ArticleMolecular biology of the cell2006
Phosphoinositide 3-kinase activity controls the chemoattractant-mediated activation and adaptation of adenylyl cyclase.
Article in Molecular biology of the cell, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 44 citations in OpenAlex.
- Atypical PI3Ks coordinate chemotaxis, signaling dynamics, and multicellular development inbioRxiv : the preprint server for biology · 2026Article
- Adenylate cyclase A amplification and functional diversification during Polyspondylium pallidum development.EvoDevo · 2022Article
- Exosomes mediate LTB4 release during neutrophil chemotaxis.PLoS biology · 2021Article
- Ras, PI3K and mTORC2 - three's a crowd?Journal of cell science · 2020Review
- Caffeine inhibits PI3K and mTORC2 in Dictyostelium and differentially affects multiple other cAMP chemoattractant signaling effectors.Molecular and cellular biochemistry · 2019Article
- Mechanisms of Cell Polarization.Current opinion in systems biology · 2017Article
- Adenylyl cyclase mRNA localizes to the posterior of polarized DICTYOSTELIUM cells during chemotaxis.BMC cell biology · 2017Article
- Fold-change detection and scale invariance of cell-cell signaling in social amoeba.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Protein kinase A regulates the Ras, Rap1 and TORC2 pathways in response to the chemoattractant cAMP inJournal of cell science · 2017Article
- Self-organization of chemoattractant waves in Dictyostelium depends on F-actin and cell-substrate adhesion.Journal of the Royal Society, Interface · 2016Article
- Exosomes Mediate LTB4 Release during Neutrophil Chemotaxis.PLoS biology · 2016Article
- From intracellular signaling to population oscillations: bridging size- and time-scales in collective behavior.Molecular systems biology · 2015Article
- Phosphorylation of chemoattractant receptors regulates chemotaxis, actin reorganization and signal relay.Journal of cell science · 2013Article
- The green tea catechin epigallocatechin gallate (EGCG) blocks cell motility, chemotaxis and development in Dictyostelium discoideum.PloS one · 2013Article
- LTB4 is a signal-relay molecule during neutrophil chemotaxis.Developmental cell · 2012Article
- Direct biochemical measurements of signal relay during Dictyostelium development.The Journal of biological chemistry · 2011Article
- Expression of Y53A-actin in Dictyostelium disrupts the cytoskeleton and inhibits intracellular and intercellular chemotactic signaling.The Journal of biological chemistry · 2010Article
- Eukaryotic chemotaxis: a network of signaling pathways controls motility, directional sensing, and polarity.Annual review of biophysics · 2010Review
- Real-time measurements of cAMP production in live Dictyostelium cells.Journal of cell science · 2009Article
- The group migration of Dictyostelium cells is regulated by extracellular chemoattractant degradation.Molecular biology of the cell · 2009Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The binding of chemoattractants to cognate G protein-coupled receptors activates a variety of signaling cascades that provide spatial and temporal cues required for chemotaxis. When subjected to uniform stimulation, these responses are transient, showing an initial peak of activation followed by a period of adaptation, in which activity subsides even in the presence of stimulus. A tightly regulated balance between receptor-mediated stimulatory and inhibitory pathways controls the kinetics of activation and subsequent adaptation. In Dictyostelium, the adenylyl cyclase expressed during aggregation (ACA), which synthesizes the chemoattractant cAMP, is essential to relay the signal to neighboring cells. Here, we report that cells lacking phosphoinositide 3-kinase (PI3K) activity are deficient in signal relay. In LY294002-treated cells, this defect is because of a loss of ACA activation. In contrast, in cells lacking PI3K1 and PI3K2, the signal relay defect is because of a loss of ACA adaptation. We propose that the residual low level of 3-phosphoinositides in pi3k(1-/2-) cells is sufficient to generate the initial peak of ACA activity, yet is insufficient to sustain the inhibitory phase required for its adaptation. Thus, PI3K activity is poised to regulate both ACA activation and adaptation, thereby providing a link to ensure the proper balance of counteracting signals required to maintain optimal chemoresponsiveness.
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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.