ArticleCancer research2011
PIPKIγ regulates β-catenin transcriptional activity downstream of growth factor receptor signaling.
Article in Cancer research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 21 citations in OpenAlex.
- PIPKIγ promotes non-homologous end joining through LIG4 to enhance radiotherapy resistance in triple-negative breast cancer.Cell death & disease · 2025Article
- Pip5k1γ promotes anabolism of nucleus pulposus cells and intervertebral disc homeostasis by activating CaMKII-Ampk pathway in aged mice.Aging cell · 2024Article
- Pip5k1c Loss in Chondrocytes Causes Spontaneous Osteoarthritic Lesions in Aged Mice.Aging and disease · 2023Article
- PI(4,5)PScience advances · 2023Article
- Posttranslational Modifications of Smurfs: Emerging Regulation in Cancer.Frontiers in oncology · 2020Review
- Type Iγ phosphatidylinositol phosphate kinase promotes tumor growth by facilitating Warburg effect in colorectal cancer.EBioMedicine · 2019Article
- Type Iγ phosphatidylinositol phosphate kinase dependent cell migration and invasion are dispensable for tumor metastasis.American journal of cancer research · 2019Article
- MiR-155 promotes epithelial-mesenchymal transition in hepatocellular carcinoma cells through the activation of PI3K/SGK3/β-catenin signaling pathways.Oncotarget · 2016Article
- Enhancement of β-catenin activity by BIG1 plus BIG2 via Arf activation and cAMP signals.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- IQGAP1 is a phosphoinositide effector and kinase scaffold.Advances in biological regulation · 2016Review
- Phosphatidylinositol phosphate 5-kinase Iγi2 in association with Src controls anchorage-independent growth of tumor cells.The Journal of biological chemistry · 2013Article
- IQGAP1 is a novel phosphatidylinositol 4,5 bisphosphate effector in regulation of directional cell migration.The EMBO journal · 2013Article
- ARF6-regulated endocytosis of growth factor receptors links cadherin-based adhesion to canonical Wnt signaling in epithelia.Molecular and cellular biology · 2013Article
- Phosphatidylinositol 4,5-bisphosphate: targeted production and signaling.BioEssays : news and reviews in molecular, cellular and developmental biology · 2013Review
- Acute alcohol exposure impairs fracture healing and deregulates β-catenin signaling in the fracture callus.Alcoholism, clinical and experimental research · 2012Article
- Phosphoinositide signaling regulates the exocyst complex and polarized integrin trafficking in directionally migrating cells.Developmental cell · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Increased β-catenin transcriptional activity downstream of the Wnt/Wingless signaling pathway has been observed in many human tumors, most notably colorectal carcinomas. However, β-catenin activation is also observed in many human malignancies with no observable Wnt activity. Wnt-independent pathways that activate β-catenin remain undefined, yet have the potential to play a significant role during tumorigenesis. Here, we report that phosphotidylinositol phosphate kinase Iγ (PIPKIγ), an enzyme that generates phosphoinositide messengers in vivo, directly associates with β-catenin and increases β-catenin activity downstream of growth factor stimulation. PIPKIγ expression and kinase activity enhance β-catenin phosphorylation on residues that promote nuclear importation and transcriptional activity. Lastly, we show that β-catenin is required for PIPKIγ-dependent increased cell proliferation. These results reveal a novel mechanism in which PIPKIγ expression and catalytic activity enhance β-catenin nuclear translocation and expression of its target genes to promote tumorigenic phenotypes.
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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.