Src-kinase-dependent epidermal growth factor receptor transactivation in salivary mucin secretion in response to β-adrenergic G-protein-coupled receptor activation

@article{Slomiany2004SrckinasedependentEG,
  title={Src-kinase-dependent epidermal growth factor receptor transactivation in salivary mucin secretion in response to $\beta$-adrenergic G-protein-coupled receptor activation},
  author={Bronislaw L. Slomiany and Amalia Slomiany},
  journal={InflammoPharmacology},
  year={2004},
  volume={12},
  pages={233-245}
}
The principal regulatory factors that control the flow and make-up of salivary secretion are neurotransmitters, released by parasympathetic and sympathetic innervation, that trigger activation of G protein-coupled receptors (GPCRs) on the acinar cells of salivary glands and stimulate the generation of soluble second messengers. In this study, we report that activation of GPCR by β-adrenergic agonist leading to stimulation in salivary mucin secretion occurs with the involvement of epidermal… 

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References

SHOWING 1-10 OF 40 REFERENCES
Gs Protein-coupled Receptor Agonists Induce Transactivation of the Epidermal Growth Factor Receptor in T84 Cells
TLDR
GsPCR agonists rapidly transactivate the EGFr in T84 cells by a signaling pathway involving cAMP and PKA, through a mechanism that likely involves PI3K, which is required for the full expression of cAMP-dependent Cl- secretory responses.
Sensitization of Epidermal Growth Factor-induced Signaling by Bradykinin Is Mediated by c-Src
Communication between receptor tyrosine kinase (RTK)- and G protein-coupled receptor (GPCR)-mediated signaling systems has received increasing attention in recent years. Here, we report that
The β2-Adrenergic Receptor Mediates Extracellular Signal-regulated Kinase Activation via Assembly of a Multi-receptor Complex with the Epidermal Growth Factor Receptor*
TLDR
GPCR activation mimics growth factor-mediated stimulation of the epidermal growth factor receptor (EGFR) with respect to many facets of RTK function, and RTK transactivation is revealed to be a process involving both association of receptors of distinct classes and the interaction of the transactivated RTK with the cells endocytic machinery.
c-Src Is Activated by the Epidermal Growth Factor Receptor in a Pathway That Mediates JNK and ERK Activation by Gonadotropin-releasing Hormone in COS7 Cells*
TLDR
The unique pathway elucidated here in which c-Src and PI3K are sequentially activated downstream of the EGF receptor may serve as a prototype of signaling mechanisms by GnRHR and by additional GPCRs in various cell types.
Distinct Roles for Src Tyrosine Kinase in β2-Adrenergic Receptor Signaling to MAPK and in Receptor Internalization*
TLDR
The data demonstrate that although Src and β-arrestin 2 play essential roles in β2-adrenergic receptor internalization, they are not required for the activation of the mitogen-activated protein kinase (MAPK) pathway by the β2+ receptor.
Src and Pyk2 Mediate G-protein-coupled Receptor Activation of Epidermal Growth Factor Receptor (EGFR) but Are Not Required for Coupling to the Mitogen-activated Protein (MAP) Kinase Signaling Cascade*
TLDR
It is shown that Src kinases are critical for activation of Pyk2 in response to GPCR-stimulation and thatPyk2 and Src are essential for GPCr-induced tyrosine phosphorylation of EGFR, and that Pyk1, Src, and SRC are dispensable for G PCR-induced activation of MAP kinase.
Neurotransmitter Control of Secretion
  • B. Baum
  • Biology
    Journal of dental research
  • 1987
TLDR
It is very well established that the principal control of salivary secretion is derived from autonomic innervation, which provides the intracellular signal for secretory events (protein, fluid, electrolyte secretion) to begin.
Dependence of Peroxisome Proliferator-activated Receptor Ligand-induced Mitogen-activated Protein Kinase Signaling on Epidermal Growth Factor Receptor Transactivation*
TLDR
PPARα and γ ligands activate two distinct signaling cascades in GN4 cells leading to MAPK activation, suggesting a possible role for Pyk2 as an upstream activator of p38.
Role of adrenergic and cholinergic mediators in salivary phospholipids secretion.
...
...