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Phosphorylated KDR can be located in the nucleus of neoplastic cells

Phosphorylated KDR can be located in the nucleus of neoplastic cells
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摘要 KDR (kinase 插入领域受体) phosphorylation 导致最后带到房间增长和幸存的几效果。一旦它被激活, KDR 与原子核由交流的精确机制正在开始被理解,但是还没是完全 unravelled。二在在文学报导的动物细胞线上的 vitro 研究表明了那,跟随有 VEGF 的刺激, KDR 实际上是在原子核以内的 translocated。我们的目的是调查这 translocation 是否在 vitro 并且在 vivo 发生在人的房间。用扫描共焦的显微镜学的激光,在房间线和瘤样品的 phosphorylated 和全部的 KDR 的可变原子本地化被发现。在人的肿瘤的房间线, hypoxic 刺激极大地增加了全部的 KDR,但是少些的原子数量以便 phosphorylated 形式。仅仅在组织缺氧和 VEGF 刺激以后,有在这些房间的原子核观察的 phosphorylated 和全部的 KDR 的可比较地增加的表情。我们断定肿瘤的房间在原子核显示出总数和 phosphorylated KDR 的可变表情。要证实的原子地点遗体的精确功能的意思。 KDR (kinase insert domain receptor) phosphorylation induces several effects which lead eventually to cell proliferation and survival. The precise mechanisms by which KDR, once it is activated, communicates with the nucleus are starting to be understood but have not yet been completely unravelled. Two in vitro studies on animal cell lines reported in the literature have demonstrated that, following stimulation with VEGF, KDR is actually translocated within the nucleus. Our aim was to investigate whether this translocation occurs in human cells both in vitro and in vivo. Using laser scanning confocal microscopy, a variable nuclear localization of phosphorylated and total KDR in cell lines and tumour samples was found. In human neoplastic cell lines, hypoxic stimulation greatly increased the nuclear amount of total KDR but less so that of the phosphorylated form. Only after hypoxia and VEGF stimulation there was a comparably increased expression of phosphorylated and total KDR observed in the nuclei of these cells. We conclude that neoplastic cells show a variable expression of total and phosphorylated KDR in the nucleus. The precise functional meaning of nuclear location remains to be established.
出处 《Cell Research》 SCIE CAS CSCD 2006年第1期93-98,共6页 细胞研究(英文版)
关键词 KDR 磷酸化 原子核 肿瘤细胞 治疗 KDR, human neoplasma, hypoxia, nucleus
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参考文献31

  • 1Carmeliet P, Jain RK. Angiogenesis in cancer and other diseases.Nature 2000; 407:249-57.
  • 2Yancopoulos GD, Davis S, Gale NW, et al. Vascular-specific growth factors and blood vessel formation. Nature 2000;407:242-8.
  • 3Fidler IJ. Regulation of neoplastic angiogenesis. J Natl Cancer Inst Monogr 2001; 28:10-4.
  • 4Ferrara N.VEGF: an update on biological and therapeutic aspects. Curr Opin Biotechnol 2000; 11:617-24.
  • 5Ferrara N. Role of vascular endothelial growth factor in regulation of physiological angiogenesis. Am J Physiol Cell Physiol 2001; 280:C1358-66.
  • 6de Vries C, Escobedo JA, Ueno H. et al. The fms-like tyrosine kinase, a receptor for vascular endothelial growth factor. Science 1992; 255:989-91.
  • 7Lee J, Gray A, Yuan J. et al. Vascular endothelial growth factor-related protein: a ligand and specific activator of the tyrosine kinase receptor Flt4. Proc Natl Acad Sci U S A 1996; 93:1988-92.
  • 8Terman BI, Dougher-Vermazen M, Carrion ME, et al. Identification of the KDR tyrosine kinase as a receptor for vascular endothelial cell growth factor. Biochem Biophys Res Commun 1992; 187:1579-86.
  • 9Soker S, Takashima S, Miao HQ, Neufeld G, Klagsbrun M.Neuropilin-1 is expressed by endothelial and tumor cells as an isoform-specific receptor for vascular endothelial growth factor.Cell 1998; 92:735-45.
  • 10Petrova TV, Makinen T, Alitalo K. Signaling via vascular endothelial growth factor receptors. Exp Cell Res 1999; 253:117-30.

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