de.mpg.escidoc.pubman.appbase.FacesBean
Deutsch
 
Hilfe Wegweiser Datenschutzhinweis Impressum Kontakt
  DetailsucheBrowse

Datensatz

DATENSATZ AKTIONENEXPORT
  Homeobox genes d11-d13 and a13 control mouse autopod cortical bone and joint formation.

Villavicencio-Lorini, P., Kuss, P., Friedrich, J., Haupt, J., Farooq, M., Turkmen, S., et al. (2010). Homeobox genes d11-d13 and a13 control mouse autopod cortical bone and joint formation. Journal of Clinical Investigation, 120(6), 1994-2004. doi:10.1172/JCI41554 41554.

Item is

Basisdaten

einblenden: ausblenden:
Datensatz-Permalink: http://hdl.handle.net/11858/00-001M-0000-0010-7AE8-5 Versions-Permalink: http://hdl.handle.net/11858/00-001M-0000-0010-7AE9-3
Genre: Zeitschriftenartikel
Alternativer Titel : J Clin Invest

Dateien

einblenden: Dateien
ausblenden: Dateien
:
JCI41554.pdf (beliebiger Volltext), 9MB
Beschreibung:
-
Sichtbarkeit:
Öffentlich
MIME-Typ / Prüfsumme:
application/pdf / [MD5]
Technische Metadaten:
Copyright Datum:
-
Copyright Info:
eDoc_access: PUBLIC
Lizenz:
-

Externe Referenzen

einblenden:

Urheber

einblenden:
ausblenden:
 Urheber:
Villavicencio-Lorini, P.1, Autor              
Kuss, P.1, Autor              
Friedrich, J.2, Autor
Haupt, J.2, Autor
Farooq, M., Autor
Turkmen, S.3, Autor              
Duboule, D., Autor
Hecht, J.1, Autor              
Mundlos, S.1, Autor              
Affiliations:
1Research Group Development & Disease (Head: Stefan Mundlos), Max Planck Institute for Molecular Genetics, Max Planck Society, escidoc:1433557              
2Max Planck Society, escidoc:persistent13              
3Dept. of Human Molecular Genetics (Head: Hans-Hilger Ropers), Max Planck Institute for Molecular Genetics, Max Planck Society, escidoc:1433549              

Inhalt

einblenden:
ausblenden:
Schlagwörter: Alleles; Animals; Bone and Bones/*metabolism; Cartilage/*metabolism; Extremities; Mice, Knockout; Peptides; Signal Transduction/genetics; Transcription Factors/biosynthesis/*genetics/*metabolism
 Zusammenfassung: The molecular mechanisms that govern bone and joint formation are complex, involving an integrated network of signaling pathways and gene regulators. We investigated the role of Hox genes, which are known to specify individual segments of the skeleton, in the formation of autopod limb bones (i.e., the hands and feet) using the mouse mutant synpolydactyly homolog (spdh), which encodes a polyalanine expansion in Hoxd13. We found that no cortical bone was formed in the autopod in spdh/spdh mice; instead, these bones underwent trabecular ossification after birth. Spdh/spdh metacarpals acquired an ovoid shape and developed ectopic joints, indicating a loss of long bone characteristics and thus a transformation of metacarpals into carpal bones. The perichondrium of spdh/spdh mice showed abnormal morphology and decreased expression of Runt-related transcription factor 2 (Runx2), which was identified as a direct Hoxd13 transcriptional target. Hoxd11-/-Hoxd12-/-Hoxd13-/- triple-knockout mice and Hoxd13-/-Hoxa13+/- mice exhibited similar but less severe defects, suggesting that these Hox genes have similar and complementary functions and that the spdh allele acts as a dominant negative. This effect was shown to be due to sequestration of other polyalanine-containing transcription factors by the mutant Hoxd13 in the cytoplasm, leading to their degradation. These data indicate that Hox genes not only regulate patterning but also directly influence bone formation and the ossification pattern of bones, in part via Runx2.

Details

einblenden:
ausblenden:
Sprache(n): eng - Englisch
 Datum: 2010-06-01
 Publikationsstatus: Im Druck publiziert
 Seiten: -
 Ort, Verlag, Ausgabe: -
 Inhaltsverzeichnis: -
 Art der Begutachtung: -
 Art des Abschluß: -

Veranstaltung

einblenden:

Entscheidung

einblenden:

Projektinformation

einblenden:

Quelle 1

einblenden:
ausblenden:
Titel: Journal of Clinical Investigation
  Alternativer Titel : J Clin Invest
Genre der Quelle: Zeitschrift
 Urheber:
Affiliations:
Ort, Verlag, Ausgabe: -
Seiten: - Band / Heft: 120 (6) Artikelnummer: - Start- / Endseite: 1994 - 2004 Identifikator: ISSN: 0021-9738