Advanced Centre for Treatment Research and Education in Cancer, Tata Memorial Centre, Kharghar Node, Navi Mumbai, India.
Cell Mol Life Sci. 2011 Apr;68(8):1439-54. doi: 10.1007/s00018-010-0531-3. Epub 2010 Sep 23.
A decrease in the levels of the desmosomal plaque protein, plakophilin3 (PKP3), leads to a decrease in desmosome size and cell-cell adhesion. To test the hypothesis that PKP3 is required for desmosome formation, the recruitment of desmosomal components to the cell surface was studied in the PKP3 knockdown clones. The PKP3 knockdown clones showed decreased cell border staining for multiple desmosomal proteins, when compared to vector controls, and did not form desmosomes in a calcium switch assay. Further analysis demonstrated that PKP3, plakoglobin (PG) and E-cadherin are present at the cell border at low concentrations of calcium. Loss of either PG or E-cadherin led to a decrease in the levels of PKP3 and other desmosomal proteins at the cell border. The results reported here are consistent with the model that PG and E-cadherin recruit PKP3 to the cell border to initiate desmosome formation.
桥粒斑蛋白 3（PKP3）水平降低会导致桥粒大小和细胞间黏附减少。为了验证 PKP3 对于桥粒形成是必需的这一假设，研究人员在 PKP3 敲低克隆中研究了桥粒成分向细胞表面的募集情况。与载体对照相比，PKP3 敲低克隆的多个桥粒蛋白的细胞边缘染色减少，并且在钙转换测定中未形成桥粒。进一步的分析表明，PKP3、桥粒斑蛋白（PG）和 E-钙黏蛋白在低钙浓度下存在于细胞边缘。PG 或 E-钙黏蛋白的缺失导致细胞边缘 PKP3 和其他桥粒蛋白水平降低。这里报道的结果与以下模型一致，即 PG 和 E-钙黏蛋白将 PKP3 募集到细胞边缘以启动桥粒形成。
