ArticleThe Journal of biological chemistry2014
EphrinB1 interacts with CNK1 and promotes cell migration through c-Jun N-terminal kinase (JNK) activation.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 34 citations in OpenAlex.
- A Multiomics and Bioinformatics Analysis of the Role and Mechanism ofInternational journal of genomics · 2026Article
- EFNB1 drives glioma progression and shapes the immune microenvironment: a potential prognostic biomarker.Discover oncology · 2025Article
- PLK1 phosphorylates RhoGDI1 and promotes cancer cell migration and invasion.Cancer cell international · 2024Article
- Scaffolding Protein Connector Enhancer of Kinase Suppressor of Ras 1 (CNKSR1) Regulates MAPK Inhibition Responsiveness in Pancreas Cancer via Crosstalk with AKT Signaling.Molecular cancer research : MCR · 2023Article
- EFNB1 Acts as a Novel Prognosis Marker in Glioblastoma through Bioinformatics Methods and Experimental Validation.Journal of oncology · 2021Article
- Disease-associated synaptic scaffold protein CNK2 modulates PSD size and influences localisation of the regulatory kinase TNIK.Scientific reports · 2020Article
- Beyond Synthetic Lethality: Charting the Landscape of Pairwise Gene Expression States Associated with Survival in Cancer.Cell reports · 2019Article
- Ephrins and Eph Receptor Signaling in Tissue Repair and Fibrosis.Current rheumatology reports · 2019Review
- TBC1d24-ephrinB2 interaction regulates contact inhibition of locomotion in neural crest cell migration.Nature communications · 2018Article
- Nephrin-Binding Ephrin-B1 at the Slit Diaphragm Controls Podocyte Function through the JNK Pathway.Journal of the American Society of Nephrology : JASN · 2018Article
- EphrinB1 promotes cancer cell migration and invasion through the interaction with RhoGDI1.Oncogene · 2018Article
- Expression of the scaffold connector enhancer of kinase suppressor of Ras 1 (CNKSR1) is correlated with clinical outcome in pancreatic cancer.BMC cancer · 2017Article
- Paradoxes of the EphB1 receptor in malignant brain tumors.Cancer cell international · 2017Review
- Δ9-Tetrahydrocannabinol (Δ9-THC) Promotes Neuroimmune-Modulatory MicroRNA Profile in Striatum of Simian Immunodeficiency Virus (SIV)-Infected Macaques.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2016Article
- The C. elegans NR4A nuclear receptor gene nhr-6 promotes cell cycle progression in the spermatheca lineage.Developmental dynamics : an official publication of the American Association of Anatomists · 2015Article
- The multi-targeted tyrosine kinase inhibitor vandetanib plays a bifunctional role in non-small cell lung cancer cells.Scientific reports · 2015Article
- EphB/ephrinB signaling in cell adhesion and migration.Molecules and cells · 2015Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
The Eph receptors and their membrane-bound ligands, ephrins, play important roles in various biological processes such as cell adhesion and movement. The transmembrane ephrinBs transduce reverse signaling in a tyrosine phosphorylation-dependent or -independent, as well as PDZ-dependent manner. Here, we show that ephrinB1 interacts with Connector Enhancer of KSR1 (CNK1) in an EphB receptor-independent manner. In cultured cells, cotransfection of ephrinB1 with CNK1 increases JNK phosphorylation. EphrinB1/CNK1-mediated JNK activation is reduced by overexpression of dominant-negative RhoA. Overexpression of CNK1 alone is sufficient for activation of RhoA; however, both ephrinB1 and CNK1 are required for JNK phosphorylation. Co-immunoprecipitation data showed that ephrinB1 and CNK1 act as scaffold proteins that connect RhoA and JNK signaling components, such as p115RhoGEF and MKK4. Furthermore, adhesion to fibronectin or active Src overexpression increases ephrinB1/CNK1 binding, whereas blocking Src activity by a pharmacological inhibitor decreases not only ephrinB1/CNK1 binding, but also JNK activation. EphrinB1 overexpression increases cell motility, however, CNK1 depletion by siRNA abrogates ephrinB1-mediated cell migration and JNK activation. Moreover, Rho kinase inhibitor or JNK inhibitor treatment suppresses ephrinB1-mediated cell migration. Taken together, our findings suggest that CNK1 is required for ephrinB1-induced JNK activation and cell migration.
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