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  1. Article ; Online: Nogo/RTN4 isoforms and RTN3 expression protect SH-SY5Y cells against multiple death insults.

    Teng, Felicia Yu Hsuan / Tang, Bor Luen

    Molecular and cellular biochemistry

    2013  Volume 384, Issue 1-2, Page(s) 7–19

    Abstract: Among the members of the reticulon (RTN) family, Nogo-A/RTN4A, a prominent myelin-associated neurite growth inhibitory protein, and RTN3 are highly expressed in neurons. However, neuronal cell-autonomous functions of Nogo-A, as well as other members of ... ...

    Abstract Among the members of the reticulon (RTN) family, Nogo-A/RTN4A, a prominent myelin-associated neurite growth inhibitory protein, and RTN3 are highly expressed in neurons. However, neuronal cell-autonomous functions of Nogo-A, as well as other members of the RTN family, are unclear. We show here that SH-SY5Y neuroblastoma cells stably over-expressing either two of the three major isoforms of Nogo/RTN4 (Nogo-A and Nogo-B) or a major isoform of RTN3 were protected against cell death induced by a battery of apoptosis-inducing agents (including serum deprivation, staurosporine, etoposide, and H2O2) compared to vector-transfected control cells. Nogo-A, -B, and RTN3 are particularly effective in terms of protection against H2O2-induced increase in intracellular reactive oxygen species levels and ensuing apoptotic and autophagic cell death. Expression of these RTNs upregulated basal levels of Bax, activated Bax, and activated caspase 3, but did not exhibit an enhanced ER stress response. The protective effect of RTNs is also not dependent on classical survival-promoting signaling pathways such as Akt and Erk kinase pathways. Neuron-enriched Nogo-A/Rtn4A and RTN3 may, therefore, exert a protective effect on neuronal cells against death stimuli, and elevation of their levels during injury may have a cell-autonomous survival-promoting function.
    MeSH term(s) Antineoplastic Agents, Phytogenic/pharmacology ; Apoptosis/genetics ; Butadienes/pharmacology ; Carrier Proteins/biosynthesis ; Carrier Proteins/metabolism ; Caspase 3/metabolism ; Cell Line, Tumor ; Chromones/pharmacology ; Endoplasmic Reticulum Stress ; Enzyme Activation ; Enzyme Inhibitors/pharmacology ; Etoposide/pharmacology ; Extracellular Signal-Regulated MAP Kinases/antagonists & inhibitors ; Extracellular Signal-Regulated MAP Kinases/metabolism ; G2 Phase Cell Cycle Checkpoints ; Humans ; Hydrogen Peroxide/pharmacology ; Membrane Proteins/biosynthesis ; Membrane Proteins/metabolism ; Morpholines/pharmacology ; Myelin Proteins/genetics ; Myelin Proteins/metabolism ; Nerve Tissue Proteins/biosynthesis ; Nerve Tissue Proteins/metabolism ; Nitriles/pharmacology ; Nogo Proteins ; Oxidants/pharmacology ; Protein Isoforms/genetics ; Protein Isoforms/metabolism ; Proto-Oncogene Proteins c-akt/antagonists & inhibitors ; Proto-Oncogene Proteins c-akt/metabolism ; Staurosporine/pharmacology ; bcl-2-Associated X Protein/biosynthesis ; bcl-2-Associated X Protein/metabolism
    Chemical Substances Antineoplastic Agents, Phytogenic ; Butadienes ; Carrier Proteins ; Chromones ; Enzyme Inhibitors ; Membrane Proteins ; Morpholines ; Myelin Proteins ; Nerve Tissue Proteins ; Nitriles ; Nogo Proteins ; Oxidants ; Protein Isoforms ; RTN3 protein, human ; RTN4 protein, human ; U 0126 ; bcl-2-Associated X Protein ; 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one (31M2U1DVID) ; Etoposide (6PLQ3CP4P3) ; Hydrogen Peroxide (BBX060AN9V) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Extracellular Signal-Regulated MAP Kinases (EC 2.7.11.24) ; Caspase 3 (EC 3.4.22.-) ; Staurosporine (H88EPA0A3N)
    Language English
    Publishing date 2013-08-18
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 184833-1
    ISSN 1573-4919 ; 0300-8177
    ISSN (online) 1573-4919
    ISSN 0300-8177
    DOI 10.1007/s11010-013-1776-6
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  2. Article: NF-kappaB signaling in neurite growth and neuronal survival.

    Teng, Felicia Yu Hsuan / Tang, Bor Luen

    Reviews in the neurosciences

    2010  Volume 21, Issue 4, Page(s) 299–313

    Abstract: The nuclear factor kappa B (NF-kappaB) transcription factor system plays multiple roles in the function of the nervous system during development and postnatal physiology. In the developing nervous system, neurite outgrowth could be regulated by both ... ...

    Abstract The nuclear factor kappa B (NF-kappaB) transcription factor system plays multiple roles in the function of the nervous system during development and postnatal physiology. In the developing nervous system, neurite outgrowth could be regulated by both canonical and alternative NF-kappaB signaling pathways. The degree and site of NF-kappaB activation could promote or inhibit neuronal survival in a complex, signal and subunit-dependent manner. The significance and mechanistic basis of some of NF-kappaB activity in neurons have remained controversial. We discuss our current understanding and recent findings with regard to the roles of NF-kappaB in the neurite outgrowth and neuronal survival, and how NF-kappaB activation is associated with the pathophysiology of ischemic/ traumatic injuries and neurodegenerative diseases.
    MeSH term(s) Animals ; Cell Survival/drug effects ; Enzyme Inhibitors/pharmacology ; Humans ; NF-kappa B/metabolism ; Nerve Growth Factor/pharmacology ; Nervous System/cytology ; Nervous System/drug effects ; Nervous System/growth & development ; Neurites/drug effects ; Neurites/physiology ; Neurons/drug effects ; Neurons/metabolism ; Neurons/ultrastructure ; Signal Transduction/drug effects ; Signal Transduction/physiology
    Chemical Substances Enzyme Inhibitors ; NF-kappa B ; Nerve Growth Factor (9061-61-4)
    Language English
    Publishing date 2010-11-17
    Publishing country Germany
    Document type Journal Article ; Review
    ZDB-ID 639035-3
    ISSN 2191-0200 ; 0334-1763
    ISSN (online) 2191-0200
    ISSN 0334-1763
    DOI 10.1515/revneuro.2010.21.4.299
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  3. Article ; Online: Cell autonomous function of Nogo and reticulons: The emerging story at the endoplasmic reticulum.

    Teng, Felicia Yu Hsuan / Tang, Bor Luen

    Journal of cellular physiology

    2008  Volume 216, Issue 2, Page(s) 303–308

    Abstract: The myelin-associated membrane protein reticulon-4 (RTN4)/Nogo has been extensively studied with regards to its neurite outgrowth inhibitory function, both in limiting plasticity in the healthy adult brain and regeneration during central nervous system ... ...

    Abstract The myelin-associated membrane protein reticulon-4 (RTN4)/Nogo has been extensively studied with regards to its neurite outgrowth inhibitory function, both in limiting plasticity in the healthy adult brain and regeneration during central nervous system injury. These activities are presumably associated with Nogo splice isoforms expressed on the cell surface and function largely in trans, exerting an influence as an intercellular membrane-bound ligand. Nogo, and other reticulon paralogues and orthologues, are however mainly localized to the endoplasmic reticulum (ER), and are likely to have cell autonomous functions that are not yet clear. Emerging evidence suggests that Nogo may have a role in modulating the morphology and functions of the ER. This role is apparently not essential for cell viability under normal growth conditions, but may be manifested under certain stress conditions.
    MeSH term(s) Animals ; Apoptosis/physiology ; Cell Membrane/metabolism ; Central Nervous System/cytology ; Central Nervous System/metabolism ; Endoplasmic Reticulum/metabolism ; Endoplasmic Reticulum/ultrastructure ; Growth Inhibitors/metabolism ; Humans ; Myelin Proteins/genetics ; Myelin Proteins/metabolism ; Nerve Tissue Proteins/genetics ; Nerve Tissue Proteins/metabolism ; Nogo Proteins ; Oxidative Stress ; Protein Isoforms/genetics ; Protein Isoforms/metabolism
    Chemical Substances Growth Inhibitors ; Myelin Proteins ; Nerve Tissue Proteins ; Nogo Proteins ; Protein Isoforms ; RTN4 protein, human
    Language English
    Publishing date 2008-08
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 3116-1
    ISSN 1097-4652 ; 0021-9541
    ISSN (online) 1097-4652
    ISSN 0021-9541
    DOI 10.1002/jcp.21434
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  4. Article: Nogo-A and Nogo-66 receptor in amyotrophic lateral sclerosis.

    Teng, Felicia Yu Hsuan / Tang, Bor Luen

    Journal of cellular and molecular medicine

    2008  Volume 12, Issue 4, Page(s) 1199–1204

    Abstract: Nogo/reticulon (RTN)-4 has been strongly implicated as a disease marker for the motor neuron disease amyotrophic lateral sclerosis (ALS). Nogo isoforms, including Nogo-A, are ectopically expressed in the skeletal muscle of ALS mouse models and patients ... ...

    Abstract Nogo/reticulon (RTN)-4 has been strongly implicated as a disease marker for the motor neuron disease amyotrophic lateral sclerosis (ALS). Nogo isoforms, including Nogo-A, are ectopically expressed in the skeletal muscle of ALS mouse models and patients and their levels correlate with the disease severity. The notion of a direct involvement of Nogo-A in ALS aetiology is supported by the findings that Nogo-A deletion in mice reduces muscle denervation and prolongs survival, whereas overexpression of Nogo-A destabilizes motor nerve terminals and promotes denervation. Another intriguing, and somewhat paradoxical, recent finding revealed that binding of the Nogo-66 receptor (NgR) by either agonistic or antagonistic Nogo-66-derived peptides protects against p75 neurotrophin receptor (p75(NTR))-dependent motor neuron death. Ligand binding by NgR could result in subsequent engagement of p75(NTR), and this association could preclude pro-apoptotic signalling by the latter. Understanding the intricate interplay among Nogo isoforms, NgR and p75(NTR) in ALS disease progression may provide important, therapeutically exploitable information.
    MeSH term(s) Amyotrophic Lateral Sclerosis/metabolism ; Amyotrophic Lateral Sclerosis/pathology ; Amyotrophic Lateral Sclerosis/therapy ; Animals ; Cell Death ; Humans ; Motor Neurons/cytology ; Motor Neurons/metabolism ; Myelin Proteins/metabolism ; Nogo Proteins ; Protein Isoforms/metabolism ; Receptor, Nerve Growth Factor/metabolism
    Chemical Substances Myelin Proteins ; Nogo Proteins ; Protein Isoforms ; RTN4 protein, human ; Receptor, Nerve Growth Factor ; Rtn4 protein, mouse
    Language English
    Publishing date 2008-04-15
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2074559-X
    ISSN 1582-4934 ; 1582-1838 ; 1582-4934
    ISSN (online) 1582-4934
    ISSN 1582-1838 ; 1582-4934
    DOI 10.1111/j.1582-4934.2008.00351.x
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  5. Article ; Online: Emerging cues mediating astroglia lineage restriction of progenitor cells in the injured/diseased adult CNS.

    Teng, Felicia Yu Hsuan / Hor, Catherine Hong Huan / Tang, Bor Luen

    Differentiation; research in biological diversity

    2009  Volume 77, Issue 2, Page(s) 121–127

    Abstract: Other than specific neurogenic regions, the adult central nervous system (CNS) is not conducive for neuronal regeneration and neurogenesis, particularly at sites of injury or neurodegeneration. Engraftment of neural stem/progenitor cells into non- ... ...

    Abstract Other than specific neurogenic regions, the adult central nervous system (CNS) is not conducive for neuronal regeneration and neurogenesis, particularly at sites of injury or neurodegeneration. Engraftment of neural stem/progenitor cells into non-neurogenic regions or sites of injury/disease invariably results mainly in astroglia differentiation. The reasons for such a lineage restriction have not been well defined. Recent findings have brought to light some underlying novel mechanistic basis for this preferential differentiation into astroglia. The more oxidized state of pathological brain tissue leads to upregulation of the protein deacetylase sirtuin 1 (Sirt1). Sirt1 appears to stabilize a co-repressor complex of Hairy/enhancer of split (Hes)1, thereby suppressing expression of the proneuronal transcription factor Mash1, and directs progenitor cell differentiation towards the glia lineage. Sirt1 upregulated by CNS inflammation may also inhibit neuronal differentiation. Myelin-associated inhibitors such as Nogo, acting through the Nogo-66 receptor (NgR), also appear to promote neural stem/progenitor cell differentiation into astrocytes. Understanding the molecular basis of glia lineage restriction of neural progenitors in the injured or diseased CNS would provide handles to improving the success of stem cell-based transplantation therapy.
    MeSH term(s) Adult ; Astrocytes/pathology ; Basic Helix-Loop-Helix Transcription Factors/metabolism ; Cell Differentiation ; Cell Lineage ; Central Nervous System/pathology ; Homeodomain Proteins/metabolism ; Humans ; Models, Biological ; Sirtuin 1 ; Sirtuins/metabolism ; Stem Cells/pathology ; Transcription Factor HES-1
    Chemical Substances Basic Helix-Loop-Helix Transcription Factors ; Homeodomain Proteins ; Transcription Factor HES-1 ; HES1 protein, human (149348-15-2) ; SIRT1 protein, human (EC 3.5.1.-) ; Sirtuin 1 (EC 3.5.1.-) ; Sirtuins (EC 3.5.1.-)
    Language English
    Publishing date 2009-02
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 184540-8
    ISSN 1432-0436 ; 0301-4681
    ISSN (online) 1432-0436
    ISSN 0301-4681
    DOI 10.1016/j.diff.2008.09.013
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  6. Article: Axonal regeneration in adult CNS neurons--signaling molecules and pathways.

    Teng, Felicia Yu Hsuan / Tang, Bor Luen

    Journal of neurochemistry

    2006  Volume 96, Issue 6, Page(s) 1501–1508

    Abstract: Failure of severed adult CNS axons to regenerate could be attributed to both a reduced intrinsic capacity to grow and an heightened susceptibility to inhibitory factors of the CNS extracellular environment. A particularly interesting and useful paradigm ... ...

    Abstract Failure of severed adult CNS axons to regenerate could be attributed to both a reduced intrinsic capacity to grow and an heightened susceptibility to inhibitory factors of the CNS extracellular environment. A particularly interesting and useful paradigm for investigating CNS axonal regeneration is its enhancement at the CNS branch of dorsal root ganglion (DRG) neurons after conditional lesioning of their peripheral branch. Recent reports have implicated the involvement of two well-known signaling pathways utilizing separate transcription factors; the Cyclic AMP (cAMP) response element binding protein (CREB) and signal transducer and activator of transcription 3 (STAT3), in conditional lesioning. The former appears to be the pathway activated by neurotrophic factors and Bcl-2, while the latter is responsible for the neurogenic effect of cytokines [such as the leukemia inhibitory factor (LIF) and interleukin-6 (IL-6) elevated at lesion sites]. Recent findings also augmented earlier notions that modulations of the activity of another class of cellular signaling intermediate, the conventional protein kinase C (PKC), could result in a contrasting growth response by CNS neurons to myelin-associated inhibitors. We discuss these signaling pathways and mechanisms, in conjunction with other recent reports of regeneration enhancement and also within the context of what is known about aiding regeneration of injured CNS axons.
    MeSH term(s) Animals ; Central Nervous System/injuries ; Central Nervous System/physiology ; Cyclic AMP Response Element-Binding Protein/metabolism ; Growth Cones/metabolism ; Growth Inhibitors/antagonists & inhibitors ; Growth Inhibitors/metabolism ; Humans ; Nerve Growth Factors/metabolism ; Nerve Regeneration/physiology ; Protein Kinase C/metabolism ; STAT3 Transcription Factor/metabolism ; Signal Transduction/physiology
    Chemical Substances Cyclic AMP Response Element-Binding Protein ; Growth Inhibitors ; Nerve Growth Factors ; STAT3 Transcription Factor ; Protein Kinase C (EC 2.7.11.13)
    Language English
    Publishing date 2006-03
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 80158-6
    ISSN 1471-4159 ; 0022-3042 ; 1474-1644
    ISSN (online) 1471-4159
    ISSN 0022-3042 ; 1474-1644
    DOI 10.1111/j.1471-4159.2006.03663.x
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  7. Article: No go for brain tumors?

    Teng, Felicia Yu Hsuan / Tang, Bor Luen

    Journal of molecular neuroscience : MN

    2005  Volume 25, Issue 1, Page(s) 1–6

    Abstract: The Nogo gene and its products are well known as adult central nervous system (CNS) myelin inhibitors of neuronal regeneration. We review here experimental findings that might link Nogo to CNS malignancy. These links are founded on two very different ... ...

    Abstract The Nogo gene and its products are well known as adult central nervous system (CNS) myelin inhibitors of neuronal regeneration. We review here experimental findings that might link Nogo to CNS malignancy. These links are founded on two very different modes of cellular action by Nogo isoforms. Acting intracellularly and in conjunction with other molecules, cytoplasmic domains of Nogo might predispose cancer cells to apoptotic susceptibility. On the other hand, extracellular domains of Nogo might inhibit the migration and invasion of CNS tumors. Depending on the physiological context, Nogo isoforms might therefore be antitumorigenic or have tumor-suppressing activities.
    MeSH term(s) Antineoplastic Agents/metabolism ; Brain Neoplasms/genetics ; Central Nervous System/pathology ; Central Nervous System/physiology ; Growth Inhibitors/genetics ; Growth Inhibitors/metabolism ; Humans ; Myelin Proteins/genetics ; Myelin Proteins/metabolism ; Nogo Proteins ; Protein Isoforms/genetics ; Protein Isoforms/metabolism ; Proto-Oncogene Proteins/genetics ; Proto-Oncogene Proteins/metabolism
    Chemical Substances Antineoplastic Agents ; Growth Inhibitors ; Myelin Proteins ; Nogo Proteins ; Protein Isoforms ; Proto-Oncogene Proteins ; RTN4 protein, human
    Language English
    Publishing date 2005-03-11
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1043392-2
    ISSN 0895-8696
    ISSN 0895-8696
    DOI 10.1385/jmn:25:1:001
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  8. Article: Concepts of protein sorting or targeting signals and membrane topology in undergraduate teaching*.

    Tang, Bor Luen / Teng, Felicia Yu Hsuan

    Biochemistry and molecular biology education : a bimonthly publication of the International Union of Biochemistry and Molecular Biology

    2005  Volume 33, Issue 3, Page(s) 188–193

    Abstract: The process of protein biogenesis culminates in its correct targeting to specific subcellular locations where it serves a function. Contemporary molecular and cell biology investigations often involve the exogenous expression of epitope- or fluorescent ... ...

    Abstract The process of protein biogenesis culminates in its correct targeting to specific subcellular locations where it serves a function. Contemporary molecular and cell biology investigations often involve the exogenous expression of epitope- or fluorescent protein-tagged recombinant molecules as well as subsequent analysis of protein-protein interactions in vitro and in vivo. Fundamental knowledge of targeting signals that direct a polypeptide to various organelles or membrane domains is essential for the proper design of such recombinant molecules. A fundamental concept of membrane compartmentalization is also often useful for the interpretation of the preliminary results of interaction screens. Knowledge in targeting signals and post-translational dynamics of proteins should therefore be given sufficient emphasis in an undergraduate biochemistry or molecular biology curriculum. Such knowledge is essential, particularly for undergraduates or fresh graduates embarking on research projects in a cell and molecular biology laboratory.
    Language English
    Publishing date 2005-05
    Publishing country United States
    Document type Journal Article
    ISSN 1470-8175
    ISSN 1470-8175
    DOI 10.1002/bmb.2005.494033032448
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  9. Article: Nogo signaling and non-physical injury-induced nervous system pathology.

    Teng, Felicia Yu Hsuan / Tang, Bor Luen

    Journal of neuroscience research

    2005  Volume 79, Issue 3, Page(s) 273–278

    Abstract: The Nogo gene products were described first as myelin-associated inhibitors that prevent neuronal regeneration upon injury. Recent findings have also implicated Nogo in several neuronal pathologies that are not induced by physical injury. Nogo-A may be ... ...

    Abstract The Nogo gene products were described first as myelin-associated inhibitors that prevent neuronal regeneration upon injury. Recent findings have also implicated Nogo in several neuronal pathologies that are not induced by physical injury. Nogo-A may be an important determinant of autoimmune demyelinating diseases, as active immunization with Nogo-A fragments attenuates the symptoms of experimental autoimmune encephalomyelitis (EAE). Nogo-A levels are elevated markedly in hippocampal neurons of patients with temporal lobe epilepsy (TLE), in brain and muscle of patients with amyotrophic lateral sclerosis (ALS), and in schizophrenic patients. 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. We speculate on possible linkages between the effect of aberrant elevation of Nogo levels and the signaling consequences that could lead to nervous system pathology.
    MeSH term(s) Amyotrophic Lateral Sclerosis/metabolism ; Amyotrophic Lateral Sclerosis/physiopathology ; Animals ; Central Nervous System Diseases/metabolism ; Central Nervous System Diseases/physiopathology ; Encephalomyelitis, Autoimmune, Experimental/metabolism ; Encephalomyelitis, Autoimmune, Experimental/physiopathology ; Epilepsy/metabolism ; Epilepsy/physiopathology ; GPI-Linked Proteins ; Humans ; Myelin Proteins/genetics ; Myelin Proteins/metabolism ; Nerve Degeneration/metabolism ; Nerve Degeneration/physiopathology ; Nogo Proteins ; Nogo Receptor 1 ; Receptors, Cell Surface/genetics ; Receptors, Cell Surface/metabolism ; Signal Transduction/physiology
    Chemical Substances GPI-Linked Proteins ; Myelin Proteins ; Nogo Proteins ; Nogo Receptor 1 ; RTN4 protein, human ; RTN4R protein, human ; Receptors, Cell Surface
    Language English
    Publishing date 2005-02-01
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 195324-2
    ISSN 1097-4547 ; 0360-4012
    ISSN (online) 1097-4547
    ISSN 0360-4012
    DOI 10.1002/jnr.20361
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  10. Article: Why do Nogo/Nogo-66 receptor gene knockouts result in inferior regeneration compared to treatment with neutralizing agents?

    Teng, Felicia Yu Hsuan / Tang, Bor Luen

    Journal of neurochemistry

    2005  Volume 94, Issue 4, Page(s) 865–874

    Abstract: IN-1, the monoclonal antibody against the exon 3-encoded N-terminal domain of Nogo-A, and the Nogo-66 receptor (NgR) antagonist NEP1-40 have both shown efficacy in promoting regeneration in animal spinal cord injury models, the latter even when ... ...

    Abstract IN-1, the monoclonal antibody against the exon 3-encoded N-terminal domain of Nogo-A, and the Nogo-66 receptor (NgR) antagonist NEP1-40 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 NEP1-40. Disruption of the Nogo gene by various groups yielded results ranging from significant regenerative improvement in young mice to no improvement. Likewise, knockout of NgR produced some improvement in raphespinal and rubrospinal axonal regeneration, but not that of corticospinal neurons. Other than invoking possible differences in genetic background, we suggest here some possible and testable explanations for the above phenomena. These possibilities include effects of IN-1 and NEP1-40 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.
    MeSH term(s) Animals ; Antibodies, Monoclonal/pharmacology ; GPI-Linked Proteins ; Mice ; Mice, Knockout/genetics ; Myelin Proteins/deficiency ; Myelin Proteins/genetics ; Myelin Proteins/pharmacology ; Nerve Regeneration/drug effects ; Nogo Proteins ; Nogo Receptor 1 ; Peptide Fragments/pharmacology ; Receptors, Cell Surface/deficiency ; Receptors, Cell Surface/genetics ; Spinal Cord Injuries/metabolism ; Spinal Cord Injuries/physiopathology
    Chemical Substances Antibodies, Monoclonal ; GPI-Linked Proteins ; Myelin Proteins ; NEPI-40 protein, mouse ; Nogo Proteins ; Nogo Receptor 1 ; Peptide Fragments ; Receptors, Cell Surface ; Rtn4 protein, mouse ; Rtn4r protein, mouse
    Language English
    Publishing date 2005-08
    Publishing country England
    Document type Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 80158-6
    ISSN 1471-4159 ; 0022-3042 ; 1474-1644
    ISSN (online) 1471-4159
    ISSN 0022-3042 ; 1474-1644
    DOI 10.1111/j.1471-4159.2005.03238.x
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