Gli regulation by the opposing activities of Fused and Suppressor of Fused

Murone, Maximilien; Luoh, Shiuh-Ming; Stone, Donald S.; Li, Wenlu; Gurney, Austin; Armanini, Mark; Grey, Christa; Rosenthal, Arnon; Sauvage, Frédéric J. de

doi:10.1038/35010610

Cited by 132 publications

(149 citation statements)

References 15 publications

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“…Taken together, our data demonstrate that mFu could enhance the activity of Gli1 and Gli2 proteins and both the kinase domain and Cterminal regulatory region of mFu are required for the full activation of Gli, though the potential kinase activity appears not to be crucial. These data are similar to those obtained with hFU (Murone et al 2000;Østerlund et al 2004;Daoud and Blanchet-Tournier 2005).…”

Section: Expression Of Mfu In Brain and Testissupporting

confidence: 91%

A possible role of mouse Fused (STK36) in Hedgehog signaling and Gli transcription factor regulation

Maloveryan

Finta²,

Østerlund

et al. 2007

J. Cell Commun. Signal.

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The segment polarity gene Fused (Fu) encodes a putative serine-threonine kinase Fu, which has been shown to play a key role in the Hedgehog signaling pathway of Drosophila. Human FU (hFU) has been shown to enhance the activity of Gli transcription factors, targets of the signaling pathway. However, Fu −/− mice do not show aberrant embryonic development indicating that mouse Fu (mFu) is dispensable for Hedgehog signaling until birth. In order to investigate if there are important differences between hFU and mFu, we cloned the cDNA, analyzed expression and tested the ability of mFu to regulate Gli proteins. Of the tested tissues only brain and testis showed significant expression. However, in transient overexpression analyses mFu was able to enhance Gli induced transcription in a manner similar to hFU. Thus, we turned to RNAi in order to test if mFu would be important for Hedgehog signaling after all. In one cell line with reduced mFu expression the Hedgehog signaling was severely hampered, indicating that mFu may have a role in Hedgehog signaling and Gli regulation in some cellular situations.

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Section: Expression Of Mfu In Brain and Testissupporting

confidence: 91%

A possible role of mouse Fused (STK36) in Hedgehog signaling and Gli transcription factor regulation

Maloveryan

Finta²,

Østerlund

et al. 2007

J. Cell Commun. Signal.

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“…Studies involving mammalian Su(fu) support this hypothesis. Over-expression of human SU(FU) in cultured mammalian cells triggers increased cytoplasmic GLI-1 and decreased expression of Gli reporter construct(s) [88][89][90].…”

Section: Suppressor Of Fusedmentioning

confidence: 99%

Regulation of Hedgehog signaling: a complex story

Ogden

Ascano

Stegman

et al. 2004

Biochemical Pharmacology

102

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The Hedgehog (Hh) signal transduction pathway plays critical instructional roles during development. Activating mutations in human Hh signaling components predispose to a variety of tumor types, and have been observed in sporadic tumors occurring in a wide range of organs. Multiple insights into the regulation of Hh signaling have been achieved through studies using Drosophila melanogaster as a model organism. In Drosophila, regulation of the transcription factor

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“…After binding of Ihh to PTCH, Smo, which is repressed by PTCH, is activated and transduces signals into the cytoplasm though the intracellular signaling molecule, Fused, and the transcription factors, the Gli family members, which contain a zinc finger domain (Murone et al, 2000;Koebernick and Pieler, 2002). Activated Gli family members translocate from the cytoplasm to the nucleus and regulate the transcription of target genes (Murone et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

Ihh/Gli2 Signaling Promotes Osteoblast Differentiation by Regulating Runx2 Expression and Function

Shimoyama

Wada

Ikeda

et al. 2007

MBoC

156

115

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Genetic and cell biological studies have indicated that Indian hedgehog (Ihh) plays an important role in bone development and osteoblast differentiation. However, the molecular mechanism by which Ihh regulates osteoblast differentiation is complex and remains to be fully elucidated. In this study, we investigated the role of Ihh signaling in osteoblast differentiation using mesenchymal cells and primary osteoblasts. We observed that Ihh stimulated alkaline phosphatase (ALP) activity, osteocalcin expression, and calcification. Overexpression of Gli2-but not Gli3-induced ALP, osteocalcin expression, and calcification of these cells. In contrast, dominant-negative Gli2 markedly inhibited Ihh-dependent osteoblast differentiation. Ihh treatment or Gli2 overexpression also up-regulated the expression of Runx2, an essential transcription factor for osteoblastogenesis, and enhanced the transcriptional activity and osteogenic action of Runx2. Coimmunoprecipitation analysis demonstrated a physical interaction between Gli2 and Runx2. Moreover, Ihh or Gli2 overexpression failed to increase ALP activity in Runx2-deficient mesenchymal cells. Collectively, these results suggest that Ihh regulates osteoblast differentiation of mesenchymal cells through up-regulation of the expression and function of Runx2 by Gli2.

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Gli regulation by the opposing activities of Fused and Suppressor of Fused

Cited by 132 publications

References 15 publications

A possible role of mouse Fused (STK36) in Hedgehog signaling and Gli transcription factor regulation

A possible role of mouse Fused (STK36) in Hedgehog signaling and Gli transcription factor regulation

Regulation of Hedgehog signaling: a complex story

Ihh/Gli2 Signaling Promotes Osteoblast Differentiation by Regulating Runx2 Expression and Function

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