ArticleCell death & disease2010
Differential effects of the phosphatidylinositol 4-kinases, PI4KIIα and PI4KIIIβ, on Akt activation and apoptosis.
Article in Cell death & disease, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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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.
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Who cites it
43 citing papers in PubMed, 66 citations in OpenAlex.
- PI4K and PIPK families in breast cancer: subtype-specific oncogenic mechanisms and precision therapeutic strategies.Molecular biology reports · 2026Review
- Knockout of PI4-Kinase A in GnRH Neurons Causes their Prepubertal Death.bioRxiv : the preprint server for biology · 2026Article
- Golgi Drivers of Cancer.Sub-cellular biochemistry · 2026Review
- PI4-kinase A is essential for survival of the GnRH neurons.Frontiers in endocrinology · 2026Article
- Oxygen tension-dependent variability in the cancer cell kinome impacts signaling pathways and response to targeted therapies.iScience · 2024Article
- A Plethora of Functions Condensed into Tiny Phospholipids: The Story of PI4P and PI(4,5)PCells · 2023Review
- Membrane trafficking in breast cancer progression: protein kinase D comes into play.Frontiers in cell and developmental biology · 2023Review
- High expression of PI4K2A predicted poor prognosis of colon adenocarcinoma (COAD) and correlated with immunity.Cancer medicine · 2023Article
- Supercritical fluid chromatography-mass spectrometry enables simultaneous measurement of all phosphoinositide regioisomers.Communications chemistry · 2022Article
- The diaryl-imidazopyridazine anti-plasmodial compound, MMV652103, exhibits anti-breast cancer activity.EXCLI journal · 2022Article
- A PI4KIIIα protein complex is required for cell viability during Drosophila wing development.Developmental biology · 2020Article
- Using Phosphatidylinositol Phosphorylation as Markers for Hyperglycemic Related Breast Cancer.International journal of molecular sciences · 2020Article
- Anti-angiogenic effects of VEGF stimulation on endothelium deficient in phosphoinositide recycling.Nature communications · 2020Article
- Integrin-independent support of cancer drug resistance by tetraspanin CD151.Cellular and molecular life sciences : CMLS · 2019Article
- A complex between phosphatidylinositol 4-kinase IIα and integrin α3β1 is required forThe Journal of biological chemistry · 2019Article
- A large scale high-throughput screen identifies chemical inhibitors of phosphatidylinositol 4-kinase type II alpha.Journal of lipid research · 2019Article
- Article
- Identification of a novel biomarker in tangeretin‑induced cell death in AGS human gastric cancer cells.Oncology reports · 2018Article
- Phospholipidation of nuclear proteins by the human papillomavirus E6 oncoprotein: implication in carcinogenesis.Oncotarget · 2018Article
- PI4KIIα regulates insulin secretion and glucose homeostasis via a PKD-dependent pathway.Biophysics reports · 2018Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
In this study, we investigated the role of PI4P synthesis by the phosphatidylinositol 4-kinases, PI4KIIα and PI4KIIIβ, in epidermal growth factor (EGF)-stimulated phosphoinositide signaling and cell survival. In COS-7 cells, knockdown of either isozyme by RNA interference reduced basal levels of PI4P and PI(4,5)P(2), without affecting receptor activation. Only knockdown of PI4KIIα inhibited EGF-stimulated Akt phosphorylation, indicating that decreased PI(4,5)P(2) synthesis observed by loss of either isoform could not account for this PI4KIIα-specific effect. Phospholipase Cγ activation was also differentially affected by knockdown of either PI4K isozyme. Overexpression of kinase-inactive PI4KIIα, which induces defective endosomal trafficking without reducing PI(4,5)P(2) levels, also reduced Akt activation. Furthermore, PI4KIIα knockdown profoundly inhibited cell proliferation and induced apoptosis as evidenced by the cleavage of caspase-3 and its substrate poly(ADP-ribose) polymerase. However, in MDA-MB-231 breast cancer cells, apoptosis was observed subsequent to knockdown of either PI4KIIα or PI4KIIIβ and this correlated with enhanced proapoptotic Akt phosphorylation. The differential effects of phosphatidylinositol 4-kinase knockdown in the two cell lines lead to the conclusion that phosphoinositide turnover is inhibited through PI4P substrate depletion, whereas impaired antiapoptotic Akt signaling is an indirect consequence of dysfunctional endosomal trafficking.
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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.