U3 Small Nucleolar Ribonucleoprotein 6, Homolog (UTP6)

HCA66 is able to modulate selectively Apaf-1-dependent apoptosis through its direct association with the CED4 domain of Apaf-1. Expression of HCA66 was able to potentiate Apaf-1, but not receptor-mediated apoptosis, by increasing downstream caspase activity following cytochrome c release from the mitochondria. Cells depleted of HCA66 were severely impaired for apoptosome-dependent apoptosis. Expression of the Apaf-1-interacting domain of HCA66 had the opposite effect of the full-length protein, interfering with the Apaf-1 apoptotic pathway. HCA66 maps to chromosome 17q11.2 and is among the genes heterozygously deleted in neurofibromatosis type 1 (NF1) microdeletion syndrome patients. Reduced expression of HCA66 could render NF1 microdeleted patients-derived cells less susceptible to apoptosis.