Tenascin-R (TNR)

Tenascin-R (TNR) is a neural extracellular matrix glycoprotein almost exclusively expressed in the central nervous system, where it is primarily produced by oligodendrocytes and select neuron types[1][5][7][9]. It is the smallest member of the tenascin family and is composed of a modular structure, including an N-terminal cysteine-rich region, multiple epidermal growth factor (EGF)-like repeats, nine fibronectin type III domains, and a C-terminal region homologous to fibrinogen chains[1][5][9]. Tenascin-R plays a crucial role in neural cell adhesion, regulation of neurite outgrowth (both promotion and inhibition depending on cellular context), modulation of synaptic and ion channel functions, and organization of perineuronal nets essential for neuroprotection and extracellular matrix integrity[2][3][4][7][9]. It interacts with multiple cell-surface molecules, notably the IgCAMs contactin1, neurofascin, contactin2 (TAG-1), sodium channel subunits, integrins, and chondroitin sulfate proteoglycans such as aggrecan and brevican[2][3][4][9]. Tenascin-R deficiency in mice leads to deficits in neurogenesis, synaptic stability, anxiety-like behaviors, motor dysfunction, and susceptibility to neurodevelopmental or neurodegenerative conditions[3][4][7][8]. There are currently no direct therapeutic drugs, but its role as a structural and functional modulator in the CNS makes it a potential biomarker and investigational target in neurology and psychiatry[7][8].

Other names

Tenascin-RTNRTN-RJanusinRestrictinrestrictinjanusinNEDSTOJ1-160/180