ArticleMolecular and cellular biology1998
A function for phosphatidylinositol 3-kinase beta (p85alpha-p110beta) in fibroblasts during mitogenesis: requirement for insulin- and lysophosphatidic acid-mediated signal transduction.
Article in Molecular and cellular biology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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
37 citing papers in PubMed, 127 citations in OpenAlex.
- The efficacy of PI3Kγ and EGFR inhibitors on the suppression of the characteristics of cancer stem cells.Scientific reports · 2022Article
- PI3Kβ-A Versatile Transducer for GPCR, RTK, and Small GTPase Signaling.Endocrinology · 2019Review
- TGX-221 inhibits proliferation and induces apoptosis in human glioblastoma cells.Oncology reports · 2017Article
- PI3Kδ and PI3Kγ isoforms have distinct functions in regulating pro-tumoural signalling in the multiple myeloma microenvironment.Blood cancer journal · 2017Article
- MiR-30a-5p Overexpression May Overcome EGFR-Inhibitor Resistance through Regulating PI3K/AKT Signaling Pathway in Non-small Cell Lung Cancer Cell Lines.Frontiers in genetics · 2016Article
- Effect of NK4 transduction in bone marrow-derived mesenchymal stem cells on biological characteristics of pancreatic cancer cells.International journal of molecular sciences · 2014Article
- NK4 gene therapy inhibits HGF/Met-induced growth of human cholangiocarcinoma cells.Digestive diseases and sciences · 2013Article
- Signaling via class IA Phosphoinositide 3-kinases (PI3K) in human, breast-derived cell lines.PloS one · 2013Article
- p110δ PI3 kinase pathway: emerging roles in cancer.Frontiers in oncology · 2013Article
- Clinical development of phosphatidylinositol 3-kinase inhibitors for cancer treatment.BMC medicine · 2012Review
- The Biological Role of PI3K Pathway in Lung Cancer.Pharmaceuticals (Basel, Switzerland) · 2012Article
- Targeting the PI3K pathway for cancer therapy.Future medicinal chemistry · 2012Review
- Multi-level targeting of the phosphatidylinositol-3-kinase pathway in non-small cell lung cancer cells.PloS one · 2012Article
- Characterization and targeting of phosphatidylinositol-3 kinase (PI3K) and mammalian target of rapamycin (mTOR) in renal cell cancer.Journal of translational medicine · 2011Article
- Clinical activity of mammalian target of rapamycin inhibitors in solid tumors.Targeted oncology · 2011Review
- Nuclear but not cytosolic phosphoinositide 3-kinase beta has an essential function in cell survival.Molecular and cellular biology · 2011Article
- Synchronization in G0/G1 enhances the mitogenic response of cells overexpressing the human insulin receptor A isoform to insulin.Cell biology and toxicology · 2010Article
- PI3K: from the bench to the clinic and back.Current topics in microbiology and immunology · 2010Review
- Phosphatidylinositol 3-kinase: the oncoprotein.Current topics in microbiology and immunology · 2010Review
- Targeting PI3K signalling in cancer: opportunities, challenges and limitations.Nature reviews. Cancer · 2009Review
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 4 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have previously shown that phosphatidylinositol 3-kinase alpha (PI 3-Kalpha) (p85alpha-p110alpha) is required for DNA synthesis induced by various growth factors (S. Roche, M. Koegl, and S. A. Courtneidge, Proc. Natl. Acad. Sci. USA 91:9185-9189, 1994) in fibroblasts. In the present study, we have investigated the function of PI 3-Kbeta (p85alpha-p110beta) during mitogenesis. By using antibodies specific to p110beta we showed that PI 3-Kbeta is expressed in NIH 3T3 cells. PI 3-Kbeta and PI 3-Kalpha have common features: PI 3-Kbeta is tightly associated with a protein serine kinase that phosphorylates p85alpha, it interacts with the Src-middle T antigen complex and the activated platelet-derived growth factor (PDGF) receptor in fibroblasts in vivo, and it becomes tyrosine phosphorylated after PDGF stimulation. PI 3-Kbeta was also activated in Swiss 3T3 and Cos7 cells stimulated with lysophosphatidic acid (LPA), a mitogen that interacts with a heterotrimeric G protein-coupled receptor. In contrast PI 3-Kalpha was activated to a lesser extent in these cells. Microinjection of neutralizing antibodies specific for p110beta into quiescent fibroblasts inhibited DNA synthesis induced by both insulin and LPA but poorly affected PDGF receptor signaling. Therefore, PI 3-Kbeta plays an important role in transmitting the mitogenic response induced by some, but not all, growth factors. Finally, we show that while oncogenic V12Ras interacts with type I PI 3-Ks, it could induce DNA synthesis in the absence of active PI 3-Kalpha and PI 3-Kbeta, suggesting that Ras uses other effectors for DNA synthesis.
Indexed as
Identifiers
What 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.