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KAKEN_26860528seika.pdf
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Download
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:182.9 KB
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| Last updated |
:Jan 6, 2017 |
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Total downloads since Jan 6, 2017 : 439
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| Title |
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ADAM10による腸管腫瘍形成機構の解明
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| Kana |
ADAM10 ニ ヨル チョウカン シュヨウ ケイセイ キコウ ノ カイメイ
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ADAM10 ni yoru chokan shuyo keisei kiko no kaimei
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Mechanism of intestinal tumor formation through ADAM10
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股野, 麻未
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マタノ, マミ
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Matano, Mami
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慶應義塾大学・医学部・研究員
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Research team head
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科研費研究者番号 : 20439889
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2016
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科学研究費補助金研究成果報告書
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2015
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我々は, ADAM10 floxマウスとvillin-CreERマウスを交配させ, 上皮特異的なADAM10ノックアウトマウスを作製した。タモキシフェンによるノックアウト誘導により, 腸管上皮の著名な胚細胞の数の上昇と幹細胞の減少を観察しえた。ADAM10ノックアウト上皮は幹細胞機能分化および分化亢進のため, 継時的な消失を示した。ADAM10はNotchリガンドの細胞内ドメインの切断によるシグナル活性化に関与しており, 本ノックアウトマウスではNotchシグナル活性の低下を認めたことから, Notchシグナル制御異常が幹細胞消失を誘導したと考えられた。
Our research group generated an epithelium specific ADAM10 knock-out mice through crossing ADAM10 flox mouse with villin-CreER mice. Tamoxifen induced knock out resulted in increased goblet cells and decreased intestinal stem cells. This can be explained by increased stem cell differentiation. ADAM10 is involved in Notch signal activation through degradation of the intracellular domain. Indeed, ADAM10 knock-out intestinal epithelium inactivated Notch signal, resulting in loss of intestinal stem cells.
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研究種目 : 若手研究(B)
研究期間 : 2014～2015
課題番号 : 26860528
研究分野 : 消化器内科学
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