ArticleThe Biochemical journal2006
dDYRK2 and Minibrain interact with the chromatin remodelling factors SNR1 and TRX.
Article in The Biochemical journal, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 28 citations in OpenAlex.
- Targeting DYRKs in Cardiovascular Diseases: From Biological Mechanisms to Therapeutic Translation.International journal of molecular sciences · 2026Review
- Review
- DYRK1A promotes viral entry of highly pathogenic human coronaviruses in a kinase-independent manner.PLoS biology · 2023Article
- Differential maturation and chaperone dependence of the paralogous protein kinases DYRK1A and DYRK1B.Scientific reports · 2022Article
- Review
- Ocular Phenotype Associated withGenes · 2021Article
- DYRK1A: a down syndrome-related dual protein kinase with a versatile role in tumorigenesis.Cellular and molecular life sciences : CMLS · 2021Review
- Minibrain-related kinase/dual-specificity tyrosine-regulated kinase 1B implication in stem/cancer stem cells biology.World journal of stem cells · 2020Review
- The crystal structure of the protein kinase HIPK2 reveals a unique architecture of its CMGC-insert region.The Journal of biological chemistry · 2019Article
- Mutational analysis of two residues in the DYRK homology box of the protein kinase DYRK1A.BMC research notes · 2018Article
- Drosophila Studies on Autism Spectrum Disorders.Neuroscience bulletin · 2017Review
- DYRK1B mutations associated with metabolic syndrome impair the chaperone-dependent maturation of the kinase domain.Scientific reports · 2017Article
- DYRK1A, a Dosage-Sensitive Gene Involved in Neurodevelopmental Disorders, Is a Target for Drug Development in Down Syndrome.Frontiers in behavioral neuroscience · 2016Review
- Disruptive de novo mutations of DYRK1A lead to a syndromic form of autism and ID.Molecular psychiatry · 2016Article
- The Drosophila wings apart gene anchors a novel, evolutionarily conserved pathway of neuromuscular development.Genetics · 2013Article
- Structures of Down syndrome kinases, DYRKs, reveal mechanisms of kinase activation and substrate recognition.Structure (London, England : 1993) · 2013Article
- Trisomy 21 and early brain development.Trends in neurosciences · 2012Review
- Protein kinase DYRK2 is a scaffold that facilitates assembly of an E3 ligase.Nature cell biology · 2009Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The DYRKs (dual specificity tyrosine phosphorylation-regulated kinases) are a conserved family of protein kinases that autophosphorylate a tyrosine residue in their activation loop by an intra-molecular mechanism and phosphorylate exogenous substrates on serine/threonine residues. Little is known about the identity of true substrates for DYRK family members and their binding partners. To address this question, we used full-length dDYRK2 (Drosophila DYRK2) as bait in a yeast two-hybrid screen of a Drosophila embryo cDNA library. Of 14 independent dDYRK2 interacting clones identified, three were derived from the chromatin remodelling factor, SNR1 (Snf5-related 1), and three from the essential chromatin component, TRX (trithorax). The association of dDYRK2 with SNR1 and TRX was confirmed by co-immunoprecipitation studies. Deletion analysis showed that the C-terminus of dDYRK2 modulated the interaction with SNR1 and TRX. DYRK family member MNB (Minibrain) was also found to co-precipitate with SNR1 and TRX, associations that did not require the C-terminus of the molecule. dDYRK2 and MNB were also found to phosphorylate SNR1 at Thr102 in vitro and in vivo. This phosphorylation required the highly conserved DH-box (DYRK homology box) of dDYRK2, whereas the DH-box was not essential for phosphorylation by MNB. This is the first instance of phosphorylation of SNR1 or any of its homologues and implicates the DYRK family of kinases with a role in chromatin remodelling.
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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.