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1. 发明授权

US06586203B1 ARF-P19, a novel regulator of the mammalian cell cycle 有权
公开(公告)号：US06586203B1
公开(公告)日：2003-07-01
申请号：US09129855
申请日：1998-08-06
申请人： Charles J. Sherr , Dawn Quelle , Martine F. Roussel , Frederique Zindy
发明人： Charles J. Sherr , Dawn Quelle , Martine F. Roussel , Frederique Zindy
IPC分类号： C12P2106
CPC分类号： C07K14/4703 , A01K2217/05 , A01K2217/075 , A61K38/00 , A61K48/00 , C07K14/4738 , C07K2319/00
摘要： The INK4A (MTS1, CDKN2) gene encodes a specific inhibitor (InK4a-p16) of the cyclin D-dependent kinases CDK4 and CDK6. InK4a-p16 can block these kinase from phosphorylating the retinoblastoma protein (pRb), preventing exit from the G1 phase of the cell cycle. Deletions and mutations involving the gene encoding InK4a-p16, INK4A, occur frequently in cancer cells, implying that INK4a-p16, like pRb, suppresses tumor formulation. However, a completely unrelated protein (ARF-p19) arises in major part from an alternative reading frame of the mouse INK4A gene. Expression of an ARF-p19 cDNA (SEQ ID NO:1) in rodent fibroblasts induces both G1 and G2 phase arrest. Economical reutilization of protein coding sequences in this manner is without precedent in mammalian genomes, and the unitary inheritance of INK4a-p16 and ARF-p19 may reflect a dual requirement for both proteins in cell cycle control.

2. 发明授权

US06407062B1 ARF-P19, a novel regulator of the mammalian cell cycle 有权
标题翻译： ARF-P19是哺乳动物细胞周期的新型调节剂
公开(公告)号：US06407062B1
公开(公告)日：2002-06-18
申请号：US09480718
申请日：2000-01-07
申请人： Charles J. Sherr , Dawn Quelle , Martine F. Roussel , Frederique Zindy , Jason D. Weber
发明人： Charles J. Sherr , Dawn Quelle , Martine F. Roussel , Frederique Zindy , Jason D. Weber
IPC分类号： C07K1400
CPC分类号： C07K14/4738 , A01K2217/05 , A01K2217/075 , A61K38/00 , A61K48/00 , C07K14/4703 , C07K2319/00
摘要： The INK4A (MTS1, CDKN2) gene encodes a specific inhibitor (InK4a-p16) of the cyclin D-dependent kinases CDK4 and CDK6. InK4a-p16 can block these kinase from phosphorylating the retinoblastoma protein (pRb), preventing exit from the G1 phase of the cell cycle. Deletions and mutations involving the gene encoding InK4a-p16, INK4A, occur frequently in cancer cells, implying that INK4a-p16, like pRb, suppresses tumor formulation. However, a completely unrelated protein (ARF-p19) arises in major part from an alternative reading frame of the mouse INK4A gene. Expression of an ARF-p19 cDNA (SEQ ID NO:1) in rodent fibroblasts induces both G1 and G2 phase arrest. Economical reutilization of protein coding sequences in this manner is without precedent in mammalian genomes, and the unitary inheritance of INK4a-p16 and ARF-p19 may reflect a dual requirement for both proteins in cell cycle control.
摘要翻译： INK4A（MTS1，CDKN2）基因编码细胞周期蛋白D-依赖性激酶CDK4和CDK6的特异性抑制剂（InK4a-p16）。 InK4a-p16可以阻断这些激酶磷酸化视网膜母细胞瘤蛋白（pRb），从而阻止细胞周期的G1期退出。涉及编码InK4a-p16，INK4A的基因的缺失和突变频繁发生在癌细胞中，意味着像pRb一样的INK4a-p16抑制了肿瘤的制备。然而，完全不相关的蛋白质（ARF-p19）主要来自小鼠INK4A基因的替代阅读框架。 ARF-p19 cDNA（SEQ ID NO：1）在啮齿动物成纤维细胞中的表达诱导G1期和G2期停滞。蛋白质编码序列的经济再利用在哺乳动物基因组中是没有先例的，INK4a-p16和ARF-p19的单位遗传可能反映了细胞周期控制中两种蛋白质的双重要求。

3. 发明授权

US6046032A ARF-P19, a novel regulator of the mammalian cell cycle 失效
公开(公告)号：US6046032A
公开(公告)日：2000-04-04
申请号：US129855
申请日：1998-08-06
申请人： Charles J. Sherr , Dawn Quelle , Martine F. Roussel , Frederique Zindy
发明人： Charles J. Sherr , Dawn Quelle , Martine F. Roussel , Frederique Zindy
摘要： The INK4A (MTS1, CDKN2) gene encodes a specific inhibitor (InK4a-p16) of the cyclin D-dependent kinases CDK4 and CDK6. InK4a-p16 can block these kinase from phosphorylating the retinoblastoma protein (pRb), preventing exit from the G1 phase of the cell cycle. Deletions and mutations involving the gene encoding InK4a-p16, INK4A, occur frequently in cancer cells, implying that INK4a-p16, like pRb, suppresses tumor formulation. However, a completely unrelated protein (ARF-p19) arises in major part from an alternative reading frame of the mouse INK4A gene. Expression of an ARF-p19 cDNA (SEQ ID NO:1) in rodent fibroblasts induces both G1 and G2 phase arrest. Economical reutilization of protein coding sequences in this manner is without precedent in mammalian genomes, and the unitary inheritance of INK4a-p16 and ARF-p19 may reflect a dual requirement for both proteins in cell cycle control.

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