The myelin oligodendrocyte glycoprotein directly binds nerve growth factor to modulate central axon circuitry
| Autor: | David D. McKemy, Jonah R. Chan, Sarah Jahn, H.-Christian von Büdingen, Feng Mei, Yun-An A Shen, Hugh H. Reid, Ariele L. Greenfield |
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| Jazyk: | angličtina |
| Rok vydání: | 2015 |
| Předmět: |
Genotype
Cell Survival Central nervous system Molecular Sequence Data Plasma protein binding CHO Cells Biology Transfection Myelin oligodendrocyte glycoprotein Rats Sprague-Dawley Myelin Cricetulus immune system diseases Report Ganglia Spinal Nerve Growth Factor medicine Animals Amino Acid Sequence Axon Receptor trkA Research Articles Mice Knockout integumentary system hemic and immune systems Cell Biology Axons Coculture Techniques nervous system diseases 3. Good health Cell biology Oligodendroglia medicine.anatomical_structure Nerve growth factor Phenotype nervous system Spinal Cord Immunology Knockout mouse biology.protein Myelin-Oligodendrocyte Glycoprotein Signal transduction Protein Binding Signal Transduction |
| Zdroj: | The Journal of Cell Biology Chan, Jonah; von, H-C; Mei, F; Greenfield, A; Jahn, S; Shen, Y-AA; et al.(2015). The myelin oligodendrocyte glycoprotein directly binds nerve growth factor to modulate central axon circuitry. UC San Francisco: Retrieved from: http://www.escholarship.org/uc/item/9td8q9wz |
| ISSN: | 1540-8140 0021-9525 |
| Popis: | Myelin oligodendrocyte glycoprotein, expressed on the outermost lamellae of the myelin sheath, is a novel and specific binding partner for NGF that may modulate local concentrations of the neurotrophin in the spinal cord microenvironment. Myelin oligodendrocyte glycoprotein (MOG) is a central nervous system myelin-specific molecule expressed on the outer lamellae of myelin. To date, the exact function of MOG has remained unknown, with MOG knockout mice displaying normal myelin ultrastructure and no apparent specific phenotype. In this paper, we identify nerve growth factor (NGF) as a binding partner for MOG and demonstrate that this interaction is capable of sequestering NGF from TrkA-expressing neurons to modulate axon growth and survival. Deletion of MOG results in aberrant sprouting of nociceptive neurons in the spinal cord. Binding of NGF to MOG may offer widespread implications into mechanisms that underlie pain pathways. |
| Databáze: | OpenAIRE |
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