ArticleMolecular biology of the cell2005
The Wnt-NLK signaling pathway inhibits A-Myb activity by inhibiting the association with coactivator CBP and methylating histone H3.
Article in Molecular biology of the cell, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 44 citations in OpenAlex.
- Review
- TAK1: A Molecular Link Between Liver Inflammation, Fibrosis, Steatosis, and Carcinogenesis.Frontiers in cell and developmental biology · 2021Review
- Diamond Blackfan anemia is mediated by hyperactive Nemo-like kinase.Nature communications · 2020Article
- Integrative microRNA and mRNA deep-sequencing expression profiling in endemic Burkitt lymphoma.BMC cancer · 2017Article
- Post-Translational Modifications of the TAK1-TAB Complex.International journal of molecular sciences · 2017Review
- TIPE2 (Tumor Necrosis Factor α-induced Protein 8-like 2) Is a Novel Negative Regulator of TAK1 Signal.The Journal of biological chemistry · 2016Article
- NLK functions to maintain proliferation and stemness of NSCLC and is a target of metformin.Journal of hematology & oncology · 2015Article
- Deciphering Seed Sequence Based Off-Target Effects in a Large-Scale RNAi Reporter Screen for E-Cadherin Expression.PloS one · 2015Article
- Expression of Nemo-like kinase after spinal cord injury in rats.Journal of molecular neuroscience : MN · 2014Article
- Association of nuclear-localized Nemo-like kinase with heat-shock protein 27 inhibits apoptosis in human breast cancer cells.PloS one · 2014Article
- Article
- Article
- Nemo-like kinase associated with proliferation and apoptosis by c-Myb degradation in breast cancer.PloS one · 2013Article
- Transcriptional corepressors HIPK1 and HIPK2 control angiogenesis via TGF-β-TAK1-dependent mechanism.PLoS biology · 2013Article
- A-MYB (MYBL1) stimulates murine testis-specific Ldhc expression via the cAMP-responsive element (CRE) site.Biology of reproduction · 2012Article
- Article
- Regulation of FOXO1 by TAK1-Nemo-like kinase pathway.The Journal of biological chemistry · 2010Article
- Human SMAD4 is phosphorylated at Thr9 and Ser138 by interacting with NLK.Molecular and cellular biochemistry · 2010Article
- PPAR-gamma Signaling Crosstalk in Mesenchymal Stem Cells.PPAR research · 2010Article
- RFX2 is a candidate downstream amplifier of A-MYB regulation in mouse spermatogenesis.BMC developmental biology · 2009Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The c-myb proto-oncogene product (c-Myb) regulates proliferation and differentiation of hematopoietic cells. Recently we have shown that c-Myb is degraded in response to Wnt-1 stimulation via a pathway involving TAK1 (TGF-beta-activated kinase), HIPK2 (homeodomain-interacting protein kinase 2), and NLK (Nemo-like kinase). NLK and HIPK2 bind directly to c-Myb and phosphorylate c-Myb at multiple sites, inducing its ubiquitination and proteasome-dependent degradation. The mammalian myb gene family contains two members in addition to c-myb, A-myb, and B-myb. Here, we report that the Wnt-NLK pathway also inhibits A-Myb activity, but by a different mechanism. As in the case of c-Myb, both NLK and HIPK2 bound directly to A-Myb and inhibited its activity. NLK phosphorylated A-Myb, but did not induce A-Myb degradation. Overexpression of NLK inhibited the association between A-Myb and the coactivator CBP, thus, blocking A-Myb-induced trans-activation. The kinase activity of NLK is required for the efficient inhibition of the association between A-Myb and CBP, although the kinase-negative form of NLK also partly inhibits the interaction between A-Myb and CBP. Furthermore, NLK induced the methylation of histone H3 at lysine-9 at A-Myb-bound promoter regions. Thus, the Wnt-NLK pathway inhibits the activity of each Myb family member by different mechanisms.
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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.