ArticleThe EMBO journal1996
EGF or PDGF receptors activate atypical PKClambda through phosphatidylinositol 3-kinase.
Article in The EMBO journal, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
70 citing papers in PubMed, 272 citations in OpenAlex.
- Conditional Ablation of PKCλ/ι in CD4Biomolecules · 2025Article
- Glyoxalase 1 and protein kinase Cλ as potential therapeutic targets for late-stage breast cancer.Oncology letters · 2021Article
- Identification of Key Phospholipids That Bind and Activate Atypical PKCs.Biomedicines · 2021Article
- Article
- A high-throughput screen identifies that CDK7 activates glucose consumption in lung cancer cells.Nature communications · 2019Article
- Protein kinase Cε regulates nuclear translocation of extracellular signal-regulated kinase, which contributes to bradykinin-induced cyclooxygenase-2 expression.Scientific reports · 2018Article
- A Review of Anti-Angiogenic Targets for Monoclonal Antibody Cancer Therapy.International journal of molecular sciences · 2017Review
- Chronic insulin treatment phosphorylates the renal Na-K-ATPase α1-subunit at serine 16/23 and reduces its activity involving PI3-kinase-dependent PKC activation.American journal of physiology. Renal physiology · 2016Article
- PKC iota promotes cellular proliferation by accelerated G1/S transition via interaction with CDK7 in esophageal squamous cell carcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Protein kinase Cζ exhibits constitutive phosphorylation and phosphatidylinositol-3,4,5-triphosphate-independent regulation.The Biochemical journal · 2016Article
- Review
- Targeting aPKC disables oncogenic signaling by both the EGFR and the proinflammatory cytokine TNFα in glioblastoma.Science signaling · 2014Article
- aPKCλ maintains the integrity of the glomerular slit diaphragm through trafficking of nephrin to the cell surface.Journal of biochemistry · 2014Article
- Regulation of polarized morphogenesis by protein kinase C iota in oncogenic epithelial spheroids.Carcinogenesis · 2014Article
- Atypical protein kinase Cλ is critical for growth factor receptor-induced dorsal ruffle turnover and cell migration.The Journal of biological chemistry · 2013Article
- Polarized regulation of glycogen synthase kinase-3β is important for glioma cell invasion.PloS one · 2013Article
- The Roles of VHL-Dependent Ubiquitination in Signaling and Cancer.Frontiers in oncology · 2012Article
- Regulation of Cdk7 activity through a phosphatidylinositol (3)-kinase/PKC-ι-mediated signaling cascade in glioblastoma.Carcinogenesis · 2012Article
- Article
- Genetic variability of the mTOR pathway and prostate cancer risk in the European Prospective Investigation on Cancer (EPIC).PloS one · 2011Article
10 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
Overexpression of a TPA-insensitive PKC member, an atypical protein kinase C (aPKClambda), results in an enhancement of the transcriptional activation of TPA response element (TRE) in cells stimulated with epidermal growth factor (EGF) or platelet-derived growth factor (PDGF). EGF or PDGF also caused a transient increase in the in vivo phosphorylation level and a change in the intracellular localization of aPKClambda from the nucleus to the cytosol, indicating the activation of aPKClambda in response to this growth factor stimulation. These immediate signal-dependent changes in aKPClambda were observed for a PDGF receptor add-back mutant (Y40/51) that possesses only two of the five major autophosphorylation sites and binds PI3-kinase, and were inhibited by wortmannin, an inhibitor of PI3-kinase. Furthermore, an N-terminal fragment of the catalytic subunit of PI3-kinase, p110alpha, inhibited aPKClambda-dependent activation of TRE in Y40/51 cells stimulated with PDGF. Overexpression of p110alpha resulted in an enhancement of TRE expression in response to PDGF and the regulatory domain of aPKClambda inhibited this TRE activation in Y40/51 cells. These results provide the first in vivo evidence supporting the presence of a novel signalling pathway from receptor tyrosine kinases to aPKClambda through PI3-kinase.
Indexed as
Identifiers
8631300PMC450277W1550981215What Socratic holds
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 Socratic graph.