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Cited by 428

The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.

Loss of the retrograde motor for IFT disrupts localization of Smo to cilia and prevents the expression of both activator and repressor functions of Gli

Open access
May, Scott R., Ashique, Amir M., Karlen, Mattias, Wang, Baolin, Shen, Yiguo, Zarbalis, Kostantinos, Reiter, Jeremy, Ericson, Johan, Peterson, Andrew S.·2005·Developmental Biology

Abstract

Sonic Hedgehog (Shh) signals are transduced into nuclear ratios of Gli transcriptional activator versus repressor. The initial part of this process is accomplished by Shh acting through Patched (Ptc) to regulate Smoothened (Smo) activity. The mechanisms by which Ptc regulates Smo, and Smo activity is transduced to processing of Gli proteins remain unclear. Recently, a forward genetic approach in mice identified a role for intraflagellar transport (IFT) genes in Shh signal transduction, downstream of Patched (Ptc) and Rab23. Here, we show that the retrograde motor for IFT is required in the mouse for the phenotypic expression of both Gli activator and repressor function and for effective proteolytic processing of Gli3. Furthermore, we show that the localization of Smo to primary cilia is disrupted in mutants. These data indicate that primary cilia act as specialized signal transduction organelles required for coupling Smo activity to the biochemical processing of Gli3 protein.

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Crossref · 10.1016/j.ydbio.2005.08.050

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Metadata

Authors
May, S. R., Ashique, A. M., Karlen, M., Wang, B., Shen, Y., Zarbalis, K., Reiter, J., Ericson, J., & Peterson, A. S.
Venue
Developmental Biology
Publisher
Elsevier BV
Published
2005-11
Volume
287
Issue
2
Pages
378-389
ISSN
0012-1606 (ISSN-L)
OpenAlex
W2039238855
Cited by
428
References
7
FWCI
15.29
Type
journal article
Language
en
Open access
bronze

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