Involved in the microtubule organization in interphase cells. Overexpression induces the fragmentation of the Golgi, and causes lysosomes to disperse toward the cell periphery; it also interferes with mitotic spindle assembly. May play a role in ovarian carcinogenesis. Interacts with gamma-tubulin and TUBGCP4. Interacts with anaphase promoting complex/cyclosome (APC/C). Interacts with CDC20 and FZR1. Isoform 2 interacts with LCA5 and USH2A. In interphase cells, NINL is transported to the centrosomes by the dynein-dynactin motor complex (PubMed:16254247). During centrosome maturation, PLK1 directly phosphorylates NINL resulting in its release into the cytoplasm (PubMed:16254247). Expressed in KYSE-150 esophageal carcinoma, HeLa cervical carcinoma and U2OS osteosarcoma cells. Expression is regulated in a cell cycle-dependent manner and peaks during G2/M phase (at protein level). Expressed in fetal heart, skeletal muscle, liver, lung and cochlea, and in adult brain, testis, kidney and retina. The KEN and D (destructive) boxes are required for the cell cycle-controlled NINL degradation by the APC/C pathway. Phosphorylated by PLK1 which disrupts its centrosome association and interaction with gamma-tubulin. Ubiquitinated by the APC/C complex leading to its degradation. Truncated N-terminus. Truncated C-terminus.