在MDCK-II细胞中，对在其PKA靶向基序（(152)SRRTS）处带有未磷酸化氨基酸的GFP-AQP5嵌合蛋白进行转运。
Trafficking of GFP-AQP5 chimeric proteins conferred with unphosphorylated amino acids at their PKA-target motif ((152)SRRTS) in MDCK-II cells.
作者信息
Karabasil Mileva Ratko, Hasegawa Takahiro, Azlina Ahmad, Purwanti Nunuk, Purevjav Javkhlan, Yao Chenjuan, Akamatsu Tetsuya, Hosoi Kazuo
机构信息
Department of Molecular Oral Physiology, Institute of Health Biosciences, the University of Tokushima Graduate School, Japan.
出版信息
J Med Invest. 2009 Feb;56(1-2):55-63. doi: 10.2152/jmi.56.55.
Three constructs having mutated PKA-target motif at (152)SRRTS of AQP5, an exocrine type water channel, were prepared and fused to C-terminus of green fluorescence protein cDNA to examine the effects of blocking of phosphorylation at (152)SRRTS (a consensus PKA-target motif of AQP5) on translocation or trafficking of the chimeric proteins expressed in the Madin-Darby canine kidney-II (MDCK-II) cells. H-89 treatment increased translocation of wild-type GFP-AQP5 to the apical membrane. All 3 mutant molecules translocated 1.5 to 2 times more than the control wild-type GFP-AQP5. Colchicine but not cytochalasin B inhibited the translocation of wild-type GFP-AQP5. Present results suggest dephosphorylation of this consensus sequence increase GFP-AQP5 translocation, and that microtubules but not microfilaments are involved in this event.
制备了三种在水通道蛋白5（一种外分泌型水通道）的（152）SRRTS处具有突变PKA靶向基序的构建体，并将其与绿色荧光蛋白cDNA的C末端融合，以研究阻断（152）SRRTS（水通道蛋白5的共有PKA靶向基序）处的磷酸化对在犬肾Madin-Darby II型（MDCK-II）细胞中表达的嵌合蛋白的转运或运输的影响。H-89处理增加了野生型GFP-水通道蛋白5向顶端膜的转运。所有3种突变分子的转运量比对照野生型GFP-水通道蛋白5多1.5至2倍。秋水仙碱而非细胞松弛素B抑制野生型GFP-水通道蛋白5的转运。目前的结果表明，该共有序列的去磷酸化增加了GFP-水通道蛋白5的转运，并且微管而非微丝参与了这一过程。
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