The specific function of this protein has yet to be determined; however, it has been speculated to play a role in transcriptional regulation and/or chromatin and histone metabolism.[8]
Research done by Salomé Adam, Sophie E. Polo, and Geneviève Almouzni indicate that HIRA proteins are involved in restarting transcription after UVC damage.[9] Function of HIRA gene can be effectively examined by siRNA knockdown based on an independent validation.[10]
It is considered the primary candidate gene in some haploinsufficiency syndromes such as DiGeorge syndrome, and insufficient production of the gene may disrupt normal embryonic development.[8]
^"Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
^"Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
^Halford S, Wadey R, Roberts C, Daw SC, Whiting JA, O'Donnell H, Dunham I, Bentley D, Lindsay E, Baldini A (Mar 1994). "Isolation of a putative transcriptional regulator from the region of 22q11 deleted in DiGeorge syndrome, Shprintzen syndrome and familial congenital heart disease". Hum Mol Genet. 2 (12): 2099–107. doi:10.1093/hmg/2.12.2099. PMID8111380.
^Lamour V, Lécluse Y, Desmaze C, Spector M, Bodescot M, Aurias A, Osley MA, Lipinski M (Sep 1995). "A human homolog of the S. cerevisiae HIR1 and HIR2 transcriptional repressors cloned from the DiGeorge syndrome critical region". Hum Mol Genet. 4 (5): 791–9. doi:10.1093/hmg/4.5.791. PMID7633437.
Lorain S, Lécluse Y, Scamps C, Mattéi MG, Lipinski M (2001). "Identification of human and mouse HIRA-interacting protein-5 (HIRIP5), two mammalian representatives in a family of phylogenetically conserved proteins with a role in the biogenesis of Fe/S proteins". Biochim. Biophys. Acta. 1517 (3): 376–83. doi:10.1016/S0167-4781(00)00300-6. PMID11342215.