The biological activity of vascular endothelial growth factor (VEGF), the major cytokine regulating the process of angiogenesis is tightly controlled at multiple levels including processes involving post-translational modification such as ADP-ribosylation and glycosylation. ADP-ribosylation is a reversible NAD⁺-dependent modification, catalyzed by poly ADP-ribose polymerase (PARP) or ADP-ribosyl transferase (ADPRTs) and has been reported by us and others as a modification that reduces the biological activity of VEGF. The factors responsible for any such modification should occur in the secretory pathway, i.e., in the endoplasmic reticulum and Golgi. Our investigation carried out in this direction revealed that ADP-ribosylation of VEGF requires the interplay between members of poly ADP-ribose polymerase (PARP) family in the secretory pathway, viz., ER associated PARP-16 and Golgi associated Tankyrase-2 (TNKS-2). The data presented in this manuscript suggest that PARP-16 catalysis the priming mono ADP-ribosylation of VEGF which is a prerequisite for poly ADP-ribosylation of VEGF by TNKS-2.

调节血管生成过程的主要细胞因子血管内皮生长因子（VEGF）的生物学活性在多个水平上受到严格控制，包括涉及翻译后修饰（例如ADP-核糖基化和糖基化）的过程。ADP-核糖基化是可逆的NAD ⁺依赖性修饰，由聚ADP-核糖聚合酶（PARP）或ADP-核糖基转移酶（ADPRTs）催化，被我们和其他人报道为降低VEGF生物活性的修饰。引起任何此类修饰的因素应发生在分泌途径中，即在内质网和高尔基体中。我们朝这个方向进行的研究显示，VEGF的ADP-核糖基化需要分泌途径中的聚ADP-核糖聚合酶（PARP）家族成员之间的相互作用，即ER相关的PARP-16和Golgi相关的Tankyrase-2（TNKS -2）。该手稿中的数据表明，PARP-16催化VEGF的引发单ADP-核糖基化，这是TNKS-2对VEGF进行聚ADP-核糖基化的先决条件。