ArticleMolecular and cellular biology2005
Role of phosphoinositide 3-kinase regulatory isoforms in development and actin rearrangement.
Article in Molecular and cellular biology, 2005. 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.
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Who cites it
70 citing papers in PubMed, 126 citations in OpenAlex.
- p85β acts as a transcription cofactor and cooperates with BCLAF1 in the nucleus.Nature communications · 2025Article
- Non-catalytic role of phosphoinositide 3-kinase in mesenchymal cell migration through non-canonical induction of p85β/AP2-mediated endocytosis.Nature communications · 2024Article
- Therapeutic Role of Synthetic Lethality inJournal of immunotherapy and precision oncology · 2024Review
- SPECC1L: a cytoskeletal protein that regulates embryonic tissue dynamics.Biochemical Society transactions · 2023Article
- ARID1A-deficient bladder cancer is dependent on PI3K signaling and sensitive to EZH2 and PI3K inhibitors.JCI insight · 2022Article
- Interrelation between α-Cardiac Actin Treadmilling and Myocardin-Related Transcription Factor-A Nuclear Shuttling in Cardiomyocytes.International journal of molecular sciences · 2022Article
- Differential regulation of cranial and cardiac neural crest by serum response factor and its cofactors.eLife · 2022Article
- The Crossroads between RAS and RHO Signaling Pathways in Cellular Transformation, Motility and Contraction.Genes · 2021Review
- Insulin-PI3K signalling: an evolutionarily insulated metabolic driver of cancer.Nature reviews. Endocrinology · 2020Review
- Dysregulated actin dynamics in activated PI3Kδ syndrome.Clinical immunology (Orlando, Fla.) · 2020Article
- Synthesis and Evaluation of Novel 2H-Benzo[e]-[1,2,4]thiadiazine 1,1-Dioxide Derivatives as PI3Kδ Inhibitors.Molecules (Basel, Switzerland) · 2019Article
- MAP kinase and autophagy pathways cooperate to maintain RAS mutant cancer cell survival.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- MAPK and PI3K signaling: At the crossroads of neural crest development.Developmental biology · 2018Review
- Endothelial cell rearrangements during vascular patterning require PI3-kinase-mediated inhibition of actomyosin contractility.Nature communications · 2018Article
- Isoform-specific activities of the regulatory subunits of phosphatidylinositol 3-kinases - potentially novel therapeutic targets.Expert opinion on therapeutic targets · 2018Review
- Phosphoinositide 3-Kinase Is Integral for the Acute Activity of Leptin and Insulin in Male Arcuate NPY/AgRP Neurons.Journal of the Endocrine Society · 2018Article
- A RAB35-p85/PI3K axis controls oscillatory apical protrusions required for efficient chemotactic migration.Nature communications · 2018Article
- The regulation of tumor-suppressive microRNA, miR-126, in chronic lymphocytic leukemia.Cancer medicine · 2017Article
- PDGFRβ regulates craniofacial development through homodimers and functional heterodimers with PDGFRα.Genes & development · 2016Article
- Genetic insights into the mechanisms of Fgf signaling.Genes & development · 2016Review
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
7 authors at 4 institutions in 3 countries.
Funding
Abstract
Class Ia phosphoinositide 3-kinases (PI3Ks) are heterodimers of p110 catalytic and p85 regulatory subunits that mediate a variety of cellular responses to growth and differentiation factors. Although embryonic development is not impaired in mice lacking all isoforms of the p85alpha gene (p85alpha-/- p55alpha-/- p50alpha-/-) or in mice lacking the p85beta gene (p85beta-/-) (D. A. Fruman, F. Mauvais-Jarvis, D. A. Pollard, C. M. Yballe, D. Brazil, R. T. Bronson, C. R. Kahn, and L. C. Cantley, Nat Genet. 26:379-382, 2000; K. Ueki, C. M. Yballe, S. M. Brachmann, D. Vicent, J. M. Watt, C. R. Kahn, and L. C. Cantley, Proc. Natl. Acad. Sci. USA 99:419-424, 2002), we show here that loss of both genes results in lethality at embryonic day 12.5 (E12.5). The phenotypes of these embryos, including subepidermal blebs flanking the neural tube at E8 and bleeding into the blebs during the turning process, are similar to defects observed in platelet-derived growth factor receptor alpha null (PDGFRalpha-/-) mice (P. Soriano, Development 124:2691-2700, 1997), suggesting that PI3K is an essential mediator of PDGFRalpha signaling at this developmental stage. p85alpha-/- p55alpha+/+ p50alpha+/+ p85beta-/- mice had similar but less severe defects, indicating that p85alpha and p85beta have a critical and redundant function in development. Mouse embryo fibroblasts deficient in all p85alpha and p85beta gene products (p85alpha-/- p55alpha-/- p50alpha-/- p85beta-/-) are defective in PDGF-induced membrane ruffling. Overexpression of the Rac-specific GDP-GTP exchange factor Vav2 or reintroduction of p85alpha or p85beta rescues the membrane ruffling defect. Surprisingly, reintroduction of p50alpha also restored PDGF-dependent membrane ruffling. These results indicate that class Ia PI3K is critical for PDGF-dependent actin rearrangement but that the SH3 domain and the Rho/Rac/Cdc42-interacting domain of p85, which lacks p50alpha, are not required for this response.
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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.