Inhibition of inositol 1,4,5-trisphosphate-induced Ca
            <sup>2+</sup>
            release by cAMP-dependent protein kinase in a living cell

Tertyshnikova, Svetlana; Fein, Alan M.

doi:10.1073/pnas.95.4.1613

Cited by 91 publications

(66 citation statements)

References 55 publications

(56 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Opening of IP3R-operated stores and activation of TRPC1 and voltage-gated channels result in an increase of Ca 2+ spike activity. Activated Smo also inhibits PKA, which can inhibit IP3-induced Ca 2+ release (43). Hence, modulation of Ca 2+ spike activity may occur by pathways that are parallel or convergent to the one operated by PLC.…”

Section: Discussionmentioning

confidence: 99%

Sonic hedgehog signaling is decoded by calcium spike activity in the developing spinal cord

Belgacem

Borodinsky

2011

Proc. Natl. Acad. Sci. U.S.A.

138

199

View full text Add to dashboard Cite

Evolutionarily conserved hedgehog proteins orchestrate the patterning of embryonic tissues, and dysfunctions in their signaling can lead to tumorigenesis. In vertebrates, Sonic hedgehog (Shh) is essential for nervous system development, but the mechanisms underlying its action remain unclear. Early electrical activity is another developmental cue important for proliferation, migration, and differentiation of neurons. Here we demonstrate the interplay between Shh signaling and Ca 2+ dynamics in the developing spinal cord. Ca 2+ imaging of embryonic spinal cells shows that Shh acutely increases Ca 2+ spike activity through activation of the Shh coreceptor Smoothened (Smo) in neurons. Smo recruits a heterotrimeric GTP-binding protein-dependent pathway and engages both intracellular Ca 2+ stores and Ca 2+ influx. The dynamics of this signaling are manifested in synchronous Ca 2+ spikes and inositol triphosphate transients apparent at the neuronal primary cilium. Interaction of Shh and electrical activity modulates neurotransmitter phenotype expression in spinal neurons. These results indicate that electrical activity and second-messenger signaling mediate Shh action in embryonic spinal neurons.

show abstract

Section: Discussionmentioning

confidence: 99%

Sonic hedgehog signaling is decoded by calcium spike activity in the developing spinal cord

Belgacem

Borodinsky

2011

Proc. Natl. Acad. Sci. U.S.A.

138

199

View full text Add to dashboard Cite

show abstract

“…Consistent with this effect, a number of studies have found that the inositol 1,4,5-trisphosphate (IP 3 ) receptor (IP 3 R) is phosphorylated by PKA, apparently resulting in reduced Ca 2+ release from the endoplasmic reticulum (ER) in response to IP 3 [121,122]. It is now known that there are at least three types of IP 3 R and that, in ASM, cAMP and cGMP both promote the PKG-dependent phosphorylation at Ser 1755 of the type 1 IP 3 R that predominates in this tissue [123].…”

Section: Modulation Of Cytosolic Free Calcium Concentrationmentioning

confidence: 87%

Beyond the dogma: novel 2-adrenoceptor signalling in the airways

Giembycz

Newton²

2006

European Respiratory Journal

131

118

View full text Add to dashboard Cite

b 2 -Adrenoceptor agonists evoke rapid bronchodilatation and are the mainstay of the treatment of asthma symptoms worldwide. The mechanism of action of this class of compounds is believed to involve the stimulation of adenylyl cyclase and subsequent activation of the cyclic adenosine monosphosphate (cAMP)/cAMP-dependent protein kinase cascade.This classical model of b 2 -adrenoceptor-mediated signal transduction is deeply entrenched, but there is compelling evidence that agonism of b 2 -adrenoceptors can lead to the activation of multiple effector pathways, which now compels researchers in academia and the pharmaceutical industry alike to think beyond the traditional dogma. Therefore, the regulation by b 2 -adrenoceptor agonists of responses, including airways smooth muscle tone and the secretory capacity of the epithelium and pro-inflammatory/immune cells, may be highly complex, involving both cAMPdependent and -independent mechanisms that, in many cases, may act in concert.In this article, the current status of b 2 -adrenoceptor-mediated signalling in the airways is reviewed in the context of understanding mechanisms that may underlie both the beneficial and detrimental effects of these drugs in asthma symptom management.

show abstract

“…This indicates that the distinctive calcium response in MRL T cells upon CD3 engagement is not due to fuller stores or increased influx from the extracellular space following store depletion, but rather a result of prolonged activation of the InsP 3 receptor. Certain mechanisms have already been suggested to explain this early signaling defect in a variety of cell types, such as mitochondrial hyperpolarization with deficient calcium sequestration from the cytosol (61) or loss of protein kinase A I-mediated phospholipase C␥1 down-regulation with an increase in InsP 3 (62)(63)(64). The latter seems less plausible as a mechanism in MRL mice, as a similar percentage of T cells responded to anti-CD3 stimulation, which indicates that InsP 3 production is comparable.…”

Section: Discussionmentioning

confidence: 99%

Naive CD4+ T Cells from Lupus-Prone Fas-Intact MRL Mice Display TCR-Mediated Hyperproliferation Due to Intrinsic Threshold Defects in Activation

Zielinski

Jacob

Bouzahzah

et al. 2005

The Journal of Immunology

View full text Add to dashboard Cite

Autoreactive T cell activation is a consistent feature of murine lupus; however, the mechanism of such activation remains unclear. We hypothesized that naive CD4+ T cells in lupus have a lower threshold of activation through their TCR-CD3 complex that renders them more susceptible to stimulation with self-Ags. To test this hypothesis, we compared proliferation, IL-2 production, and single cell calcium signaling of naive CD4+ T cells isolated from Fas-intact MRL/+Fas-lpr mice with H-2k-matched B10.BR and CBA/CaJ controls, following anti-CD3 stimulation in the presence or absence of anti-CD28. We also assessed the responsiveness of naive CD4+ T cells isolated from Fas-intact MRL and control mice bearing a rearranged TCR specific for amino acids 88–104 of pigeon cytochrome c to cognate and low affinity peptide Ags presented by bone marrow-matured dendritic cells. TCR transgenic and wild-type CD4+ T cells from MRL mice displayed a lower threshold of activation than control cells, a response that was class II MHC dependent. The rise in intracellular calcium in MRL vs controls was enhanced and prolonged following anti-CD3 triggering, suggestive of proximal defects in TCR-engendered signaling as the mechanism for the observed hyperactivity. These findings were observed as early as 1–2 mo postweaning and, based on analysis of F1 T cells, appeared to be dominantly expressed. This genetically altered threshold for activation of MRL T cells, a consequence of a proximal defect in CD3-mediated signal transduction, may contribute to the abrogation of T cell tolerance to self-Ags in lupus.

show abstract

Inhibition of inositol 1,4,5-trisphosphate-induced Ca ²⁺ release by cAMP-dependent protein kinase in a living cell

Cited by 91 publications

References 55 publications

Sonic hedgehog signaling is decoded by calcium spike activity in the developing spinal cord

Sonic hedgehog signaling is decoded by calcium spike activity in the developing spinal cord

Beyond the dogma: novel 2-adrenoceptor signalling in the airways

Naive CD4+ T Cells from Lupus-Prone Fas-Intact MRL Mice Display TCR-Mediated Hyperproliferation Due to Intrinsic Threshold Defects in Activation

Contact Info

Product

Resources

About

Inhibition of inositol 1,4,5-trisphosphate-induced Ca 2+ release by cAMP-dependent protein kinase in a living cell

Cited by 91 publications

References 55 publications

Sonic hedgehog signaling is decoded by calcium spike activity in the developing spinal cord

Sonic hedgehog signaling is decoded by calcium spike activity in the developing spinal cord

Beyond the dogma: novel 2-adrenoceptor signalling in the airways

Naive CD4+ T Cells from Lupus-Prone Fas-Intact MRL Mice Display TCR-Mediated Hyperproliferation Due to Intrinsic Threshold Defects in Activation

Contact Info

Product

Resources

About

Inhibition of inositol 1,4,5-trisphosphate-induced Ca ²⁺ release by cAMP-dependent protein kinase in a living cell