Activation of muscarinic M4 receptor augments NGF-induced pro-survival Akt signaling in PC12 cells

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

doi:10.1016/j.cellsig.2005.04.009

Cited by 30 publications

(28 citation statements)

References 51 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%

“…Not surprisingly, a diverse range of G i -coupled receptors are capable of regulating tuberin. For example, all three opioid receptor subtypes ( ␦ , , ), ␣ 2 -adrenoceptor, and muscarinic M 4 receptor are capable of inducing the phosphorylation of tuberin in both transfected and native cellular models [29,30,73] . Tuberin is rapidly phosphorylated in response to the G i -coupled receptor agonists.…”

Section: Mechanisms Of Tuberin Regulation By Gpcrsmentioning

confidence: 99%

“…Our recent study showed that co-activation of G icoupled M 4 muscarinic acetylcholine receptor (mAChR) and NGF receptor resulted in augmentation of Akt activity and tuberin phosphorylation in a G ␤ ␥ -and PI3K-dependent manner [30] . There is also evidence that suggests that activated M 4 mAChR is able to work together with NGF receptor to enhance cell survival.…”

Section: Cooperation Between Rtk and Gpcrmentioning

confidence: 99%

“…Apart from demonstrating the role of tuberin in the regulation of cell growth and proliferation, results from several laboratories over the past few years have provided new insights into how tuberin might affect cell survival, cell adhesion, cell morphology, cell migration, neuronal differentiation, regulation of cellular energy, post-Golgi transport, or protein trafficking in the cell [29][30][31][32][33][34][35] . A particularly interesting feature of tuberin is the presence of multiple serine, threonine and tyrosine phosphorylation sites [36,37] , suggesting that the functional activity of tuberin could be potentially regulated by different signaling molecules.…”

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

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%

Section: Mechanisms Of Tuberin Regulation By Gpcrsmentioning

confidence: 99%

Section: Cooperation Between Rtk and Gpcrmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

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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“…Signaling through G i/o -coupled muscarinic acetylcholine receptors appears to cooperate with NGF in activating the PI3K/Akt pathway and promoting neuronal survival [14][15][16]. Treatment of PC12 cells with pertussis toxin (PTX; which inactivates G i/o ) reduced NGF-induced Akt phosphorylation, but has no effect on the Akt response elicited by epidermal growth factor (EGF).…”

Section: The Functions Of G Protein Signaling In Neuronal Differentiamentioning

confidence: 99%

G protein signaling controls the differentiation of multiple cell lineages

Wang¹,

Wong²

2009

BioFactors

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G protein‐coupled receptors (GPCRs) detect a great diversity of extracellular stimuli ranging from hormonal peptides, chemokines, neurotransmitters, lipids, nucleotides, amino acids, biogenic amines to ions. G protein‐coupled pathways regulate a rich collection of biological processes involved in normal physiological function of the body as well as in pathological progression of diseases. In addition to their function in postmitotic steady‐state tissues, GPCRs have been implicated in the differentiation of stem cells and tissue specific progenitor cells during development. Examples of these include the functions of nucleotides and neuropeptides in neuronal differentiation and axon growth, chemokines in lymphocyte differentiation and activation, and other GPCR‐mediated processes in the differentiation of adipocytes, osteoblasts and smooth muscle cells. This review summarizes the recent advances in our understanding of the importance of GPCR‐linked signaling cascades in the differentiation of different cell lineages. © 2009 International Union of Biochemistry and Molecular Biology, Inc.

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Novel perspectives of neural stem cell differentiation: From neurotransmitters to therapeutics

et al. 2008

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In the past years, many reports have described the existence of neural progenitor and stem cells in the adult central nervous system capable of generating new neurons, astrocytes, and oligodendrocytes. This discovery has overturned the central assumption in the neuroscience field, of no new neurons being originated in the brain after birth and provided the fundaments to understand the molecular basis of neural differentiation and to develop new therapies for neural tissue repair. Although the mechanisms underlying cell fate during neural development are not yet understood, the importance of intrinsic and extrinsic factors and of an appropriate microenvironment is well known. In this context, emerging evidence strongly suggests that glial cells play a key role in controlling multiple steps of neurogenesis. Those cells, of particular radial glia, are important for migration, cell specification, and integration of neurons into a functional neural network. This review aims to present an update in the neurogenesis area and highlight the modulation of neural stem cell differentiation by neurotransmitters, growth factors, and their receptors, with possible applications for cell therapy strategies of neurological disorders.

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Activation of muscarinic M4 receptor augments NGF-induced pro-survival Akt signaling in PC12 cells

Cited by 30 publications

References 51 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

G protein signaling controls the differentiation of multiple cell lineages

Novel perspectives of neural stem cell differentiation: From neurotransmitters to therapeutics

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