ALX homeobox 4
Dernière mise à jour 7 avr. 2026
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The ALX4 gene provides instructions for making a member of the homeobox protein family. Homeobox proteins direct the formation of body structures during early embryonic development. The ALX4 protein is necessary for normal development of the head.
Normal function
The ALX4 gene provides instructions for making a member of the homeobox protein family. Homeobox proteins direct the formation of body structures during early embryonic development. The ALX4 protein is necessary for normal development of the head.
The ALX4 protein is a transcription factor, which means that it attaches (binds) to DNA and controls the activity of certain genes. Specifically, the protein controls the activity of genes that regulate cell growth and division (proliferation), cell maturation and specialization (differentiation), cell movement (migration), and cell survival. The ALX4 protein also interacts with other transcription factors to help regulate these functions and ensure that cells start and stop growing at specific times and that they are positioned correctly during development.
Conditions referring to this gene or chromosome
Other names
homeodomain transcription factor ALX4
KIAA1788
PFM
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Lectures complémentaires et références
- ALX homeobox 4; MedlinePlus, National Library of Medicine.
- Cain B, Yuan Z, Thoman E, Kovall RA, Gebelein B. The ALX4 dimer structure provides insight into how disease alleles impact function. Nat Commun. 2025 May 23;16(1):4800. doi: 10.1038/s41467-025-59728-9.
- Griessenauer CJ, Veith P, Mortazavi MM, Stewart C, Grochowsky A, Loukas M, Tubbs RS. Enlarged parietal foramina: a review of genetics, prognosis, radiology, and treatment. Childs Nerv Syst. 2013 Apr;29(4):543-7. doi: 10.1007/s00381-012-1982-7. Epub 2012 Dec 4.
- Kayserili H, Uz E, Niessen C, Vargel I, Alanay Y, Tuncbilek G, Yigit G, Uyguner O, Candan S, Okur H, Kaygin S, Balci S, Mavili E, Alikasifoglu M, Haase I, Wollnik B, Akarsu NA. ALX4 dysfunction disrupts craniofacial and epidermal development. Hum Mol Genet. 2009 Nov 15;18(22):4357-66. doi: 10.1093/hmg/ddp391. Epub 2009 Aug 19.
- Mavrogiannis LA, Wilkie AOM. Enlarged Parietal Foramina. 2004 Mar 30 [updated 2025 Jun 26]. In: Adam MP, Bick S, Mirzaa GM, Wallace SE, Amemiya A, editors. GeneReviews(R) [Internet]. Seattle (WA): University of Washington, Seattle; 1993-2026. Available from http://www.ncbi.nlm.nih.gov/books/NBK1128/
- Romeike BF, Wuyts W. Proximal chromosome 11p contiguous gene deletion syndrome phenotype: case report and review of the literature. Clin Neuropathol. 2007 Jan-Feb;26(1):1-11. doi: 10.5414/npp26001.
- Wakui K, Gregato G, Ballif BC, Glotzbach CD, Bailey KA, Kuo PL, Sue WC, Sheffield LJ, Irons M, Gomez EG, Hecht JT, Potocki L, Shaffer LG. Construction of a natural panel of 11p11.2 deletions and further delineation of the critical region involved in Potocki-Shaffer syndrome. Eur J Hum Genet. 2005 May;13(5):528-40. doi: 10.1038/sj.ejhg.5201366.
- Wu YQ, Badano JL, McCaskill C, Vogel H, Potocki L, Shaffer LG. Haploinsufficiency of ALX4 as a potential cause of parietal foramina in the 11p11.2 contiguous gene-deletion syndrome. Am J Hum Genet. 2000 Nov;67(5):1327-32. doi: 10.1016/S0002-9297(07)62963-2. Epub 2000 Oct 3.
- Wuyts W, Cleiren E, Homfray T, Rasore-Quartino A, Vanhoenacker F, Van Hul W. The ALX4 homeobox gene is mutated in patients with ossification defects of the skull (foramina parietalia permagna, OMIM 168500). J Med Genet. 2000 Dec;37(12):916-20. doi: 10.1136/jmg.37.12.916.
- Wuyts W, Waeber G, Meinecke P, Schuler H, Goecke TO, Van Hul W, Bartsch O. Proximal 11p deletion syndrome (P11pDS): additional evaluation of the clinical and molecular aspects. Eur J Hum Genet. 2004 May;12(5):400-6. doi: 10.1038/sj.ejhg.5201163.
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