The Iowa African-American Journal, January 2000, Vol. 6, no. 1

Newsletter for the Iowa Commission on the Status of African-Americans

The Iowa African-American Journal, July 2000, Vol. 6, no. 2

Newsletter for the Iowa Commission on the Status of African-Americans

The Iowa African-American Journal, November 2000, Vol. 6, no. 3

Newsletter for the Iowa Commission on the Status of African-Americans

The Iowa African-American Journal, Spring/Fall 2001, Vol. 7, no. 1

Newsletter for the Iowa Commission on the Status of African-Americans

The Iowa African-American Journal, Spring/Fall 2002, Vol. 8, no. 1

Newsletter for the Iowa Commission on the Status of African-Americans

The Iowa African-American Journal, Winter 2002/Spring 2003, Vol. 8, no. 2

Newsletter for the Iowa Commission on the Status of African-Americans

The Iowa African-American Journal, October 1999, Vol. 5, no. 4

Newsletter for the Iowa Commission on the Status of African-Americans

[Archives de l'Opéra. Régie. Journal de régie. Deuxième série]

Journal contenant pour chaque jour les répétitions, les réglages, les représentations avec le programme et les distributions. Notes concernant les événements survenus au cours de la journée. - Contient 2 pièces additionnelles

[Archives de l'Opéra. Régie. Journal de régie. Première série]

Calendrier des spectacles et des répétitions. - Ne comporte plus la liste du personnel de la régie. - Contient 10 pièces additionnelles

Mutations in the heparan-sulfate proteoglycan glypican 6 (GPC6) impair endochondral ossification and cause recessive omodysplasia.

Glypicans are a family of glycosylphosphatidylinositol (GPI)-anchored, membrane-bound heparan sulfate (HS) proteoglycans. Their biological roles are only partly understood, although it is assumed that they modulate the activity of HS-binding growth factors. The involvement of glypicans in developmental morphogenesis and growth regulation has been highlighted by Drosophila mutants and by a human overgrowth syndrome with multiple malformations caused by glypican 3 mutations (Simpson-Golabi-Behmel syndrome). We now report that autosomal-recessive omodysplasia, a genetic condition characterized by short-limbed short stature, craniofacial dysmorphism, and variable developmental delay, maps to chromosome 13 (13q31.1-q32.2) and is caused by point mutations or by larger genomic rearrangements in glypican 6 (GPC6). All mutations cause truncation of the GPC6 protein and abolish both the HS-binding site and the GPI-bearing membrane-associated domain, and thus loss of function is predicted. Expression studies in microdissected mouse growth plate revealed expression of Gpc6 in proliferative chondrocytes. Thus, GPC6 seems to have a previously unsuspected role in endochondral ossification and skeletal growth, and its functional abrogation results in a short-limb phenotype.