Dlx3 is a crucial regulator of hair follicle differentiation and cycling. Dlx3 transcription is mediated throughWnt, and colocalization of Dlx3 withphospho-SMAD1/5/8 is involved in the regulation of transcription byBMP signaling.[7] Dlx3 transcription is also induced byBMP-2 throughtransactivation withSMAD1 andSMAD4.[8]
Many vertebrate homeo box-containing genes have been identified on the basis of their sequence similarity withDrosophila developmental genes. Members of the Dlx gene family contain ahomeobox that is related to that of Distal-less (Dll), a gene expressed in the head and limbs of the developing fruit fly. The Distal-less (Dlx) family of genes comprises at least 6 different members,DLX1-DLX6. This gene is located in a tail-to-tail configuration with another member of the gene family on the long arm ofchromosome 17.[6]
^"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.
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Haldeman RJ, Cooper LF, Hart TC, et al. (2005). "Increased bone density associated with DLX3 mutation in the tricho-dento-osseous syndrome".Bone.35 (4):988–97.doi:10.1016/j.bone.2004.06.003.PMID15454107.
Dong J, Amor D, Aldred MJ, et al. (2005). "DLX3 mutation associated with autosomal dominant amelogenesis imperfecta with taurodontism".Am. J. Med. Genet. A.133 (2):138–41.doi:10.1002/ajmg.a.30521.PMID15666299.S2CID8482065.
Islam M, Lurie AG, Reichenberger E (2006). "Clinical features of tricho-dento-osseous syndrome and presentation of three new cases: an addition to clinical heterogeneity".Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, and Endodontics.100 (6):736–42.doi:10.1016/j.tripleo.2005.04.017.PMID16301156.
Morsczeck C (2006). "Gene expression of runx2, Osterix, c-fos, DLX-3, DLX-5, and MSX-2 in dental follicle cells during osteogenic differentiation in vitro".Calcif. Tissue Int.78 (2):98–102.doi:10.1007/s00223-005-0146-0.PMID16467978.S2CID7621703.