ArticleMolecular biology of the cell2017
NLK-mediated phosphorylation of HDAC1 negatively regulates Wnt signaling.
Article in Molecular biology of the cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 34 citations in OpenAlex.
- CI-994 is a dual modulator of class I HDACs and Wnt/β-catenin signaling for the treatment of Alzheimer's disease.Alzheimer's research & therapy · 2026Article
- Evolutionary analysis through structural modeling of FAM222 proteins reveals a novel disordered conserved domain in vertebrates that interacts with NLK.Scientific reports · 2025Article
- Revealing Dynamics of Protein Phosphorylation: A Study on the Cashmere Fineness Disparities in Liaoning Cashmere Goats.Molecular biotechnology · 2025Article
- Exosome-mediated Transfer of lncRNA in Liver Associated Diseases; Uncovered Truths.Cell biochemistry and biophysics · 2025Review
- The ROS/CaMK II/β-Catenin Signaling Axis Affects the Osteogenic Potential of BMSCs and Disrupts Implant Osseointegration: An In Vitro Study.International journal of dentistry · 2025Article
- Investigating the molecular mechanisms of microRNA‑409‑3p in tumor progression: Towards targeted therapeutics (Review).International journal of oncology · 2024Review
- Landscape of NcRNAs involved in drug resistance of breast cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023Review
- Article
- The phosphorylation to acetylation/methylation cascade in transcriptional regulation: how kinases regulate transcriptional activities of DNA/histone-modifying enzymes.Cell & bioscience · 2022Review
- Modulation of Placental Breast Cancer Resistance Protein by HDAC1 in Mice: Implications for Optimization of Pharmacotherapy During Pregnancy.Reproductive sciences (Thousand Oaks, Calif.) · 2021Article
- Nemo-Like Kinase in Development and Diseases: Insights from Mouse Studies.International journal of molecular sciences · 2020Review
- Modulation of Biliary Cancer Chemo-Resistance Through MicroRNA-Mediated Rewiring of the Expansion of CD133+ Cells.Hepatology (Baltimore, Md.) · 2020Article
- Exosome-transferred long non-coding RNA ASMTL-AS1 contributes to malignant phenotypes in residual hepatocellular carcinoma after insufficient radiofrequency ablation.Cell proliferation · 2020Article
- Diamond Blackfan anemia is mediated by hyperactive Nemo-like kinase.Nature communications · 2020Article
- Phospholipase C inhibits apoptosis of porcine primary granulosa cells cultured in vitro.Journal of ovarian research · 2019Article
- Knockdown of Nemo‑like kinase promotes metastasis in non‑small‑cell lung cancer.Oncology reports · 2019Article
- HDAC1 was involved in placental breast cancer resistance protein regulation in vitro: A preliminary study.Journal of cellular and molecular medicine · 2019Article
- Article
- Revisiting Histone Deacetylases in Human Tumorigenesis: The Paradigm of Urothelial Bladder Cancer.International journal of molecular sciences · 2019Review
- Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Wnt signaling pathway is essential in regulating various cellular processes. Different mechanisms of inhibition for Wnt signaling have been proposed. Besides β-catenin degradation through the proteasome, nemo-like kinase (NLK) is another molecule that is known to negatively regulate Wnt signaling. However, the mechanism by which NLK mediates the inhibition of Wnt signaling was not known. In the present study, we used primary embryonic fibroblast cells isolated from NLK-deficient mice and showed that these cells proliferate faster and have a shorter cell cycle than wild-type cells. In NLK-knockout cells, we observed sustained interaction between Lef1 and β-catenin, leading to elevated luciferase reporter of β-catenin/Lef1-mediated transcriptional activation. The mechanism for the reduced β-catenin/Lef1 promoter activation was explained by phosphorylation of HDAC1 at serine 421 via NLK. The phosphorylation of HDAC1 was achieved only in the presence of wild-type NLK because a catalytically inactive mutant of NLK was unable to phosphorylate HDAC1 and reduced the luciferase reporter of β-catenin/Lef1-mediated transcriptional activation. This result suggests that NLK and HDAC1 together negatively regulate Wnt signaling, which is vital in preventing aberrant proliferation of nontransformed primary fibroblast cells.
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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.