ReviewBiochemical pharmacology2014
Atypical protein kinase Cι as a human oncogene and therapeutic target.
Review in Biochemical pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
57 citing papers in PubMed, 96 citations in OpenAlex.
- A proof-of-concept trial of protein kinase C iota inhibition with auranofin for the paclitaxel-induced acute pain syndrome.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2017Trial
- PKC-iota drives EGFR-TKI resistance in EGFR-mutated NSCLC by phosphorylating FASN to reprogram lipid metabolism.Translational lung cancer research · 2026Article
- Targeting protein kinase C signaling cascades in alzheimer's disease: emerging neuroprotective roles of aurothioglucose.Inflammopharmacology · 2026Review
- The chordoid gliomaScience signaling · 2025Article
- Protein kinase C iota (PKCι) and pVHL are both needed for lysosomal degradation of α5 integrin in renal carcinoma cells.Molecular biology reports · 2025Article
- Into the fold: advances in understanding aPKC membrane dynamics.The Biochemical journal · 2023Article
- Investigating pathogenic SNP of PKCι in HCV-induced hepatocellular carcinoma.Scientific reports · 2023Article
- Control of atypical PKCι membrane dissociation by tyrosine phosphorylation within a PB1-C1 interdomain interface.The Journal of biological chemistry · 2023Article
- Investigation of UTR Variants by Computational Approaches Reveal Their Functional Significance inGenes · 2023Article
- Enhanced activity of Alzheimer disease-associated variant of protein kinase Cα drives cognitive decline in a mouse model.Nature communications · 2022Article
- Protein kinase Cι mediates immunosuppression in lung adenocarcinoma.Science translational medicine · 2022Article
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- Upgrade of an old drug: Auranofin in innovative cancer therapies to overcome drug resistance and to increase drug effectiveness.Medicinal research reviews · 2022Review
- Protein kinase CCell reports · 2021Article
- 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
- Recurrent copy number gains drive PKCι expression and PKCι-dependent oncogenic signaling in human cancers.Advances in biological regulation · 2020Article
- A new pipeline for pathophysiological analysis of the mammary gland based on organoid transplantation and organ clearing.Journal of cell science · 2020Article
- Protein kinase Cι promotes UBF1-ECT2 binding on ribosomal DNA to drive rRNA synthesis and transformed growth of non-small-cell lung cancer cells.The Journal of biological chemistry · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Protein kinase inhibitors represent a major class of targeted therapeutics that has made a positive impact on treatment of cancer and other disease indications. Among the promising kinase targets for further therapeutic development are members of the Protein Kinase C (PKC) family. The PKCs are central components of many signaling pathways that regulate diverse cellular functions including proliferation, cell cycle, differentiation, survival, cell migration, and polarity. Genetic manipulation of individual PKC isozymes has demonstrated that they often fulfill distinct, nonredundant cellular functions. Participation of PKC members in different intracellular signaling pathways reflects responses to varying extracellular stimuli, intracellular localization, tissue distribution, phosphorylation status, and intermolecular interactions. PKC activity, localization, phosphorylation, and/or expression are often altered in human tumors, and PKC isozymes have been implicated in various aspects of transformation, including uncontrolled proliferation, migration, invasion, metastasis, angiogenesis, and resistance to apoptosis. Despite the strong relationship between PKC isozymes and cancer, to date only atypical PKCiota has been shown to function as a bona fide oncogene, and as such is a particularly attractive therapeutic target for cancer treatment. In this review, we discuss the role of PKCiota in transformation and describe mechanism-based approaches to therapeutically target oncogenic PKCiota signaling in cancer.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.