Адам ағзасындағы нейрон жасушасының адгезия молекуласы (NCAM/CD56)

Mammalian protein found in Homo sapiens

Neural cell adhesion molecule (NCAM), also called CD56, is a homophilic binding glycoprotein expressed on the surface of neurons, glia and skeletal muscle. Although CD56 is often considered a marker of neural lineage commitment due to its discovery site, CD56 expression is also found in, among others, the hematopoietic system. Here, the expression of CD56 is mostly associated with, but not limited to, natural killer cells. CD56 has been detected on other lymphoid cells, including gamma delta (γδ) Τ cells and activated CD8+ T cells, as well as on dendritic cells. NCAM has been implicated as having a role in cell–cell adhesion, neurite outgrowth, synaptic plasticity, and learning and memory.

Another layer of complexity is created by the insertion of other "minor" exons in the NCAM transcript. The two most notable are:
the VASE (VAriable domain Spliced Exon) exon which is thought to correlate with an inhibition of the neurite outgrowth promoting properties of NCAM. the MSD (Muscle Specific Domain), which is thought to play a positive role in myoblast fusion. In skeletal muscle it is found in all three NCAM isoforms, increasing their MW, giving NCAM 125, NCAM 145, and NCAM 185 isoforms, but is most commonly found in the NCAM 125 isoform.

The neural cell adhesion molecule NCAM1 appears on early embryonic cells and is important in the formation of cell collectives and their boundaries at sites of morphogenesis. Later in development, NCAM1 (CD56) expression is found on various differentiated tissues and is a major CAM mediating adhesion among neurons and between neurons and muscle.

NCAM is thought to signal to induce neurite outgrowth via the fibroblast growth factor receptor (FGFR) and act upon the p59Fyn signaling pathway. In nerves, NCAM1 regulates homophilic (like like) interactions between neurons and between neurons and muscle; it associates with fibroblast growth factor receptor (FGFR) and stimulates tyrosine kinase activity of receptor to induce neurite outgrowth. When neural crest cells stop making N CAM and N cadherin, and start displaying integrin receptors, cells separate and migrate. During hematopoiesis, CD56 is the prototypic marker of NK cells, also present on subset of CD4+ T cells and CD8+ T cells. In cell adhesion, CD56 contributes to cell cell adhesion or cell matrix adhesion during embryonic development.

In anatomic pathology, pathologists make use of CD56 immunohistochemistry to recognize certain tumors. Normal cells that stain positively for CD56 include NK cells, activated T cells, the brain and cerebellum, and neuroendocrine tissues. Tumors that are CD56 positive are myeloma, myeloid leukemia, neuroendocrine tumors, Wilms' tumor, neuroblastoma, extranodal NK/T cell lymphoma, nasal type, pancreatic acinar cell carcinoma, pheochromocytoma, paraganglioma, small cell lung carcinoma, and the Ewing's sarcoma family of tumors.

A member of the NCAM superfamily, NCAM2 gene has been observed progressively downregulated in human papillomavirus positive neoplastic keratinocytes derived from uterine cervical preneoplastic lesions at different levels of malignancy. For this reason, NCAM2 is likely to be associated with tumorigenesis and may be a potential prognostic marker for uterine cervical preneoplastic lesions progression.

NCAM2 is found in lower levels in hippocampal synapses of Alzheimer's disease sufferers and is found to be broken down by beta amyloid.

NCAM has been identified as one of the target proteins for the rabies virus, allowing entry into the cell.

NCAM has been used as a target molecule for experimental antibody based immunotherapy. Successful radio immunolocalisation of metastases was demonstrated after giving injections of NCAM binding 123J UJ13a or 131J UJ13a radio immunoconjugates to children with neuroblastoma. Patients with small cell lung cancer were treated with the anti NCAM immunotoxin huN901 DM1 in two different clinical studies, revealing acceptable toxicity and signs of clinical response.