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doi: 10.1016/j.neuint.2012.01.019 206 ParkerS

Alterations in these genes result in shortening of telomeres, which in turn leads to defects in proliferation and spontaneous chromosomal rearrangements.[199] Levels of TERC, the RNA component of the telomerase complex, are reduced in all dyskeratosis congenita patients.[200] Missense pathogenic variants in WRAP53 , a gene with a protein product that facilitates trafficking of telomerase, have also been associated with an autosomal recessive form of dyskeratosis congenita.[201] Pathogenic variants in C16orf57 were identified in 6 of 132 families who did not have a variant detected in other known genes.[202] C16orf57 pathogenic variants are also associated with poikiloderma with neutropenia.[203] For more information about poikiloderma congenitale, see the Rothmund-Thomson syndrome section

GHRP-2 directly influences these centers