Transactivation of Trk Neurotrophin Receptors by G-Protein-Coupled Receptor Ligands Occurs on Intracellular Membranes

Rajagopal, Rithwick; Chen, Zhe-Yu; Lee, Francis S.; Chao, Moses V.

doi:10.1523/jneurosci.0010-04.2004

Cited by 233 publications

(185 citation statements)

References 52 publications

(75 reference statements)

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“…Trk tyrosine kinase could be clearly detected in K562, Meg-01 and HMC-1 by western blotting ( Figure 1a). As the activated TrkA is found predominantly in intracellular membranes in some systems (Rajagopal et al, 2004), we next examined the cell surface expression of TrkA in leukemia cells by labeling the cell surface expressing TrkA with biotin. As shown in Figure 1b, TrkA was detected on the cell surface in K562 cells.…”

Section: Resultsmentioning

confidence: 99%

Inhibition of Abl tyrosine kinase enhances nerve growth factor-mediated signaling in Bcr–Abl transformed cells via the alteration of signaling complex and the receptor turnover

et al. 2008

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Section: Resultsmentioning

confidence: 99%

Inhibition of Abl tyrosine kinase enhances nerve growth factor-mediated signaling in Bcr–Abl transformed cells via the alteration of signaling complex and the receptor turnover

et al. 2008

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“…GPCRdependent Trk transactivation differs from neurotrophin-dependent Trk activation in one important respect. Neurotrophins necessarily activate Trk receptors residing in the plasma membrane, whereas GPCR signaling causes activation of Trk proteins that may initiate before they exit the Golgi apparatus, and this activation may actually impede subsequent trafficking of Trk protein to the plasma membrane (Rajagopal et al, 2004). On immunoblots, Trk proteins generally can be resolved into two distinct bands.…”

Section: Trk Receptors: Not Just For Neurotrophinsmentioning

confidence: 99%

Neurotrophin receptors: Old friends with new partners

Schecterson

Bothwell

2010

Developmental Neurobiology

112

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ABSTRACT:Neurotrophins are important regulators of embryonic development and adult function of most populations of neurons in vertebrate nervous systems. This signaling system regulates many diverse activities, including survival, axon outgrowth, and synaptic plasticity. In mammals, neurotrophin action is mediated by four receptors, p75 NTR , TrkA, TrkB, and TrkC. Although early studies viewed these receptors as solitary agents in the cells outer membrane, recent discoveries reveal that the cell outer membrane is a crowded and highly interactive neighborhood. Neurotrophin receptors partner with a diverse array of membrane proteins, dramatically expanding their functional repertoire. This review will focus on some of the most recent discoveries concerning the promiscuous partnering of neurotrophin receptors. '

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“…Ligand binding to G-protein-coupled receptors (GPCRs) can lead to transactivation of Trk and other growth factor receptors (Rajagopal et al 2004). Since phospho ERK1/2 is a well-defined downstream effector of TrkA (Kaplan and Stephens 1994;Sofroniew et al 2001), it is possible that the FIG. 2.…”

Section: Mechanism Of Lhrh-induced Increase Of I Camentioning

confidence: 99%

“…This provides additional evidence against a role for transactivation of growth factor receptors in the action of LHRH. There is good evidence, however, for the operation of this mechanism for other G-proteincoupled receptors in other systems (Rajagopal et al 2004). Finally, the ability of LHRH and NGF to activate ras rather than rap-1 suggests that the former is involved in gonadotropin actions to increase Ca 2ϩ current (Figs.…”

Section: Role Of Ras-mapk In the Lhrh-induced Increase In I Camentioning

confidence: 99%

Differential Neurotrophic Regulation of Sodium and Calcium Channels in an Adult Sympathetic Neuron

Ford

Wong

et al. 2008

Journal of Neurophysiology

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Ford CP, Wong KV, Lu VB, Posse de Chaves E, Smith PA. Differential neurotrophic regulation of sodium and calcium channels in an adult sympathetic neuron. J Neurophysiol 99: 1319 -1332, 2008. First published January 23, 2008 doi:10.1152/jn.00966.2007. Adult neuronal phenotype is maintained, at least in part, by the sensitivity of individual neurons to a specific selection of neurotrophic factors and the availability of such factors in the neurons' environment. Nerve growth factor (NGF) increases the functional expression of Na ϩ channel currents (I Na ) and both N-and L-type Ca 2ϩ currents (I Ca,N and I Ca,L ) in adult bullfrog sympathetic ganglion (BFSG) B-neurons. The effects of NGF on I Ca involve the mitogen-activated protein kinase (MAPK) pathway. Prolonged exposure to the ganglionic neurotransmitter luteinizing hormone releasing hormone (LHRH) also increases I Ca,N but the transduction mechanism remains to be elucidated as does the transduction mechanism for NGF regulation of Na ϩ channels. We therefore exposed cultured BFSG B-neurons to chicken II LHRH (0.45 M; 6 -9 days) or to NGF (200 ng/ml; 9 -10 days) and used whole cell recording, immunoblot analysis, and ras or rap-1 pulldown assays to study effects of various inhibitors and activators of transduction pathways. We found that 1) LHRH signals via ras-MAPK to increase I Ca,N , 2) this effect is mediated via protein kinase C-␤ (PKC-␤-⌱⌱), 3) protein kinase A (PKA) is necessary but not sufficient to effect transduction, 4) NGF signals via phosphatidylinositol 3-kinase (PI3K) to increase I Na , and 5) long-term exposure to LHRH fails to affect I Na . Thus downstream signaling from LHRH has access to the ras-MAPK pathway but not to the PI3K pathway. This allows for differential retrograde and anterograde neurotrophic regulation of sodium and calcium channels in an adult sympathetic neuron.

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Transactivation of Trk Neurotrophin Receptors by G-Protein-Coupled Receptor Ligands Occurs on Intracellular Membranes

Cited by 233 publications

References 52 publications

Inhibition of Abl tyrosine kinase enhances nerve growth factor-mediated signaling in Bcr–Abl transformed cells via the alteration of signaling complex and the receptor turnover

Inhibition of Abl tyrosine kinase enhances nerve growth factor-mediated signaling in Bcr–Abl transformed cells via the alteration of signaling complex and the receptor turnover

Neurotrophin receptors: Old friends with new partners

Differential Neurotrophic Regulation of Sodium and Calcium Channels in an Adult Sympathetic Neuron

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