Publication | Open Access

Defects in mTR stability and telomerase activity produced by the Dkc1 A353V mutation in dyskeratosis congenita are rescued by a peptide from the dyskerin TruB domain

Protein FunctionMedicineTelomerase ActivityNatural SciencesMolecular BiologyMtr StabilityMolecular GeneticsProteomicsCell BiologyDyskerin Trub Domain