Activation of δ-, κ-, and μ-opioid receptors induces phosphorylation of tuberin in transfected HEK 293 cells and native cells

Wu, Eddy H.T.; Wong, Yung Hou

doi:10.1016/j.bbrc.2005.06.184

Cited by 14 publications

(10 citation statements)

References 40 publications

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“…Recently, some reports have also demonstrated that two GPCR ligands, adenosine and PACAP, can activate Trk receptor activity to increase the survival of neural cells through stimulation of Akt activity [126][127][128] . However, transactivation of TrkA or EGF receptor is not necessary for the stimulation of tuberin phosphorylation by G i -coupled opioid receptors and M 4 mAChR [30,129] , indicating that different GPCRs may utilize disparate pathways to regulate their downstream effectors in order to carry out their biological functions.…”

Section: Cooperation Between Rtk and Gpcrmentioning

confidence: 99%

Tuberin: A Stimulus-Regulated Tumor Suppressor Protein Controlled by a Diverse Array of Receptor Tyrosine Kinases and G Protein-Coupled Receptors

Wu²,

Wong³

2006

Neurosignals

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Tuberin, a tumor suppressor protein, is involved in various cellular functions including survival, proliferation, and growth. It has emerged as an important effector regulated by receptor tyrosine kinases (RTKs) and G protein-coupled receptors (GPCRs). Regulation of tuberin by RTKs and GPCRs is highly complex and dependent on the type of receptors and their associated signaling molecules. Apart from Akt, the first kinase recognized to phosphorylate and inactivate tuberin upon growth factor stimulation, an increasing number of kinases upstream of tuberin have been identified. Furthermore, recruitment of different scaffolding adaptor components to the activated receptors appears to play an important role in the regulation of tuberin activity. More recently, the differential regulation of tuberin by various G protein family members have also been intensively studied, it appears that G proteins can both facilitate (e.g., G_i/o) as well as inhibit (e.g., G_q) tuberin phosphorylation. In the present review, we attempt to summarize our emerging understandings of the roles of RTKs, GPCRs, and their cross-talk on the regulation of tuberin.

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Section: Cooperation Between Rtk and Gpcrmentioning

confidence: 99%

Tuberin: A Stimulus-Regulated Tumor Suppressor Protein Controlled by a Diverse Array of Receptor Tyrosine Kinases and G Protein-Coupled Receptors

Wu²,

Wong³

2006

Neurosignals

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“…As a class of ligands, opioids bind to receptors (GPCRs) on the cell membrane that are coupled to G proteins (usually Gi/o in the case of opioid receptors; Wettschureck & Offermanns 2005) both inside and outside the nervous system (Wu & Wong 2005). The effect of the activation of opioid receptors is almost uniformly inhibitory and the intracellular mechanisms that mediate the cellular hyperpolarization that causes this inhibition depends on the opening of potassium channels, and inhibition of adenylate cyclases, among other things.…”

Section: Peptides In Cardiorespiratory Regulationmentioning

confidence: 99%

Differential regulation of the central neural cardiorespiratory system by metabotropic neurotransmitters

Pilowsky

Lung

Spirovski

et al. 2009

Phil. Trans. R. Soc. B

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Central neurons in the brainstem and spinal cord are essential for the maintenance of sympathetic tone, the integration of responses to the activation of reflexes and central commands, and the generation of an appropriate respiratory motor output. Here, we will discuss work that aims to understand the role that metabotropic neurotransmitter systems play in central cardiorespiratory mechanisms. It is well known that blockade of glutamatergic, gamma-aminobutyric acidergic and glycinergic pathways causes major or even complete disruption of cardiorespiratory systems, whereas antagonism of other neurotransmitter systems barely affects circulation or ventilation. Despite the lack of an 'all-or-none' role for metabotropic neurotransmitters, they are nevertheless significant in modulating the effects of central command and peripheral adaptive reflexes. Finally, we propose that a likely explanation for the plethora of neurotransmitters and their receptors on cardiorespiratory neurons is to enable differential regulation of outputs in response to reflex inputs, while at the same time maintaining a tonic level of sympathetic activity that supports those organs that significantly autoregulate their blood supply, such as the heart, brain, retina and kidney. Such an explanation of the data now available enables the generation of many new testable hypotheses.

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“…miRNA23b interacts with the MOR1 3Ј-UTR through binding to a K Box motif (Wu et al, 2008). The MOR1 3Ј-UTR is absent from the plasmid DNA sequences in all cell lines that express cloned MOR, such as N2A-MOR and HEK-MOR Wu and Wong, 2005). N2A cells are not known to express any opioid receptors (Im et al, 2001); N2A-MOR cells were established by stably transfecting MOR1 into N2A cells.…”

mentioning

confidence: 99%

Long-Term Morphine Treatment Decreases the Association of μ-Opioid Receptor (MOR1) mRNA with Polysomes through miRNA23b

Zhang²,

Law³

et al. 2009

Mol Pharmacol

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ABSTRACT-Opioid receptor (MOR) mediates most of the pharmacological effects of opioid drugs. The expression of MOR is temporarily and spatially regulated at both the transcriptional and post-transcriptional levels. Long-term morphine treatment that induces tolerance does not alter MOR mRNA expression, suggesting no direct link between agonist treatment and MOR gene transcription. We previously identified the 3Ј-untranslated region (3Ј-UTR) of the major transcript of -opioid receptor (MOR1) and revealed a novel trans-acting factor, miRNA23b, that binds to the K box motif in the 3Ј-UTR. The interaction between miRNA23b with the MOR1 3Ј-UTR suppressed receptor translation by inhibiting polysome-mRNA association. In this report, we demonstrate that long-term morphine treatment increases miRNA23b expression in a dose-and time-dependent manner and represses the association of MOR1 mRNA with polysomes through the MOR1 3Ј-UTR. The translational luciferase reporter assay shows a suppression effect of morphine on reporter activity that requires the MOR1 3Ј-UTR. This suggests a potential link between MOR expression and morphine treatment at the post-transcriptional level in which a specific miRNA, miRNA23b, is involved.

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Activation of δ-, κ-, and μ-opioid receptors induces phosphorylation of tuberin in transfected HEK 293 cells and native cells

Cited by 14 publications

References 40 publications

Tuberin: A Stimulus-Regulated Tumor Suppressor Protein Controlled by a Diverse Array of Receptor Tyrosine Kinases and G Protein-Coupled Receptors

Tuberin: A Stimulus-Regulated Tumor Suppressor Protein Controlled by a Diverse Array of Receptor Tyrosine Kinases and G Protein-Coupled Receptors

Differential regulation of the central neural cardiorespiratory system by metabotropic neurotransmitters

Long-Term Morphine Treatment Decreases the Association of μ-Opioid Receptor (MOR1) mRNA with Polysomes through miRNA23b

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