Department of Cardiology, The Second Xiangya Hospital of Central South University, Changsha, Hunan, People's Republic China.
Mol Cell Biochem. 2009 Nov;331(1-2):225-30. doi: 10.1007/s11010-009-0163-9. Epub 2009 Jun 12.
Reticulon3 (RTN3), as a member of the reticulon family, is generally regarded as a novel human apoptosis-inducing protein. But the extensional role of RTN3 remains virtually unknown. Herein, we showed that cysteine rich with EGF like domains 1(CRELD1), a cell adhesion molecule played a critical role in atrioventricular septal defects and it had mutual effect with RTN3 in vitro. Furthermore, we discovered that ectopic CRELD1 could interact with ectopic or endogenous RTN3. CRELD1 bound with RTN3 so as to increase the localization of RTN3 on the plasma membrane and decreased the apoptotic activity of RTN3 moderately. Moreover, the tunicamycin-inducing cell apoptosis was partly suppressed by this kind of interaction mentioned above. These results suggested that CRELD1 could partly change the localization of RTN3 from the endoplasmic reticulum to the plasma membrane and modulate the apoptotic activity of RTN3 through binding with it.
Reticulon3（RTN3）作为 reticulon 家族的一员，通常被认为是一种新型的人类凋亡诱导蛋白。但 RTN3 的扩展作用实际上是未知的。在此，我们表明富含半胱氨酸的表皮生长因子样域 1（CRELD1），一种细胞黏附分子，在房室间隔缺损中起着关键作用，并且它在体外与 RTN3 有相互作用。此外，我们发现异位 CRELD1 可以与异位或内源性 RTN3 相互作用。CRELD1 与 RTN3 结合，从而增加 RTN3 在质膜上的定位，并适度降低 RTN3 的凋亡活性。此外，这种相互作用部分抑制了衣霉素诱导的细胞凋亡。这些结果表明，CRELD1 可以部分改变 RTN3 从内质网到质膜的定位，并通过与 RTN3 结合来调节其凋亡活性。
