Altered heparan sulfate structure in Glce−/− mice leads to increased Hedgehog signaling in endochondral bones
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- 作者：Tabea Dierkera ; b ; tabea.dierker@imbim.uu.se" class="auth_mail" title="E-mail the corresponding author ; Velina Bachvarovaa ; velina.bachvarova@uni-due.de" class="auth_mail" title="E-mail the corresponding author ; Yvonne Krausea ; yvonne.krause@uni-due.de" class="auth_mail" title="E-mail the corresponding author ; Jin-Ping Lib ; Jin-ping.Li@imbim.uu.se" class="auth_mail" title="E-mail the corresponding author ; Lena Kjellé ; nb ; lena.kjellen@imbim.uu.se" class="auth_mail" title="E-mail the corresponding author ; Daniela G. Seidlerc ; &dagger ; ; dgseidle@uni-muenster.de" class="auth_mail" title="E-mail the corresponding author ; Andrea Vortkampa ; andrea.vortkamp@uni-due.de" class="auth_mail" title="E-mail the corresponding author
- 关键词：Glce ; glucuronyl C5-epimerase ; Ihh ; Indian hedgehog ; Pthrp ; Parathyroid hormone related peptide
- 刊名：Matrix Biology
- 出版年：2016
- 出版时间：January 2016
- 年：2016
- 卷：49
- 期：Complete
- 页码：82-92
- 全文大小：1352 K
文摘
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Glce deficient mice show a delayed onset of hypertrophic differentiation.
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Ptch1 and Pthrp are upregulated in Glce-/- mice indicating increased Ihh signaling.
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Glce−/− chondrocytes have reduced HS 2-O- and slightly increased 6-O-sulfation.
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Binding of Ihh to HS from Glce−/− mice is reduced in vitro.
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The reduced affinity of Glce−/− HS to Ihh results in increased Ihh signaling.