコゲネシス) について
背景:
- レトロウイルス腫瘍遺伝子のv-srcは,細胞遺伝子のc-srcから発生します.
- 構造的な類似性は,c-srcが腫瘍発生的可能性をもっていることを示唆しています.
研究 の 目的:
- セルラーSRC遺伝子 (c-src) の腫瘍発生の可能性を調査する.
- pp60c-srcとpp60v-srcの変換能力を比較する.
主な方法:
- 鶏のc-src発現のためのキメリックプラズミドの構築.
- ネズミ-2細胞をキメリックDNAで変異させ,PP60c-src値が上昇した細胞系を作り出す.
- セルラーとウイルスのSRCタンパク質発現レベルとセルラー現象型の比較.
主要な成果:
- ネズミの細胞系は,正常のpp60c-srcレベルの10倍で,表型的には正常であり,アクチンケーブルを保持し,柔らかいアガー成長を示さなかった.
- pp60c-srcは,pp60v-srcの変換値を超えるレベルで生成されました.
- v-src誘発型変異による感染は,正常および高血圧 pp60c-src 細胞系の両方で発生し,丸い形状,アクチンの破壊,および軟アガーの成長が特徴です.
結論:
- pp60c-srcの過剰発現は単独では細胞変異を誘導しない.
- ウイルス腫瘍遺伝子のpp60v-srcは,細胞の同位体とは異なる強力な変異活性を持っています.
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