The activity of this enzyme is terminated by a complex that is mutated in cerebroretinal microangiopathy with calcifications and cysts; that is the CST complex. One component of this enzyme complex is Nop10, which can be mutated in dyskeratosis congenita. One component of this enzyme is encoded by a gene next to semaphorin F and delta-catenin on the p arm of chromosome 5, and is therefore deleted in (*) Cri-du-chat syndrome. This complex was originally discovered using extracts of Tetrahymena by Greider and Blackburn. Aberrant activation of this complex allows cells to bypass the Hayflick limit, and this reverse trans
The activity of this enzyme is terminated by a complex that is mutated in cerebroretinal microangiopathy with calcifications and cysts; that is the CST complex. One component of this enzyme complex is Nop10, which can be mutated in dyskeratosis congenita. One component of this enzyme is encoded by a gene next to semaphorin F and delta-catenin on the p arm of chromosome 5, and is therefore deleted in (*) Cri-du-chat syndrome. This complex was originally discovered using extracts of Tetrahymena by Greider and Blackburn. Aberrant activation of this complex allows cells to bypass the Hayflick limit, and this reverse transcriptase enzyme adds the sequence TTAGGG to its substrate. For 10 points, name this enzyme that lengthens the ends of chromosomes, and is often over-activated in cancer cells.
The activity of this enzyme is terminated by a complex that is mutated in cerebroretinal microangiopathy with calcifications and cysts; that is the CST complex.
telomerase