ArticleMolecular and cellular biology1997
Phosphatidylinositol 3-kinase mediates epidermal growth factor-induced activation of the c-Jun N-terminal kinase signaling pathway.
Article in Molecular and cellular biology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 133 citations in OpenAlex.
- Molecular Mechanisms of Anti-Estrogen Therapy Resistance and Novel Targeted Therapies.Cancers · 2022Review
- JNK Signaling in Stem Cell Self-Renewal and Differentiation.International journal of molecular sciences · 2020Review
- Gossypol induces apoptosis of multiple myeloma cells through the JUN-JNK pathway.American journal of cancer research · 2020Article
- Crosstalk Between Signaling Pathways Involved in the Regulation of Airway Smooth Muscle Cell Hyperplasia.Frontiers in pharmacology · 2019Review
- Estrogen receptor alpha drives mTORC1 inhibitor-induced feedback activation of PI3K/AKT in ER+ breast cancer.Oncotarget · 2018Article
- PI3K p110β isoform synergizes with JNK in the regulation of glioblastoma cell proliferation and migration through Akt and FAK inhibition.Journal of experimental & clinical cancer research : CR · 2016Article
- EGFR and FGFR pathways have distinct roles in Drosophila mushroom body development and ethanol-induced behavior.PloS one · 2014Article
- Primordial germ cells and gastrointestinal stromal tumors respond distinctly to a cKit overactivating allele.Human molecular genetics · 2013Article
- Phosphatidylinositol 3-kinase and antiestrogen resistance in breast cancer.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2011Review
- Mutations in the phosphatidylinositol 3-kinase pathway: role in tumor progression and therapeutic implications in breast cancer.Breast cancer research : BCR · 2011Review
- Regulation of MAPKs by growth factors and receptor tyrosine kinases.Biochimica et biophysica acta · 2007Review
- The phosphoinositide 3-kinase pathway in human cancer: genetic alterations and therapeutic implications.Current genomics · 2007Article
- Membrane-type 1 matrix metalloproteinase is regulated by sp1 through the differential activation of AKT, JNK, and ERK pathways in human prostate tumor cells.Neoplasia (New York, N.Y.) · 2007Article
- The Dbs PH domain contributes independently to membrane targeting and regulation of guanine nucleotide-exchange activity.The Biochemical journal · 2006Article
- Activated c-Jun N-terminal kinase is required for axon formation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2006Article
- Epidermal growth factor differentially augments G(i)-mediated stimulation of c-Jun N-terminal kinase activity.British journal of pharmacology · 2004Article
- An inhibitory function for JNK in the regulation of IGF-I signaling in breast cancer.Oncogene · 2003Article
- Oxygen sensing in neuroendocrine cells and other cell types: pheochromocytoma (PC12) cells as an experimental model.Endocrine pathology · 2003Review
- Prophylactic use of epidermal growth factor reduces ischemia/reperfusion intestinal damage.The American journal of pathology · 2002Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The signaling events which mediate activation of c-Jun N-terminal kinase (JNK) are not yet well characterized. To broaden our understanding of upstream mediators which link extracellular signals to the JNK pathway, we investigated the role of phosphatidylinositol (PI) 3-kinase in epidermal growth factor (EGF)-mediated JNK activation. In this report we demonstrate that a dominant negative form of PI 3-kinase as well as the inhibitor wortmannin blocks EGF-induced JNK activation dramatically. However, wortmannin does not have an effect on JNK activation induced by UV irradiation or osmotic shock. In addition, a membrane-targeted, constitutively active PI 3-kinase (p110beta) was shown to produce in vivo products and to activate JNK, while a kinase-mutated form of this protein showed no activation. On the basis of these experiments, we propose that PI 3-kinase activity plays a role in EGF-induced JNK activation in these cells.
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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 Socratic graph.