ArticleScientific reports2016
Drosophila Dullard functions as a Mad phosphatase to terminate BMP signaling.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 9 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
9 citing papers in PubMed, 16 citations in OpenAlex.
- Biochemical principles of SMAD signaling across the animal kingdom.The Biochemical journal · 2026Review
- Suppression of TGF-β/SMAD signaling by an inner nuclear membrane phosphatase complex.Nature communications · 2025Article
- Review
- Convergent insulin and TGF-β signalling drives cancer cachexia by promoting aberrant fat body ECM accumulation in a Drosophila tumour model.EMBO reports · 2023Article
- Fragile X mental retardation protein coordinates neuron-to-glia communication for clearance of developmentally transient brain neurons.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Decapentaplegic Acutely Defines the Connectivity of Central Pacemaker Neurons inThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Mad dephosphorylation at the nuclear pore is essential for asymmetric stem cell division.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- The Smad Dependent TGF-β and BMP Signaling Pathway in Bone Remodeling and Therapies.Frontiers in molecular biosciences · 2021Review
- Article
Corrections and comments
- Erratum issued
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Bone morphogenetic proteins (BMPs) are growth factors that provide essential signals for normal embryonic development and adult tissue homeostasis. A key step in initiating BMP signaling is ligand induced phosphorylation of receptor Smads (R-Smads) by type I receptor kinases, while linker phosphorylation of R-Smads has been shown to cause BMP signal termination. Here we present data demonstrating that the phosphatase Dullard is involved in dephosphorylating the Drosophila R-Smad, Mad, and is integral in controlling BMP signal duration. We show that a hypomorphic Dullard allele or Dullard knockdown leads to increased Mad phosphorylation levels, while Dullard overexpression resulted in reduced Mad phosphorylations. Co-immunoprecipitation binding assays demonstrate phosphorylated Mad and Dullard physically interact, while mutation of Dullard's phosphatase domain still allowed Mad-Dullard interactions but abolished its ability to regulate Mad phosphorylations. Finally, we demonstrate that linker and C-terminally phosphorylated Mad can be regulated by one of two terminating mechanisms, degradation by proteasomes or dephosphorylation by the phosphatase Dullard.
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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.