[5][6][7] TERC is a Long non-coding RNA (lncRNA) ranging in length from ~150nt in ciliates to 400-600nt in vertebrates, and 1,300nt in yeast (Alnafakh).

[10] The conserved CR7 domain is also localized at the 3’ end of TERC, and contains a 3nt CAB (Cajal body Localisation) box which binds TCAB1.

Telomerase expression plays a role in cellular senescence, as it is normally repressed in postnatal somatic cells resulting in progressive shortening of telomeres.

Studies in mice suggest that telomerase also participates in chromosomal repair, since de novo synthesis of telomere repeats may occur at double-stranded breaks.

[10] Unlike in other RNPs, in telomerase, the protein TERT is catalytic while the lncRNA TERC is structural, rather than acting as a ribozyme.

TERC-mediated upregulation of Lin37, Trpg1l, tyrobp, Usp16 stimulates the NF-κB pathway, resulting in increased expression and secretion of inflammatory cytokines.

[16] Unlike most lncRNAs which are assembled from introns by the spliceosome, hTR is directly transcribed from a dedicated promoter site[8] located at genomic locus 3q26.2[17] by RNA polymerase II.

Mutations in TERC have been associated with dyskeratosis congenita,[19] idiopathic pulmonary fibrosis,[20] aplastic anemia, and myelodysplasia.

Upregulation of hTR is widely observed in patients with precancerous cervical phenotype as a result of HPV infection.