Rabbit Anti-Human NRCAM (a.a. 47-451) Polyclonal antibody

Action potential initiation and propagation requires clustered Na+ (voltage-gated Na+ [Nav]) channels at axon Initial segments (AIS) and nodes of Ranvier. In addition to ion channels, these domains are characterized by cell adhesion molecules (CAMs; neurofascin-186 [NF-186] and neuron glia-related CAM [NrCAM]), cytoskeletal proteins (ankyrinG and PIV spectrin), and the extracellular chondroitin-sulfate proteoglycan brevican. Schwann cells initiate peripheral nervous system node formation by clustering NF-186, which then recruits ankyrinG and Nav channels. However, AIS assembly of this protein complex does not require glial contact. To determine the AIS assembly mechanism, we silenced expression of AIS proteins by RNA interference. AnkyrinG knockdown prevented AIS localization of all other AIS proteins. Loss of NF-186, NrCAM, Nav channels, or PIV spectrin did not affect other neuronal AIS proteins. However, loss of NF-186 blocked assembly of the brevican-based AIS extracellular matrix, and NF-186 overexpression caused somatodendritic brevican clustering. Thus, NF-186 assembles and links the specialized brevican-containing AIS extracellular matrix to the intracellular cytoskeleton.

Previous researchers have demonstrated that microRNA-505 (miR-505) is negatively correlated with progression in various malignancies. However, the detailed function and molecular mechanisms of miR-505 have yet to be completely elucidated in prostate cancer (PCa). The present study initially identified the potential role of miR-505 in PCa using in vitro experiments, and demonstrated that restoration of miR-505 inhibited proliferation, invasion and migration, yet induced cell cycle arrest and promoted apoptosis in PCa cells. The present study also demonstrated that the expression of neuron-glial-related cell adhesion molecule (NRCAM) was markedly upregulated in PCa cells when compared with benign prostate epithelium. A luciferase reporter assay demonstrated that miR-505 directly targeted NRCAM in PCa cells. In addition, NRCAM stimulation antagonized the inhibitory effects of miR-505 on the proliferation, migration, and invasion of PCa cells. Furthermore, lower levels of miR-505 and higher levels of NRCAM may serve as a predictor of worse biochemical recurrence-free survival or disease-free survival in patients with PCa. In conclusion, the present study revealed the inhibitory effects of miR-505 on PCa tumorigenesis, which potentially occur by targeting NRCAM. The combined analysis of NRCAM and miR-505 may predict disease progression in patients with PCa following radical prostatectomy.