College of Pharmacy and Research Institute of Drug Development, Chonnam National University, Gwangju, Republic of Korea.
FEBS Open Bio. 2012 Nov 29;3:16-21. doi: 10.1016/j.fob.2012.11.006. Print 2013.
Accumulated evidence suggests that aberrant regulation of δ-catenin leads to pathological consequences such as mental retardation and cognitive dysfunction. This study revealed that 14-3-3ɛ/ζ stabilizes δ-catenin, with different binding regions involved in the interaction. Furthermore, the specific inhibition of the interaction of 14-3-3 with δ-catenin reduced levels of δ-catenin and significantly impaired the capacity of δ-catenin to induce dendritic branching in both NIH3T3 fibroblasts and primary hippocampal neurons. However, the S1094A δ-catenin mutant, which cannot interact with 14-3-3ζ, still retained the capability of inducing dendrogenesis. Taken together, these results elucidate the underlying events that regulate the stability of δ-catenin and δ-catenin-induced dendrogenesis.
已有大量证据表明，δ-catenin 的异常调节会导致智力迟钝和认知功能障碍等病理后果。本研究揭示了 14-3-3ɛ/ζ 可稳定 δ-catenin，涉及不同的结合区域参与相互作用。此外，特异性抑制 14-3-3 与 δ-catenin 的相互作用会降低 δ-catenin 的水平，并显著损害 δ-catenin 在 NIH3T3 成纤维细胞和原代海马神经元中诱导树突分支的能力。然而，不能与 14-3-3ζ 相互作用的 S1094A δ-catenin 突变体仍然保留诱导树突发生的能力。综上所述，这些结果阐明了调节 δ-catenin 稳定性和 δ-catenin 诱导的树突发生的潜在事件。
