会员体验
专利管家(专利管理)
工作空间(专利管理)
风险监控(情报监控)
数据分析(专利分析)
侵权分析(诉讼无效)
联系我们
交流群
官方交流:
QQ群: 891211   
微信请扫码    >>>
现在联系顾问~
热词
    • 4. 发明授权
    • Use of VEGF and homologues to treat neuron disorders
    • 使用VEGF和同系物治疗神经元疾病
    • US07226908B2
    • 2007-06-05
    • US10257423
    • 2001-04-12
    • Peter CarmelietDésiré CollenBert Oosthuyse
    • Peter CarmelietDésiré CollenBert Oosthuyse
    • A61K38/18C07K14/475
    • A01K67/0276A01K2217/075A01K2227/105A01K2267/0312A01K2267/0318A01K2267/0356A61K38/1866A61K48/00C07K14/52C12N15/8509C12N2800/30C12N2830/002C12N2830/85
    • The present invention relates to neurological and physiological dysfunction associated with neuron disorders. In (particular, the invention relates to the involvement of vascular endothelial growth factor (VEGF) and homologues in the aetiology of motor neuron disorders. The invention further concerns a novel, mutant transgenic mouse (VEGFm/m) with a homozygous deletion in the hypoxia responsive element (HRE) of the VEGF promoter which alters the hypoxic upregulation of VEGF. These mice suffer severe adult onset muscle weakness due to progressive spinal motor neuron degeneration which is reminiscent of amyotrophic lateral sclerosis (ALS)—a fatal disorder with unknown aetiology. Furthermore, the neuropathy of these mice is not caused by vascular defects, but is due to defective VEGF-mediated survival signals to motor neurons. The present invention relates in particular to the isoform VEGF165 which stimulates survival of motor neurons via binding to neuropilin-1, a receptor known to bind semaphorin-3A which is implicated in axon retraction and neuronal death, and the VEGF Receptor-2. The present invention thus relates to the usage of VEGF, in particular VEGF165, for the treatment of neuron disorders and relates, in addition, to the usage of polymorphisms in the VEGF promotor for diagnosing the latter disorders.
    • 本发明涉及与神经元疾病相关的神经和生理功能障碍。 (特别是本发明涉及血管内皮生长因子(VEGF)和同系物参与运动神经元病症的病因,本发明还涉及一种新型突变型转基因小鼠(VEGF m / )在VEGF启动子的缺氧应答元件(HRE)中具有纯合缺失,其改变VEGF的缺氧上调,这些小鼠由于进行性脊髓运动神经元变性而受到严重的成年发作性肌无力,这使人想起肌萎缩性侧索硬化(ALS) 此外,这些小鼠的神经病变不是由血管缺陷引起的,而是由于VEGF介导的对运动神经元的存活信号的缺陷。本发明特别涉及同种型VEGF 165 其通过结合神经胶质蛋白-1刺激运动神经元的存活,神经胶质蛋白-1是已知结合轴突回缩和神经元死亡的信号素-3A的受体,以及VEGF Re ceptor-2。 因此,本发明涉及VEGF,特别是VEGF 165用于治疗神经元病症的用途,此外还涉及VEGF启动子中用于诊断后一种疾病的多态性的用途。
    • 9. 发明申请
    • Use of VEGF and homologues to treat neuron disorders
    • 使用VEGF和同系物治疗神经元疾病
    • US20110288020A1
    • 2011-11-24
    • US12928131
    • 2010-12-03
    • Peter CarmelietDésiré CollenBert Oosthuyse
    • Peter CarmelietDésiré CollenBert Oosthuyse
    • A61K38/18A61P25/00C12Q1/02A61K31/7088
    • A01K67/0276A01K2217/075A01K2227/105A01K2267/0312A01K2267/0318A01K2267/0356A61K38/1866A61K48/00C07K14/52C12N15/8509C12N2800/30C12N2830/002C12N2830/85
    • The present invention relates to neurological and physiological dysfunction associated with neuron disorders. In particular, the invention relates to the involvement of vascular endothelial growth factor (VEGF) and homologues in the aetiology of motor neuron disorders. The invention further concerns a novel, mutant transgenic mouse (VEGFm/m) with a homozygous deletion in the hypoxia responsive element (HRE) of the VEGF promoter which alters the hypoxic upregulation of VEGF. These mice suffer severe adult onset muscle weakness due to progressive spinal motor neuron degeneration which is reminiscent of amyotrophic lateral sclerosis (ALS)—a fatal disorder with unknown aetiology. Furthermore, the neuropathy of these mice is not caused by vascular defects, but is due to defective VEGF-mediated survival signals to motor neurons. The present invention relates in particular to the isoform VEGF165 which stimulates survival of motor neurons via binding to neuropilin-1, a receptor known to bind semaphorin-3A which is implicated in axon retraction and neuronal death, and the VEGF Receptor-2. The present invention thus relates to the usage of VEGF, in particular VEGF165, for the treatment of neuron disorders and relates, in addition, to the usage of polymorphisms in the VEGF promotor for diagnosing the latter disorders.
    • 本发明涉及与神经元疾病相关的神经和生理功能障碍。 特别地,本发明涉及血管内皮生长因子(VEGF)和同系物参与运动神经元疾病的病因学。 本发明还涉及在VEGF启动子的缺氧应答元件(HRE)中具有纯合缺失的新型突变转基因小鼠(VEGFm / m),其改变VEGF的缺氧上调。 这些小鼠由于进行性脊髓运动神经元变性而遭受严重的成人发作肌肉无力,其使人想起肌萎缩性侧索硬化(ALS) - 一种具有未知病因的致命性疾病。 此外,这些小鼠的神经病变不是由血管缺陷引起的,而是由于VEGF介导的运动神经元的生存信号。 本发明特别涉及通过与神经胶蛋白-1结合来刺激运动神经元的存活的同种型VEGF165,该神经蛋白-1是已知结合轴突回缩和神经元死亡的信号素-3A的受体以及VEGF受体-2。 因此,本发明涉及VEGF,特别是VEGF165用于治疗神经元病症的用途,此外还涉及VEGF启动子中用于诊断后一种疾病的多态性的用途。