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Abstract
Gli proteins are transcriptional effectors of the Hedgehog signaling pathway. They play key roles in the development of many organs and tissues, and are deregulated in birth defects and cancer. We review the molecular mechanisms of Gli protein regulation in mammals, with special emphasis on posttranslational modifications and intracellular transport. We also discuss how Gli proteins interact with co-activators and co-repressors to fine-tune the expression of Hedgehog target genes. Finally, we provide an overview of the regulation of developmental processes and tissue regeneration by Gli proteins and discuss how these proteins are involved in cancer progression, both through canonical regulation via the Hedgehog pathway and through cross-talk with other signaling pathways.
Highlights
glioma-associated oncogene transcription factors (Gli) proteins are transcriptional effectors of the Hedgehog signaling pathway
Gli2 and Gli3 are partially truncated on the C terminus, which removes their transcriptional activation domain and confers on them the ability to function as repressors of Hh target genes
Gli Proteins In Drosophila, Hh-regulated transcription is driven by a single transcription factor Cubitus interruptus (Ci), which acts both as an activator and repressor of transcription
Summary
The hedgehog (Hh) pathway, discovered in Drosophila, is a highly evolutionarily conserved signaling cascade that orchestrates key steps of multiple aspects of development [1,2], including embryonic patterning, organ morphogenesis, and growth control by regulating cell proliferation, differentiation, and migration. In the off-state of the Hh pathway, activity of Smo is inhibited by Ptch. In the off-state of the Hh pathway, activity of Smo is inhibited by Ptch1 Under these conditions, Gli and Gli are partially truncated on the C terminus, which removes their transcriptional activation domain and confers on them the ability to function as repressors of Hh target genes. Smo membrane: upon binding of the ligand, Ptch is excluded from the cilium, while Smo concentrates accumulation at the ciliary membrane activates entry of SuFu and Gli proteins into the cilium [27]. Aberrant activity of Hh signaling is associated with many symptoms of so-called ciliopathies, ciliopathies, that is, diseases caused by damaged or absent primary cilia.
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