ArticleMolecular biology of the cell2011
Disruption of PKB signaling restores polarity to cells lacking tumor suppressor PTEN.
Article in Molecular biology of the cell, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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
32 citing papers in PubMed, 47 citations in OpenAlex.
- GCL pruning of PIP3 establishes the soma-germline boundary.The Journal of cell biology · 2026Article
- Two endogenousProceedings of the National Academy of Sciences of the United States of America · 2025Article
- A chemorepellent inhibits local Ras activation to inhibit pseudopod formation to bias cell movement away from the chemorepellent.Molecular biology of the cell · 2022Article
- Article
- Review
- From environmental sensing to developmental control: cognitive evolution in dictyostelid social amoebas.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2021Article
- Phytocannabinoid-dependent mTORC1 regulation is dependent upon inositol polyphosphate multikinase activity.British journal of pharmacology · 2021Article
- DNAzymes, Novel Therapeutic Agents in Cancer Therapy: A Review of Concepts to Applications.Journal of nucleic acids · 2021Review
- Phosphorylated Rho-GDP directly activates mTORC2 kinase towards AKT through dimerization with Ras-GTP to regulate cell migration.Nature cell biology · 2019Article
- The Atypical MAP Kinase ErkB Transmits Distinct Chemotactic Signals through a Core Signaling Module.Developmental cell · 2019Article
- Akt and SGK protein kinases are required for efficient feeding by macropinocytosis.Journal of cell science · 2019Article
- An endogenous chemorepellent directs cell movement by inhibiting pseudopods at one side of cells.Molecular biology of the cell · 2019Article
- The excitable signal transduction networks: movers and shapers of eukaryotic cell migration.The International journal of developmental biology · 2019Review
- Shear force-based genetic screen reveals negative regulators of cell adhesion and protrusive activity.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Signaling networks that regulate cell migration.Cold Spring Harbor perspectives in biology · 2015Review
- Genetic control of morphogenesis in Dictyostelium.Developmental biology · 2015Review
- A large-scale screen reveals genes that mediate electrotaxis in Dictyostelium discoideum.Science signaling · 2015Article
- The Dictyostelium prestalk inducer differentiation-inducing factor-1 (DIF-1) triggers unexpectedly complex global phosphorylation changes.Molecular biology of the cell · 2015Article
- The role of phosphoinositide-regulated actin reorganization in chemotaxis and cell migration.British journal of pharmacology · 2014Review
- Moving towards a paradigm: common mechanisms of chemotactic signaling in Dictyostelium and mammalian leukocytes.Cellular and molecular life sciences : CMLS · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
By limiting phosphotidylinositol 3,4,5-triphosphate (PIP(3)) levels, tumor suppressor PTEN not only controls cell growth but also maintains cell polarity required for cytokinesis and chemotaxis. To identify the critical targets of PIP(3) that link it to the cytoskeleton, we deleted secondary genes to reverse the deficiencies of pten- cells in Dictyostelium. The polarity defects in pten- cells correlate with elevated phosphorylations of PKB substrates. Deletion of AKT orthologue, PkbA, or a subunit of its activator TORC2, reduced the phosphorylations and suppressed the cytokinesis and chemotaxis defects in pten- cells. In these double mutants, the excessive PIP(3) levels and, presumably, activation of other PIP(3)-binding proteins had little or no effect on the cytoskeleton. In bands with increased phosphorylation in pten- cells, we found PKB substrates, PI5K, GefS, GacG, and PakA. Disruption of PakA in pten- cells restored a large fraction of the cells to normal behavior. Consistently, expression of phosphomimetic PakA in pten- cells exacerbated the defects but nonphosphorylatable PakA had no effect. Thus, among many putative PTEN- and PIP(3)-dependent events, phosphorylation of PKB substrates is the key downstream regulator of cell polarity.
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.