ArticleCancer science2004
Nemo-like kinase suppresses a wide range of transcription factors, including nuclear factor-kappaB.
Article in Cancer science, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 46 citations in OpenAlex.
- Molecular characterization of FAM222B as a novel disease gene for dominant cardiovascular laterality defects.Scientific reports · 2026Article
- Atypical MAPKs in cancer.The FEBS journal · 2025Review
- Hsa_circ_0009092/miR-665/NLK signaling axis suppresses colorectal cancer progression via recruiting TAMs in the tumor microenvironment.Journal of experimental & clinical cancer research : CR · 2023Article
- Chemotherapeutic drugs: Cell death- and resistance-related signaling pathways. Are they really as smart as the tumor cells?Translational oncology · 2021Review
- Mechanisms of Maintenance of Foot-and-Mouth Disease Virus Persistence Inferred From Genes Differentially Expressed in Nasopharyngeal Epithelia of Virus Carriers and Non-carriers.Frontiers in veterinary science · 2020Article
- Phosphorylation of MAVS/VISA by Nemo-like kinase (NLK) for degradation regulates the antiviral innate immune response.Nature communications · 2019Article
- NLK-mediated phosphorylation of HDAC1 negatively regulates Wnt signaling.Molecular biology of the cell · 2017Article
- Article
- Nemo-like kinase as a negative regulator of nuclear receptor Nurr1 gene transcription in prostate cancer.BMC cancer · 2016Article
- Lentivirus-mediated knockdown of NLK inhibits small-cell lung cancer growth and metastasis.Drug design, development and therapy · 2016Article
- NLK functions to maintain proliferation and stemness of NSCLC and is a target of metformin.Journal of hematology & oncology · 2015Article
- Lentivirus‑delivered nemo‑like kinase small interfering RNA inhibits laryngeal cancer cell proliferation in vitro.Molecular medicine reports · 2015Article
- Molecular mechanisms of etoposide.EXCLI journal · 2015Review
- Expression of Nemo-like kinase was increased and negatively correlated with the expression of TCF4 in lung cancers.International journal of clinical and experimental pathology · 2015Article
- Nemo-like kinase is critical for p53 stabilization and function in response to DNA damage.Cell death and differentiation · 2014Article
- Nemo-like kinase (NLK) negatively regulates NF-kappa B activity through disrupting the interaction of TAK1 with IKKβ.Biochimica et biophysica acta · 2014Article
- Association of nuclear-localized Nemo-like kinase with heat-shock protein 27 inhibits apoptosis in human breast cancer cells.PloS one · 2014Article
- Prognostic significance of nemo-like kinase (NLK) expression in patients with gallbladder cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2013Article
- Nemo regulates cell dynamics and represses the expression of miple, a midkine/pleiotrophin cytokine, during ommatidial rotation.Developmental biology · 2013Article
- Common variation in Nemo-like kinase is associated with risk of ovarian cancer.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2012Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nemo-like kinase (NLK) is a serine/threonine kinase that suppresses the transcription activity of the beta-catenin-T-cell factor (TCF) complex through phosphorylation of TCF. Our previous study showed that NLK overexpression induces apoptosis in DLD-1 human colon cancer cells and that apoptosis induction presumably requires a mechanism other than the suppression of beta-catenin-TCF complex. Luciferase reporter gene assay with pNF-kappaB-Luc revealed that NLK could suppress transcription activity of NF-kappaB in a kinase-dependent manner. However, it appeared that transcription co-activators of NF-kappaB, such as CREB binding protein (CBP)/p300, were likely to be the direct targets of NLK, rather than NF-kappaB itself. Luciferase reporter gene analysis of GAL4-CBP fusion proteins revealed that the C-terminal region of CBP was critical for transcription suppression by NLK. In vitro kinase assay showed that NLK could phosphorylate the C-terminal domain of CBP. However, HAT activity was not suppressed by the induction of wild-type NLK in DLD-1 cells. Furthermore, we observed that NLK suppressed the transcription activity of AP-1, Smad, and p53, all of which also utilize CBP as a co-activator. The extent of suppression by NLK was similar among the transcription factors tested (50-60% reduction). Our results suggest that NLK may suppress a wide range of gene expression, possibly through CBP.
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Registered trials
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