ArticleAmerican journal of physiology. Lung cellular and molecular physiology2011
Filamin A is a phosphorylation target of membrane but not cytosolic adenylyl cyclase activity.
Article in American journal of physiology. Lung cellular and molecular physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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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.
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Who cites it
29 citing papers in PubMed, 39 citations in OpenAlex.
- Development of a Nanoscale Protein-Protein Mapping of PDE4 Interface-Disrupting Peptides.Nano letters · 2026Article
- Article
- Charting the importance of filamin A posttranslational modifications.The Biochemical journal · 2024Review
- Infection promotes Ser-214 phosphorylation important for generation of cytotoxic tau variants.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023Article
- Article
- miR‑351‑5p aggravates lipopolysaccharide‑induced acute lung injury via inhibiting AMPK.Molecular medicine reports · 2021Article
- Review
- Filamin A Regulates Cardiovascular Remodeling.International journal of molecular sciences · 2021Review
- Extracellular vesicles: another compartment for the second messenger, cyclic adenosine monophosphate.American journal of physiology. Lung cellular and molecular physiology · 2019Article
- Spectral imaging of FRET-based sensors reveals sustained cAMP gradients in three spatial dimensions.Cytometry. Part A : the journal of the International Society for Analytical Cytology · 2018Article
- Review
- Concurrent activation of βCellular signalling · 2017Article
- Chemical activation of adenylyl cyclase Rv1625c inhibits growth of Mycobacterium tuberculosis on cholesterol and modulates intramacrophage signaling.Molecular microbiology · 2017Article
- The Pseudomonas aeruginosa Exoenzyme Y: A Promiscuous Nucleotidyl Cyclase Edema Factor and Virulence Determinant.Handbook of experimental pharmacology · 2017Review
- Lipopolysaccharide-induced pulmonary endothelial barrier disruption and lung edema: critical role for bicarbonate stimulation of AC10.American journal of physiology. Lung cellular and molecular physiology · 2015Article
- G protein-coupled receptors directly bind filamin A with high affinity and promote filamin phosphorylation.Biochemistry · 2015Article
- Novel regulators of endothelial barrier function.American journal of physiology. Lung cellular and molecular physiology · 2014Review
- In vitro assays to monitor the activity of Pseudomonas aeruginosa Type III secreted proteins.Methods in molecular biology (Clifton, N.J.) · 2014Article
- HoPaCI-DB: host-Pseudomonas and Coxiella interaction database.Nucleic acids research · 2014Article
- B. anthracis associated cardiovascular dysfunction and shock: the potential contribution of both non-toxin and toxin components.BMC medicine · 2013Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Transmembrane adenylyl cyclase (AC) generates a cAMP pool within the subplasma membrane compartment that strengthens the endothelial cell barrier. This cAMP signal is steered toward effectors that promote junctional integrity and is inactivated before it accesses microtubules, where the cAMP signal causes phosphorylation of tau, leading to microtubule disassembly and barrier disruption. During infection, Pseudomonas aeruginosa uses a type III secretion system to inject a soluble AC, ExoY, into the cytosol of pulmonary microvascular endothelial cells. ExoY generates a cAMP signal that disrupts the endothelial cell barrier. We tested the hypothesis that this ExoY-dependent cAMP signal causes phosphorylation of tau, without inducing phosphorylation of membrane effectors that strengthen endothelial barrier function. To approach this hypothesis, we first discerned the membrane compartment in which endogenous transmembrane AC6 resides. AC6 was resolved in caveolin-rich lipid raft fractions with calcium channel proteins and the cell adhesion molecules N-cadherin, E-cadherin, and activated leukocyte adhesion molecule. VE-cadherin was excluded from the caveolin-rich fractions and was detected in the bulk plasma membrane fractions. The actin binding protein, filamin A, was detected in all membrane fractions. Isoproterenol activation of ACs promoted filamin phosphorylation, whereas thrombin inhibition of AC6 reduced filamin phosphorylation within the membrane fraction. In contrast, ExoY produced a cAMP signal that did not cause filamin phosphorylation yet induced tau phosphorylation. Hence, our data indicate that cAMP signals are strictly compartmentalized; whereas cAMP emanating from transmembrane ACs activates barrier-enhancing targets, such as filamin, cAMP emanating from soluble ACs activates barrier-disrupting targets, such as tau.
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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.