A TNF Receptor Family Member, TROY, Is a Coreceptor with Nogo Receptor in Mediating the Inhibitory Activity of Myelin Inhibitors

Park, Jong Bae; Yiu, Glenn; Kaneko, Shinjiro; Wang, Jing; Chang, Juan; He, Xiaolin; García, K. Christopher; He, Zhigang

doi:10.1016/j.neuron.2005.02.015

Cited by 114 publications

(168 citation statements)

References 0 publications

Supporting

Mentioning

159

Contrasting

Unclassified

Order By: Relevance

“…Intratransmembrane domain disulfide bonds, such as are present in p75 NTR , have not been described previously in other TNFR-SF family members, or in any other membrane protein for that matter. Cysteinyl residues are present at equivalent positions in the transmembrane domains of several other TNFR-SF proteins, including NRH and Troy (Bothwell, 2006), which have functions that partially overlap those of p75 NTR (Murray et al, 2004;Park et al, 2005;Shao et al, 2005;Wong et al, 2008) and which signal via association with TRAF6 (Kanning et al, 2003;Kojima et al, 2000), as p75 NTR does. It remains to be determined whether intratransmembrane domain disulfide bond formation is a feature of signaling by NRH2 and Troy.…”

Section: The Neurotrophin Receptors: a Brief Summary Of Signaling Mecmentioning

confidence: 99%

“…The observation that NgR lacks any cytoplasmic domain that might influence RhoA activity, coupled with the demonstration that p75 NTR regulates activity of RhoA (Yamashita et al, 1999), led to the discovery that p75 NTR forms a functional complex with NgR (Wang et al, 2002;Wong et al, 2002). In some neurons, Troy replaces p75 NTR as the signaltransducing NgR co-receptor (Park et al, 2005;Shao et al, 2005). Association of p75 NTR or Troy, and NgR with a third membrane protein, LINGO-1, is required for effective MAIF signaling.…”

Section: P75 Ntr : New Partnersmentioning

confidence: 99%

See 1 more Smart Citation

Neurotrophin receptors: Old friends with new partners

Schecterson

Bothwell

2010

Developmental Neurobiology

105

View full text Add to dashboard Cite

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. '

show abstract

Section: The Neurotrophin Receptors: a Brief Summary Of Signaling Mecmentioning

confidence: 99%

Section: P75 Ntr : New Partnersmentioning

confidence: 99%

Neurotrophin receptors: Old friends with new partners

Schecterson

Bothwell

2010

Developmental Neurobiology

105

View full text Add to dashboard Cite

show abstract

“…This inhibitory protein was later cloned by three independent groups [12][13][14] and is now termed NogoA. The Nogo-66 receptor (NgR1) was subsequently identified [15] and mediates the inhibitory activity of MAG and OMgp in addition to NogoA [16][17][18] in a complex that requires one or more co-receptors, including p75/Lingo-1/Taj [19][20][21][22]. Ligand binding to NgR1 results in RhoA-mediated stimulation of Rho-associated kinase (ROCK) and actinomyosin contractility, which ultimately results in inhibition of neurite outgrowth and growth cone collapse [23].…”

Section: Myelin-associated Inhibitors and Axonal Growthmentioning

confidence: 99%

Axonal growth therapeutics: regeneration or sprouting or plasticity?

Cafferty

McGee

Strittmatter

2008

Trends in Neurosciences

141

108

View full text Add to dashboard Cite

Loss of function after neurological injury frequently occurs through the interruption of axonal connectivity, rather than through cell loss. Functional deficits persist because a multitude of inhibitory factors in degenerating myelin and astroglial scar prevent axonal growth in the adult brain and spinal cord. Given the high clinical significance of achieving functional recovery through axonal growth, substantial research effort has been, and will be, devoted toward this desirable goal. Unfortunately, the labels commonly used in the literature to categorize post-injury axonal anatomy might hinder advancement. In this article, we present an argument for the importance of developing precise terms that describe axonal growth in terms of the inciting event, the distance of axonal extension and the timing of axonal growth. The phenotypes produced by molecular interventions that overcome astroglial scar or myelin-associated inhibitors are reframed and discussed in this context.

show abstract

“…Nogo-66, together with both MAG and OMgp, bind and activate the same receptor, the neuronal, glycosyl-phosphatidyl-inositol (GPI)-anchored Nogo-66 Receptor (NgR; Fournier et al, 2001;Domeniconi et al, 2002;Liu et al, 2002a;Wang et al, 2002a) with additional molecules including p75 NTR , Lingo-1 and TAJ/TROY required for signaling (Mi et al, 2004;Shao et al, 2005;Park et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

Selective temporal and regional alterations of Nogo-A and small proline-rich repeat protein 1A (SPRR1A) but not Nogo-66 receptor (NgR) occur following traumatic brain injury in the rat

Marklund

Fulp

Shimizu

et al. 2006

Experimental Neurology

View full text Add to dashboard Cite

Axons show a poor regenerative capacity following traumatic central nervous system (CNS) injury, partly due to the expression of inhibitors of axonal outgrowth, of which Nogo-A is considered the most important. We evaluated the acute expression of Nogo-A, the Nogo-66 receptor (NgR) and the novel small proline-rich repeat protein 1A (SPRR1A, previously undetected in brain), following experimental lateral fluid percussion (FP) brain injury in rats. Immunofluorescence with antibodies against Nogo-A, NgR and SPRR1A was combined with antibodies against the neuronal markers NeuN and microtubule-associated protein (MAP)-2 and the oligodendrocyte marker RIP, while Western blot analysis was performed for Nogo-A and NgR. Brain injury produced a significant increase in Nogo-A expression in injured cortex, ipsilateral external capsule and reticular thalamus from days 1-7 post-injury (P < 0.05) compared to controls. Increased expression of Nogo-A was observed in both RIP-and NeuN positive (+) cells in the ipsilateral cortex, in NeuN (+) cells in the CA3 region of the hippocampus and reticular thalamus and in RIP (+) cells in white matter tracts. Alterations in NgR expression were not observed following traumatic brain injury (TBI). Brain injury increased the extent of SPRR1A expression in the ipsilateral cortex and the CA3 at all post-injury time-points in NeuN (+) cells. The marked increases in Nogo-A and SPRR1A in several important brain regions suggest that although inhibitors of axonal growth may be upregulated, the injured brain is also capable of expressing proteins promoting axonal outgrowth following TBI. KeywordsNogo-A; Nogo-66 receptor; Small proline-rich repeat protein 1A (SPRR1A); Traumatic brain injury; Oligodendrocytes

show abstract

A TNF Receptor Family Member, TROY, Is a Coreceptor with Nogo Receptor in Mediating the Inhibitory Activity of Myelin Inhibitors

Cited by 114 publications

References 0 publications

Neurotrophin receptors: Old friends with new partners

Neurotrophin receptors: Old friends with new partners

Axonal growth therapeutics: regeneration or sprouting or plasticity?

Selective temporal and regional alterations of Nogo-A and small proline-rich repeat protein 1A (SPRR1A) but not Nogo-66 receptor (NgR) occur following traumatic brain injury in the rat

Contact Info

Product

Resources

About