title: The aristaless-like homeobox protein Alx3 as an etiopathogenic factor for diabetes mellitus.
abstract: Inactivation of the gene encoding the aristaless-related homeodomain transcription factor Alx3 results in islet cell apoptosis and impaired glucose homeostasis that worsens with age due to the appearance of insulin resistance. Alx3-deficient mice also show extrapancreatic developmental defects with variable penetrance. These include polydactyly, craniofacial midline defects, and neural tube closure defects. In humans, related congenital defects associated with mutations in ALX3 and other aristaless-related genes are being identified. Emerging evidence suggests that normal pancreatic function in humans may require the integrity of aristaless-related genes. Here, the proposal that ALX3 could be considered as a candidate gene for the etiopathogenesis of diabetes or its complications during embryonic or fetal development is discussed.
authors.affiliation: Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas CIBERDEM, Instituto de Investigaciones Biomédicas Alberto Sols, Consejo Superior de Investigaciones Científicas (CSIC)/Universidad Autónoma de Madrid, Spain. mvallejo@iib.uam.es
authors.forename: Mario
authors.initials: M
authors.lastname: Vallejo
mesh_terms: D000818:Animals; D000013:Congenital Abnormalities / Q000209:etiology; D003920:Diabetes Mellitus / Q000209:etiology*; D018398:Homeodomain Proteins / Q000235:genetics / Q000502:physiology*; D051379:Mice; D009154:Mutation
chemical_list: C113607:Alx3 protein, mouse; D018398:Homeodomain Proteins