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This study found that the hairless gene product (Hr) suppresses VDR-mediated gene activation by directly interacting with the vitamin D receptor, potentially affecting hair follicle function.

This study found that most pathogenic HR mutants associated with atrichia with papular lesions had abolished corepressor activity due to defective interactions with histone deacetylases.

This study demonstrated that both HR isoforms are expressed in keratinocytes, but HRDelta1072-1126 lacks corepressor activity and may act as a coactivator by inhibiting HDAC recruitment to the VDR transcriptional complex.

This study found that the mammalian hairless gene encodes a corepressor protein that interacts with thyroid hormone receptors, providing insights into hair loss syndromes in humans and mice.

This study concluded that the hairless protein interacts with the vitamin D receptor to repress transcription crucial for hair cycling, employing multiple protein interfaces and modulating chromatin structure.