| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.59737144 |
| These results suggest that Nogo A expressed on oligodendrocytes might interact with NgR presented by reactive astrocytes and microglia / macrophages in active demyelinating lesions of MS , although biologic effects caused by Nogo A / NgR interaction among glial cells remain unknown . . 0.59737144^^^ |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.87700937 |
| Fusion of the two NgR binding Nogo A domains creates a ligand with substantially enhanced affinity for NgR and converts a NgR antagonist peptide to an agonist . 0.87700937^^^ |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.72802369 |
| Several residues defining the structural epitope of NgR involved in interaction with Nogo were subsequently confirmed by alanine scanning mutagenesis . . 0.72802369^^^ |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| Nogo 66 , a portion of NogoA , binds to Nogo 66 receptor ( NgR ) and induces the inhibitory signaling . ^^^ |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| Nogo binds to a receptor complex that consists of Nogo receptor ( NgR ) , p75NTR , and Lingo 1 . ^^^ |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| Myelin inhibitory ligands of the Nogo 66 receptor ( NgR 1 ) limit axon regeneration in the adult CNS . ^^^ |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| Nogo domains and a Nogo receptor : implications for axon regeneration . ^^^ |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| The DNA regions identified contained MEL 1 , CACNA1H , and Nogo receptor genes . ^^^ |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| Targeting the Nogo receptor to treat central nervous system injuries . ^^^ |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| The 66 amino acid extracellular domain of Nogo ( Nogo 66 ) interacts with a high affinity receptor ( NgR ) , a glycosylphosphatidylinositol ( GPI ) linked protein with multiple leucine rich repeats . ^^^ Nogo 66 , on the other hand , specifically retards neurite outgrowth and induces growth cone collapse , possibly through its interaction with NgR and as yet unidentified transmembrane coreceptors . ^^^ |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| Because cytokines and neurotrophic factors play a key role in inflammation related axonal regeneration , we investigated : ( 1 ) the constitutive expression of Nogo and the Nogo receptor ( NgR ) mRNA in human neural cell lines ; ( 2 ) Nogo and NgR mRNA levels in the NTera 2 human teratocarcinoma cell line during retinoic acid ( RA ) induced neuronal differentiation ; and ( 3 ) their regulation in NTera 2 derived differentiated neurones ( NTera 2 N ) after exposure to a battery of cytokines and growth factors potentially produced by activated glial cells at post traumatic inflammatory lesions in the CNS . ^^^ By reverse transcriptase polymerase chain reaction analysis , the constitutive expression of Nogo A , the longest isoform of three distinct Nogo transcripts and NgR mRNA was identified in a wide variety of human neural and non neural cell lines . ^^^ In contrast , Nogo A , Nogo B , NgR and GAP 43 mRNA levels were unaltered in NTera 2 N cells by exposure to basic fibroblast growth factor , brain derived neurotrophic factor , glia derived neurotrophic factor , tumour necrosis factor alpha , interleukin 1beta , dibutyryl cyclic AMP or phorbol 12 myristate 13 acetate . ^^^ These results indicate that both Nogo A and NgR mRNA are coexpressed in various human cell types , including differentiated neurones , where their expression is unaffected by exposure to a panel of cytokines and neurotrophic factors which might be involved in inflammation related axonal regeneration in the CNS . . ^^^ |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| A 66 residue domain of Nogo ( Nogo 66 ) is expressed on the surface of oligodendrocytes and can inhibit axonal outgrowth through an axonal Nogo 66 receptor ( NgR ) . ^^^ The IN 1 monoclonal antibody recognizes Nogo A and promotes corticospinal tract regeneration and locomotor recovery ; however , the undefined nature of the IN 1 epitope in Nogo , the limited specificity of IN 1 for Nogo , and nonspecific anti myelin effects have prevented a firm conclusion about the role of Nogo 66 or NgR . ^^^ Here , we identify competitive antagonists of NgR derived from amino terminal peptide fragments of Nogo 66 . ^^^ The Nogo 66 ( 1 40 ) antagonist peptide ( NEP 1 40 ) blocks Nogo 66 or CNS myelin inhibition of axonal outgrowth in vitro , demonstrating that NgR mediates a significant portion of axonal outgrowth inhibition by myelin . ^^^ Thus , Nogo 66 and NgR have central roles in limiting axonal regeneration after CNS injury , and NEP 1 40 provides a potential therapeutic agent . . ^^^ |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| To further elucidate the mechanisms that mediate this inhibitory activity of OMgp , we screened an expression library and identified the Nogo receptor ( NgR ) as a high affinity OMgp binding protein . ^^^ |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| An interaction of Nogo on the oligodendrocyte surface with Nogo 66 Receptor ( NgR ) on axons has been suggested to play an important role in limiting axonal growth . ^^^ The NgR protein is detected selectively in neurons and is present throughout axons , indicating that Nogo A and its receptor are juxtaposed along the course of myelinated fibers . ^^^ In contrast , Nogo A is observed in myelinating oligodendrocytes , embryonic muscle , and neurons , suggesting that Nogo A has additional physiologic roles unrelated to NgR binding . ^^^ After spinal cord injury , Nogo A is upregulated to a moderate degree , whereas NgR levels are maintained at constant levels . ^^^ Taken together , these data confirm the apposition of Nogo ligand and NgR receptor in situations of limited axonal regeneration and support the hypothesis that this system regulates CNS axonal plasticity and recovery from injury . . ^^^ |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| While a GPI linked receptor for Nogo ( NgR ) has been identified , MAG ' s receptor is unknown . ^^^ Also , MAG and Nogo 66 compete for binding to NgR . ^^^ |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| The receptor for Nogo ( NgR ) has been identified as an axonal glycosyl phosphatidyl inositol ( GPI ) anchored protein , whereas the MAG receptor has remained elusive . ^^^ MAG and Nogo 66 activate NgR independently and serve as redundant NgR ligands that may limit axonal regeneration after CNS injury . . ^^^ |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| The expression of mRNA for Nogo 66 receptor ( NgR ) in unoperated adult rats and mice , and rats with nerve grafts placed in the thalamus and cerebellum to stimulate axonal regeneration , was investigated by in situ hybridization . ^^^ Thus NgR expression was not correlated with the ability of neurons to regenerate axons into nerve grafts although Nogo 66 was strongly upregulated by some cells in the distal stumps of injured sciatic nerves . ^^^ |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| An understanding of the mechanism of Nogo signaling through its receptor ( NgR ) is critical to developing strategies for overcoming Nogo mediated inhibition . ^^^ Analysis of alkaline phosphatase ( AP ) Nogo binding in COS 7 cells reveals that the leucine rich repeat domain is necessary and sufficient for Nogo binding and NgR multimerization . ^^^ The NgR glycosylphosphatidylinositol domain is not essential for inhibitory signaling but may facilitate Nogo responses . ^^^ |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| Recent findings indicate that three distinct myelin proteins , myelin associated glycoprotein ( MAG ) , Nogo , and oligodendrocyte myelin glycoprotein ( OMgp ) , inhibit axon growth by binding a common receptor , the Nogo 66 receptor ( NgR ) , and likely converge on a common signaling cascade . . ^^^ |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| In inhibiting neurite outgrowth , several myelin components , including the extracellular domain of Nogo A ( Nogo 66 ) , oligodendrocyte myelin glycoprotein ( OMgp ) and myelin associated glycoprotein ( MAG ) , exert their effects through the same Nogo receptor ( NgR ) . ^^^ |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| Myelin associated glycoprotein ( MAG ) , an inhibitor of axon regeneration , binds with high affinity to the Nogo 66 receptor ( NgR ) . ^^^ |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| The three axon growth inhibitory proteins , myelin associated glycoprotein , oligodendrocyte myelin glycoprotein and Nogo A , can all bind to the Nogo 66 receptor ( NgR ) . ^^^ Strong , rapid and transient downregulation of NgR mRNA in response to kainic acid and after wheel running in cortex and hippocampus suggests a role for NgR and Nogo A in plasticity , learning and memory . . ^^^ |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| Central to our current understanding of myelin mediated inhibition are the membrane protein Nogo and the Nogo 66 receptor ( NgR ) . ^^^ |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| Nogo 66 receptor ( NgR ) has recently been identified as the neuronal receptor of the myelin associated proteins Nogo A , oligodendrocyte protein ( OMgp ) and myelin associated glycoprotein ( MAG ) , and mediates inhibition of axonal regeneration both in vitro and in vivo . ^^^ |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| Recent studies suggest that an axon surface protein , the Nogo receptor ( NgR ) , may play a role in this process through an unprecedented degree of crossreactivity with myelin associated inhibitory ligands . ^^^ |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| The myelin derived axon outgrowth inhibitors Nogo , oligodendrocyte myelin glycoprotein , and myelin associated glycoprotein , all bind to an axonal Nogo 66 receptor ( NgR ) and at least partially account for this lack of CNS repair . ^^^ Subcutaneous treatment with the NgR antagonist peptide NEP 1 40 ( Nogo extracellular peptide , residues 1 40 ) results in extensive growth of corticospinal axons , sprouting of serotonergic fibers , upregulation of axonal growth protein SPRR1A ( small proline rich repeat protein 1A ) , and synapse re formation . ^^^ |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| Although Nogo , MAG and OMgp lack sequence homologies , they all bind to the Nogo receptor ( NgR ) , a GPI linked cell surface molecule which , in turn , binds p 75 to activate RhoA . ^^^ Some neurons , such as DRG cells , respond to Nogo and CNS myelin in vitro although they express little or no NgR in vivo which , with other data , indicates that other receptors are available for NgR ligands . ^^^ It is not clear whether antibodies against Nogo act on oligodendrocytes / myelin or by binding to neuronal Nogo , or whether they can stimulate regeneration of ascending axons in the spinal cord , most of which express little or no NgR . ^^^ |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| These cell surface proteins signal through multi subunit neuronal receptors that contain a common ligand binding glycosylphosphatidylinositol anchored subunit termed the Nogo 66 receptor ( NgR ) . ^^^ By deletion analysis , we show that the binding of soluble fragments of Nogo , MAG and NgR to cell surface NgR requires the entire leucine rich repeat ( LRR ) region of NgR , but not other portions of the protein . ^^^ Despite sharing extensive sequence similarity with NgR , two related proteins , NgR 2 and NgR 3 , which we have identified , do not bind Nogo , MAG , OMgp or NgR . ^^^ |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| Unlike oligodendrocytes , OECs expressed Nogo 66 receptor ( NgR ) mRNA . ^^^ Implanted OECs upregulated Nogo A and B , but downregulated Nogo ABC and NgR . . ^^^ |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| Currently only the Nogo receptor ( NgR ) , in complex with p 75 ( NTR ) neurotrophin receptor is known to be involved in this inhibitory signalling in neurons . ^^^ NgR is a common receptor for the three inhibitory myelin proteins Nogo A , OMgp , and MAG . ^^^ Here we describe two novel Nogo receptor gene homologs named NGRL 2 and NGRL 3 from human and mouse that , like NGR , encode putative leucine rich repeat containing GPI anchored proteins . ^^^ |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| Using this `` sensitized background , ' ' we investigated the effects of either increasing the expression or suppressing the activity of the Nogo receptor ( NgR ) . ^^^ NgR mediates the growth inhibiting effects of three myelin proteins , Nogo , OMgp ( oligodendrocyte myelin glycoprotein ) , and MAG ( myelin associated glycoprotein ) . ^^^ |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| Recent studies have shown that in vivo applications of Nogo neutralizing antibodies , peptides blocking the Nogo receptor subunit NgR , or blockers of the postreceptor components Rho A and ROCK induce long distance axonal regeneration and compensatory sprouting , accompanied by an impressive enhancement of functional recovery , in the rat and mouse spinal cord . . ^^^ |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| In vitro experiments demonstrated the participation of OMgp in growth cone collapse and inhibition of neurite outgrowth through its interaction with NgR , the receptor for Nogo . ^^^ |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| We show that Nogo A and the Nogo receptor ( NgR ) are developmentally regulated both in chick and human embryos , are first detected at developmental stages when the chick spinal cord regenerates , and are not down regulated after injury at permissive stages for regeneration . ^^^ Therefore , expression of Nogo A and NgR in pre E 13 chick spinal cords is not sufficient to inhibit regeneration . ^^^ Nogo A expression in the chick early embryo is primarily observed in axons , whereas NgR is mainly located on neuronal cell bodies , both in spinal cord and eye , and in striated muscle including the heart . ^^^ The distinctive and complementary patterns of Nogo A and NgR expression and their conservation throughout evolution support the view that Nogo signaling represents a key pathway in nervous system and striated muscle development . ^^^ |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| The central nervous system myelin components oligodendrocyte myelin glycoprotein , myelin associated glycoprotein and the Nogo 66 domain of Nogo A inhibit neurite outgrowth by binding the neuronal glycosyl phosphatidylinositol anchored Nogo 66 receptor ( NgR ) that transduces the inhibitory signal to the cell interior via a transmembrane co receptor , p75NTR . ^^^ |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| Membrane proteins such as sortilin , a member of the Vps10p family of sorting receptors , and the glycosylphosphatidylinositol linked Nogo receptor ( NgR ) and the associated adaptor lingo 1 have recently been added to the list of p 75 interacting modulators . ^^^ |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| Versican V 2 and the central inhibitory domain of Nogo A inhibit neurite growth via p75NTR / NgR independent pathways that converge at RhoA . ^^^ MAG , OMgp as well as the Nogo specific domain Nogo 66 exert their inhibitory activity by binding to a neuronal receptor complex containing the Nogo 66 receptor NgR and the neurotrophin receptor p 75 ( NTR ) . ^^^ While this suggests a converging role of the p 75 ( NTR ) / NgR receptor complex for myelin derived neurite growth inhibitors , we show here that NgR / p75 ( NTR ) is not required for mediating the inhibitory activity of the two myelin components NiG , unlike Nogo 66 a distinct domain of Nogo A , and Versican V 2 . ^^^ Finally , we demonstrate that neither NiG nor Versican V 2 interact with the p 75 ( NTR ) / NgR receptor complex and provide evidence that the binding sites of NiG and Nogo 66 are physically distinct from each other on neural tissue . ^^^ |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| In the central nervous system , regeneration of injured axons and sprouting of intact axons are suppressed by myelin derived molecules that bind to the Nogo receptor ( NgR ) . ^^^ |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| Three myelin proteins , Nogo , MAG ( myelin associated glycoprotein ) , and OMgp ( oligodendrocyte myelin glycoprotein ) , bind to the Nogo 66 receptor ( NgR ) and inhibit axonal growth in vitro . ^^^ |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| Concrete evidence for a direct role of Nogo A in the latter neuropathies is not yet available , but such a role is logically in line with new findings associated with localization of Nogo A and Nogo Nogo 66 receptor ( NgR ) mediated signaling . ^^^ |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| The Nogo 66 receptor ( NgR ) plays a pivotal role in the inhibition of neuroregeneration as the receptor for multiple neurite outgrowth inhibitors such as Nogo A . ^^^ |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| Neuronal Nogo receptor ( NgR ) binds to each of the three inhibitors and has been proposed to mediate their inhibitory signals by complexing with a signal transducing coreceptor , the neurotrophin receptor p 75 ( NTR ) . ^^^ Nogo transcripts are up regulated in NgR mutants , indicating that NgR regulates Nogo in vivo . ^^^ However , neurite outgrowth from NgR deficient postnatal dorsal root ganglion or cerebellar granule neurons is inhibited by myelin and by a Nogo 66 substrate to the same extent as is from wild type neurons , whereas p 75 ( NTR ) deficient neurons are less inhibited . ^^^ The NgR ligand binding domain promotes neurite outgrowth on Nogo 66 , regardless of the genotype of the neurons , indicating that the NgR ligand binding domain can act independent of NgR . ^^^ |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| A major obstacle for successful axon regeneration in the adult central nervous system ( CNS ) arises from inhibitory molecules in CNS myelin , which signal through a common receptor complex on neurons consisting of the ligand binding Nogo 66 receptor ( NgR ) and two transmembrane coreceptors , p 75 and LINGO 1 . ^^^ |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| Recently , findings indicate that three distinct myelin components inhibit axon growth by binding a common receptor , the Nogo 66 receptor ( NgR ) . ^^^ |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| Expression pattern of NOGO and NgR genes during human development . ^^^ We investigated the expression of the genes encoding Nogo and its receptor , NgR , between weeks eight and 23 of human embryonic development , by quantitative radioactive in situ hybridization . ^^^ At 8 weeks , we detected NOGO and NgR transcripts in developing neuronal and non neuronal structures . ^^^ During this period of development , NOGO and NgR transcripts colocalized in the cortical and ventricular zones of the brain , with expression strongest for these two genes in the postmitotic cells of the cortical plate . ^^^ In developing dental germs , NgR was more strongly expressed than NOGO at 16 and 21 weeks . ^^^ |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| RESULTS : Recent studies have reported a number of significant observations providing additional insight into the role and mechanism of regeneration , immune system response , and functional recovery after spinal cord injury ( SCI ) using incomplete paraplegic mice with Nogo A , NgR , EphA 4 , GFAP / vimentime , LIF , or Fas gene knock out . ^^^ |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| The p 75 neurotrophin receptor ( p75NTR ) collaborates with the Nogo receptor ( NgR ) and LINGO 1 to activate RhoA in response to myelin based growth inhibitors such as myelin associated glycoprotein ( MAG ) . ^^^ |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| IN 1 , the monoclonal antibody against the exon 3 encoded N terminal domain of Nogo A , and the Nogo 66 receptor ( NgR ) antagonist NEP 1 40 have both shown efficacy in promoting regeneration in animal spinal cord injury models , the latter even when administered subcutaneously 1 week after injury . ^^^ These results are supportive of the hypothesis that the Nogo NgR axis is a major path for inhibition of spinal cord axonal regeneration and uphold the promises of these neutralizing agents in clinical applications . ^^^ However , mice with targeted disruption of Nogo and NgR have , surprisingly , only modest regenerative capacity ( if any ) compared with treatment with IN 1 or NEP 1 40 . ^^^ These possibilities include effects of IN 1 and NEP 1 40 on the CNS beyond neutralization of Nogo and NgR functions , and the latter ' s possible role in the CNS beyond that of neuronal growth inhibition . . ^^^ |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| We find that mutations in the Nogo 66 receptor ( NgR ) affect cessation of ocular dominance plasticity . ^^^ Thus , physiological NgR signaling from myelin derived Nogo , MAG , and OMgp consolidates the neural circuitry established during experience dependent plasticity . ^^^ |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| 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 . ^^^ 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 . ^^^ |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| A Nogo to Nogo 66 receptor ( NgR ) pathway contributes to determining the ability of adult CNS axons to extend after traumatic injuries . ^^^ Both Nogo and NgR are mislocalized in AD brain samples . ^^^ |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| When associated with the Nogo receptor ( NgR ) , the transmembrane receptor p75NTR signals growth cone collapse . ^^^ Here , we show that optic nerve regeneration in vivo correlates with Schwann cell derived factor induced cleavage of NgR and Nogo A , and inactivation of p75NTR signalling by the induction of regulated intramembranous proteolysis ( RIP ) and the release of both extracellular ( p75ECD ) and intracellular ( p75ICD ) domains . ^^^ Hence , Schwann cell derived factors compromise inhibitory signalling by ( 1 ) antagonizing ligand / NgR binding with metalloproteinase cleaved Nogo A peptides ; ( 2 ) RIP of p75NTR ; ( 3 ) competitively blocking NgR / p75NTR clustering with soluble p75ECD ; and ( 4 ) consequent reduced downstream EGFR phosphorylation and suppression of Rho A activation . ^^^ |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| The regeneration potential of the adult mammalian central nervous system ( CNS ) is very modest , due to , among other factors , the presence of either a glial scar , or myelin associated regeneration inhibitors such as Nogo A , MAG and OMgp , which all interact with the same receptor ( NgR ) . ^^^ |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| With respect to the neuronal Nogo receptor ( NgR ) , recent data assign a key role for the GTPase Rho in the control of cellular responses leading to actin cytoskeletal rearrangements and finally resulting in axonal outgrowth inhibition and growth cone collapse in the adult human central nervous system . ^^^ RhoA activation induced by stimulation with the alkaline phosphatase tagged NgR ligand Nogo 66 ( AP Nogo 66 ) was confirmed by affinity precipitation of the GTPase with the Rho binding domain from Rhotekin . ^^^ In contrast , stimulation with AP Nogo 66 resulted in Rho dependent cell contraction with a similar time course only in the NgR expressing cell line . ^^^ |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| Therefore , we have examined the levels of mRNA encoding Nogo , OMgp and MAG , as well as the receptor components NgR , Lingo 1 and Troy in cortex and hippocampus of young ( 4 months ) , middle aged ( 16 months ) and old ( 24 months ) Fisher 344 rats . ^^^ |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| The inability to determine the structure of the buffer insoluble Nogo extracellular domain retarded further design of Nogo receptor ( NgR ) antagonists to treat CNS axonal injuries . ^^^ The Nogo 60 structure offered us rationales for further design of the structured and buffer soluble Nogo 54 , which may be used as a novel NgR antagonist . ^^^ |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| Nogo is a transmembraneous protein ; the extracellular domain is termed Nogo 66 , and a Nogo 66 receptor ( Nogo R ) has been identified . ^^^ |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| Nogo and the Nogo 66 receptor . ^^^ Cleavage of the Nogo 66 receptor from axonal surfaces renders neurons insensitive to Nogo 66 . ^^^ Nogo 66 receptor expression is sufficient to impart Nogo 66 axonal inhibition to unresponsive neurons . ^^^ |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| Here , we analyzed the expression pattern of Nogo A , Nogo B , and Nogo C and Nogo 66 receptor ( Ng66R ) mRNA during hippocampal development and lesion induced axonal sprouting . ^^^ |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| A neutralizing anti Nogo 66 receptor monoclonal antibody reverses inhibition of neurite outgrowth by central nervous system myelin . ^^^ The Nogo 66 receptor ( NgR 1 ) is a neuronal , leucine rich repeat ( LRR ) protein that binds three central nervous system ( CNS ) myelin proteins , Nogo , myelin associated glycoprotein , and oligodendrocyte myelin glycoprotein , and mediates their inhibitory effects on neurite growth . ^^^ |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| Solution structure of Nogo 40 , a Nogo 66 receptor antagonist enhancing injured spinal cord regeneration . ^^^ The recent discovery of the Nogo family of myelin inhibitors and the Nogo 66 receptor opens up a very promising avenue for the development of therapeutic agents for treating spinal cord injury . ^^^ Nogo 40 , a truncated form of Nogo 66 , has been previously shown to be a Nogo 66 receptor antagonist that is able to enhance CNS neuronal regeneration . ^^^ The solution structure of Nogo 40 revealed two well defined helices linked by an unstructured loop , representing the first structure of Nogo 66 receptor binding ligands . ^^^ |
|
| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| The Nogo 66 receptor homolog NgR 2 is a sialic acid dependent receptor selective for myelin associated glycoprotein . ^^^ The Nogo 66 receptor ( NgR 1 ) is a promiscuous receptor for the myelin inhibitory proteins Nogo / Nogo 66 , myelin associated glycoprotein ( MAG ) , and oligodendrocyte myelin glycoprotein ( OMgp ) . ^^^ |
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| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| TAJ / TROY , an orphan TNF receptor family member , binds Nogo 66 receptor 1 and regulates axonal regeneration . ^^^ The Nogo receptor complex , composed of the Nogo 66 receptor 1 ( NgR 1 ) , neurotrophin p 75 receptor ( p 75 ) , and LINGO 1 , represses axon regeneration upon binding to these myelin components . ^^^ |
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| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| LINGO 1 , initially discovered as a component of the Nogo 66 receptor complex which inhibits neurite growth , also regulates oligodendrocyte differentiation and myelination . ^^^ |
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| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| Unlike the loop domain ( Nogo 66 ) found in all Nogo isoforms that can interact with a neural specific Nogo 66 receptor , the receptor for the amino terminus of Nogo B that mediates vascular function is unknown . ^^^ |
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| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| Recent work has demonstrated that axonal regeneration in the central nervous system is limited by myelin derived Nogo binding to an axonal Nogo Receptor . ^^^ |
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| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| It associates with the Nogo receptor , a binding protein for axonal growth inhibitors , and appears to be the transducing subunit of this receptor complex . . ^^^ |
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| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| Expression of the neurotrophin receptor p75NTR is increased in the injured tissue and axon regeneration is repressed by the Nogo receptor using p75NTR as the signal transducer . ^^^ |
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| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| The neurotrophin receptor p75NTR is the coreceptor for Nogo receptor , mediating growth cone collapse in vitro by MAG , myelin oligodendrocyte glycoprotein ( Omgp ) , and Nogo . ^^^ |
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| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| Regulation of Nogo and Nogo receptor during the development of the entorhino hippocampal pathway and after adult hippocampal lesions . ^^^ Here we study the onset and maturation of Nogo A and Nogo receptor in the entorhino hippocampal formation of developing and adult mice . ^^^ Our results also show that Nogo and Nogo receptor mRNA are expressed in the adult by both principal and local circuit hippocampal neurons , and that after lesion , Nogo A is also transiently expressed by a subset of reactive astrocytes . ^^^ We found that Nogo A and Nogo receptor are differentially regulated after kainic acid or perforant pathway lesions . ^^^ |
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| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| Based on sequence homology to the known crystal structures of two other leucine rich repeat proteins , the human Nogo receptor and GPIb alpha , we propose a new structural model of GPIb beta . ^^^ |
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| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| Nogo 66 , the extracellular 66 aa loop of the Nogo A protein found in CNS myelin , interacts with the Nogo receptor and has been proposed to mediate inhibition of axonal regrowth . ^^^ Nogo 66 , the extracellular 66 aa loop of the Nogo A protein found in CNS myelin , interacts with the Nogo receptor and has been proposed to mediate inhibition of axonal regrowth . ^^^ |
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| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| The p 75 receptor ( p 75 ( NTR ) ) binds growth promoting neurotrophins ( NTs ) as well as the common receptor for growth inhibiting myelin derived proteins ( the Nogo receptor ) and so is well situated to gauge the balance of positive and negative influences on axonal plasticity . ^^^ |
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| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| The differential expression patterns of messenger RNAs encoding Nogo A and Nogo receptor in the rat central nervous system . ^^^ Nogo A and Nogo receptor have been considered to play pivotal roles in controlling axonal regeneration and neuronal plasticity . ^^^ We investigated the total distribution of Nogo A and Nogo receptor mRNAs in the adult rat central nervous system using in situ hybridization histochemistry . ^^^ |
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| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| Further , antagonism of the Nogo receptor by the peptide NEP 1 40 ( Nogo extracellular peptide residues 1 40 ) can promote axonal regeneration in rats after SCI . ^^^ |
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| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| Here we show that gangliosides , GT1b and GD1a , as well as the Nogo receptor , are functional binding partners for soluble MAG Fc . ^^^ |
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| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| The oligodendrocyte myelin glycoprotein is a ligand of the neuronal Nogo receptor and a potent inhibitor of neurite outgrowth , but its physiological function remains to be elucidated . ^^^ |
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| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| Triple and not single NTF treatments potentiated regulated intramembraneous proteolysis of p 75 ( NTR ) , and ectodomain shedding of Nogo receptor , correlated with a 30 % decrease in activation of Rho A , a key signalling molecule in the axon growth inhibitory cascade . ^^^ |
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| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| Introduction of the MASH 1 gene into mouse embryonic stem cells leads to differentiation of motoneuron precursors lacking Nogo receptor expression that can be applicable for transplantation to spinal cord injury . ^^^ The cells lacked the expression of Nogo receptor that was of great advantage for axon growth after transplantation to an injured spinal cord . ^^^ In the grafted spinal cord , gliosis was inhibited and Nogo receptor expression was scarcely detected . ^^^ |
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| Interacting proteins: Q9BZR6 and Q9NQC3 |
Pubmed |
SVM Score :0.0 |
| Conversely , activation of bHLH transcription factors induces a cluster of genes with potent axonal inhibitory functions including the gene coding for the Nogo receptor , a key transducer of myelin inhibition . ^^^ Degradation of Id 2 in neurons permits the accumulation of the Nogo receptor , thereby linking APC / C ( Cdh 1 ) activity with bHLH target genes for the inhibition of axonal growth . ^^^ |
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