ArticleGenetics1996
Functional domains of fused, a serine-threonine kinase required for signaling in Drosophila.
Article in Genetics, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
22 citing papers in PubMed, 53 citations in OpenAlex.
- Hedgehog-stimulated phosphorylation at multiple sites activates Ci by altering Ci-Ci interfaces without full Suppressor of Fused dissociation.PLoS biology · 2025Article
- Physiological analysis of the mechanism of Ci transcription factor activation through multiple Fused phosphorylation sites in Hedgehog signal transduction.bioRxiv : the preprint server for biology · 2025Article
- Article
- Regulation of the RNA-binding protein Smaug by the GPCR Smoothened via the kinase Fused.EMBO reports · 2020Article
- Contributions of Costal 2-Fused interactions to Hedgehog signaling in Drosophila.Development (Cambridge, England) · 2015Article
- The Hedgehog signal transduction network.Science signaling · 2012Review
- Dual function of UNC-51-like kinase 3 (Ulk3) in the Sonic hedgehog signaling pathway.The Journal of biological chemistry · 2010Article
- Mechanism and evolution of cytosolic Hedgehog signal transduction.Development (Cambridge, England) · 2010Review
- Costal2 functions as a kinesin-like protein in the hedgehog signal transduction pathway.Current biology : CB · 2008Article
- Fused-Costal2 protein complex regulates Hedgehog-induced Smo phosphorylation and cell-surface accumulation.Genes & development · 2007Article
- Comparative analysis of the kinomes of three pathogenic trypanosomatids: Leishmania major, Trypanosoma brucei and Trypanosoma cruzi.BMC genomics · 2005Article
- Mice deficient in the fused homolog do not exhibit phenotypes indicative of perturbed hedgehog signaling during embryonic development.Molecular and cellular biology · 2005Article
- Loss of the serine/threonine kinase fused results in postnatal growth defects and lethality due to progressive hydrocephalus.Molecular and cellular biology · 2005Article
- An intramolecular association between two domains of the protein kinase Fused is necessary for Hedgehog signaling.Molecular and cellular biology · 2004Article
- Regulation of Hedgehog signaling: a complex story.Biochemical pharmacology · 2004Review
- Hedgehog signal transduction proteins: contacts of the Fused kinase and Ci transcription factor with the kinesin-related protein Costal2.BMC developmental biology · 2002Article
- A screen for dominant mutations applied to components in the Drosophila EGF-R pathway.Proceedings of the National Academy of Sciences of the United States of America · 2002Article
- The carboxyl-terminal domain of the protein kinase fused can function as a dominant inhibitor of hedgehog signaling.Molecular and cellular biology · 2002Article
- Article
- X chromosome DNA variation in Drosophila virilis.Proceedings. Biological sciences · 1999Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
fused (fu) is a segment-polarity gene encoding a putative serine-threonine kinase. In a wild-type context, all fu mutations display the same set of phenotypes. Nevertheless, mutations of the Suppressor of fused [Su(fu)] gene define three classes of alleles (fuO, fuI, fuII). Here, we report the molecular analysis of known fu mutations and the generation of new alleles by in vitro mutagenesis. We show that the Fused (Fu) protein functions in vivo as a kinase. The N-terminal kinase and the extreme C-terminal domains are necessary for Fu+ activity while a central region appears to be dispensable. We observe a striking correlation between the molecular lesions of fu mutations and phenotype displayed in their interaction with Su(fu). Indeed, fuI alleles which are suppressed by Su(fu) mutations are defined by inframe alterations of the N-terminal catalytic domain whereas the C-terminal domain is missing or altered in all fuII alleles. An unregulated FuII protein, which can be limited to the 80 N-terminal amino acids of the kinase domain, would be responsible for the neomorphic costal-2 phenotype displayed by the fuII-Su(fu) interaction. We propose that the Fu C-terminal domain can differentially regulate the Fu catalytic domain according to cell position in the parasegment.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.