NINL
Domain
The KEN and D (destructive) boxes are required for the cell cycle-controlled NINL degradation by the APC/C pathway.
Function
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. Involved in vesicle transport in photoreceptor cells (By similarity). May play a role in ovarian carcinogenesis.
Post-translational modifications
Phosphorylated by PLK1 which disrupts its centrosome association and interaction with gamma-tubulin.
Ubiquitinated by the APC/C complex leading to its degradation.
Tissue Specificity
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.
Cellular localization
- Cytoplasm
- Cytoskeleton
- Microtubule organizing center
- Centrosome
- Cytoplasm
- 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).
Alternative names
KIAA0980, NLP, NINL, Ninein-like protein