The tenascin-C gene consists of 27 exons spanning 97.63 kb of genomic DNA.

7271 bp mRNA transcribed on the reverse strand; 6333 bp open reading frame.
The transcript starts with a non-coding exon 1 (179 bp) followed by exon 2, which contains the start codon (ATG) for translation initiation. Exon 1 is located 26827 bp upstream of exon 2.

Tenascin-C consists of structural motifs arranged in a linear order. Mammalian tenascin-C proteins contain amino-terminal heptad repeats, 14.5 EGF-like repeats, 8 constant FN III domains, whereas 9 additional FN III domains can be included in a combinatorial manner by alternative splicing, and a carboxyl-terminal fibrinogen globe. A prominent feature of tenascin-C is the assembly into hexamers, so-called hexabrachions.
The primary sequence encodes a protein of 2110 amino acids. Amino acids 1-22 represent the secretion signal, amino acids 189-621 constitute the EGF-like repeats, and amino acids 622-1882 account for the FNIII domains. SDS-Page analysis revealed a molecular weight of full-length tenascin-C of 250kDa - 300kDa per subunit under reducing conditions.
Alternative splicing within the stretch of FN III domains results in a great number and diversity in tenascin-C isoforms.

More than two decades ago, tenascin-C was discovered as an extracellular matrix protein (ECM) enriched in the stroma of gliomas and as a myotendinous antigen. Tenascin-C expression is highly regulated both during development and in the adult. Tenascin-C levels are high during embryogenesis, but almost absent during normal postnatal life with some basal expression detectable in tendons and ligaments only. In adult life, tenascin-C is also expressed within the sub-ventricular zone in the central nervous system, a region that constitutes the neural stem cell niche. A prominent feature of tenascin-C is its re-appearance in response to pathological situations such as infection, inflammation and tissue remodeling. Another striking example of a pathological situation leading to the re-expression of tenascin-C is the onset of tumorigenesis, where tenascin-C is specifically expressed in the activated tumor stroma. Tenascin-C can be induced by various stimuli, such as the pro- and anti-inflammatory cytokines, interleukins, TNFa or IFNg and growth factors such as TGFb , EGF or PDGF. Furthermore, tenascin-C inducing stimuli include mechanical stress, hypoxia, and reactive oxygen species, factors or conditions which also might play a prominent role in tumors.

Extracellular matrix.

Adhesion: Tenascin-C acts as an anti-adhesive substratum for a large variety of cells. Active inhibition of cell spreading was further confirmed by mixing tenascin-C together with fibronectin, which is a classical adhesion protein. Whereas cells on fibronectin nicely spread, form focal contacts and actin stress fibers, the same cells plated on a mixed fibronectin-tenascin-C substratum are not able to spread and do not form focal contacts and actin cables.
Migration: Tenascin-C enhances migration and invasiveness of different cancer cells.
Proliferation: Tenascin-C stimulates cancer cell proliferation.
Angiogenesis: Tenascin-C is expressed around angiogenic vessels in many tumors and there is evidence that it promotes and regulates angiogenesis in vitro and in vivo. Moreover, in glioma patients, clinical studies revealed an inhibition of tumor angiogenesis by applying antibodies directed against tenascin-C.

Tenascin-C belongs to the tenascin family, which is a highly conserved family of large oligomeric extracellular matrix proteins. Vertebrate genomes harbor four tenascin genes, which have been termed tenascin-C, tenascin-XB (TNXB), tenascin-R, and tenascin-W.

A SNP was identified resulting in an amino acid substitution (Leu1677Ile in the tenascin-C FN III domain D) which strongly associates with adult bronchial asthma. Therefore, this SNP might be an asthma marker and may be important in its pathogenesis.