Disease relevance of CADM3

• Expression of TSLL1 and TSLL2 was lost or markedly reduced in many human glioma cell lines or some prostate cancer cell lines, suggesting that loss of expression of these genes might be involved in some human cancers [1].

High impact information on CADM3

• In addition, nectins heterophilically trans-interact with nectin-like molecules (Necls), which are involved in cell adhesion, migration, and proliferation, and assist or modify their functions [2].
• Mutagenesis work demonstrated that Phe(82) is a key residue for the adhesion activity of Necl-1 [3].
• Thus, NK cells have evolved a dual receptor system that recognizes nectins and nectin-like molecules on target cells and mediates NK cell adhesion and triggering of effector functions [4].
• Tage4/Nectin-like molecule-5 heterophilically trans-interacts with cell adhesion molecule Nectin-3 and enhances cell migration [5].
• Tissue distribution analysis showed that Necl-1 was specifically expressed in the neural tissue [6].

Biological context of CADM3

• Nectins furthermore heterophilically trans-interact with nectin-like molecules (Necls), other Ig-like CAMs, and assist or modify their various functions, such as cell adhesion, migration, and proliferation [7].
• We have recently identified the human TSLL1 and TSLL2 genes, which are highly homologous to the human lung tumor suppressor gene, TSLC1 [8].

Anatomical context of CADM3

• The role of NK cell recognition of nectin and nectin-like proteins in tumor immunosurveillance [9].
• Furthermore, both murine TSLL1 and TSLL2 proteins were expressed on the plasma membrane, especially at the cell-cell attached site [8].
• RNA blot and in situ hybridization analysis showed that NECL1 predominantly expressed in the central nervous system, mainly in neuronal cell bodies in a variety of brain regions including the cerebellum, cerebral cortex and hippocampus [10].
• Among them, Nectin-like molecule 1 (Necl-1) is unique for its exclusive expression in the brain where it is localized at the contact sites among axon terminals and glia cell processes, cooperatively forming synapses.We hereby aimed to unambiguously characterize Necl-1 at the protein level in rat brain [11].

Other interactions of CADM3

• Isolation of the TSLL1 and TSLL2 genes, members of the tumor suppressor TSLC1 gene family encoding transmembrane proteins [1].

Analytical, diagnostic and therapeutic context of CADM3

• Immunofluorescence and immunoelectron microscopy revealed that Necl-1 localized at the contact sites among axons, their terminals, and glia cell processes that cooperatively formed synapses, axon bundles and myelinated axons [6].

References