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1. 发明申请

WO2010078198A1 SHORTENED ALK1 REGULATORY FRAGMENT 审中-公开
标题翻译：短暂的ALK1调节片段
公开(公告)号：WO2010078198A1
公开(公告)日：2010-07-08
申请号：PCT/US2009/069435
申请日：2009-12-23
申请人： MEDICAL COLLEGE OF GEORGIA RESEARCH INSTITUTE, INC. , SEKI, Tsugio
发明人： SEKI, Tsugio
IPC分类号： C12N15/00 , C07H21/04
CPC分类号： C07K14/71 , C12N15/85 , C12N15/86 , C12N2710/10343 , C12N2830/008
摘要： Regulatory elements for controlling expression of transgenes in angiogenic tissue are provided. One embodiment provides an isolated nucleic acid having at least 80%, 85%, 90%, 95%, 97%, 99% or 100% sequence identity to SEQ ID NO: I, or a fragment thereof that causes expression of a transgene in angiogenic tissue. Vectors containing SEQ ID NO: 1 and one or more transgenes are also provided. A preferred vector is an adenovirus vector. The transgene can encode a cytotoxin, pro-apoptotic polypeptide, or a therapeutic polypeptide. SEQ ID NO:1 regulates the expression of the transgene such that the transgene is only expressed in angiogenic tissue including, but not limited to arteries feeding ischemic tissues. Methods of using vectors containing SEQ ID NO: 1 are also provided.
摘要翻译：提供了用于控制血管生成组织中转基因表达的调节元件。一个实施方案提供了与SEQ ID NO：1具有至少80％，85％，90％，95％，97％，99％或100％序列同一性的分离的核酸或其导致转基因表达的片段血管生成组织。还提供了含有SEQ ID NO：1的载体和一种或多种转基因。优选的载体是腺病毒载体。转基因可编码细胞毒素，促凋亡多肽或治疗性多肽。 SEQ ID NO：1调节转基因的表达，使得转基因仅在血管生成组织中表达，包括但不限于进食缺血组织的动脉。还提供了使用含有SEQ ID NO：1的载体的方法。

2. 发明申请

WO2012149342A1 MOUSE MODEL FOR AVM 审中-公开
标题翻译： AVM的鼠标模型
公开(公告)号：WO2012149342A1
公开(公告)日：2012-11-01
申请号：PCT/US2012/035483
申请日：2012-04-27
申请人： GEORGIA HEALTH SCIENCES UNIVERSITY , SEKI, Tsugio , ALLEYNE, Cargill , YANASAK, Nathan
发明人： SEKI, Tsugio , ALLEYNE, Cargill , YANASAK, Nathan
IPC分类号： A01K67/027 , A61P9/00 , A61K31/54 , C12Q1/00 , C12N15/01
CPC分类号： G01N33/5088 , A01K67/0276 , A01K2217/075 , A01K2227/105 , A01K2267/0375 , C12N9/12 , C12Q1/485 , G01N2800/32 , G01N2800/7014 , G01N2800/7095
摘要： Arteriovenous malformation, or Arteriovenous vascular malformation (AVM) is a congenic disorder characterized by an abnormal connection between veins and arteries, resulting in hemorrhaging and even death. A lack of good animal models has long been an obstacle for identifying effective drugs for neurological AVM treatment. Describe herein is a mouse model for AVM that includes a viable, postnatal animal with a conditional deletion of the activin receptor-like kinase 1 (Alkl;Acvrll). The Alkl-cKO mouse model can be used to identify genes and gene products that are upregulated in subjects suffering from AVM. For example, it has been discovered Agpt2, ILip, and TNF-a, are upregulated in Alkl-cKO compared to controls. Pharmaceutical compositions for treatment of AVM are disclosed. Preferred compositions inhibit or decrease expression of angiogenic and pro-inflammatory factors, such as VEFG, Cox-2, Agpt2, ILip, TNF-α, and matrix metalloproteinases. Methods of determining efficacy of potential AVM therapeutics are also disclosed.
摘要翻译：动静脉畸形或动静脉血管畸形（AVM）是以静脉和动脉之间异常连接为特征的致病性疾病，导致出血甚至死亡。缺乏良好的动物模型长期以来一直是确定有效的神经AVM治疗药物的障碍。本文描述了AVM的小鼠模型，其包括具有激活素受体样激酶1（Alk1; Acvrll）的条件缺失的可行的出生后动物。 Alkl-cKO小鼠模型可用于鉴定在患有AVM的受试者中上调的基因和基因产物。例如，与对照相比，已经发现Agk1-cKO中的Agpt2，ILip和TNF-α被上调。公开了用于治疗AVM的药物组合物。优选的组合物抑制或降低血管生成和促炎因子如VEFG，Cox-2，Agpt2，ILip，TNF-α和基质金属蛋白酶的表达。还公开了确定潜在AVM治疗剂功效的方法。

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