The Nogo-66 receptor family in the intact and diseased CNS

Abstract

The Nogo-66 receptor family (NgR) consists in three glycophosphatidylinositol (GPI)-anchored receptors (NgR1, NgR2 and NgR3), which are primarily expressed by neurons in the central and peripheral mammalian nervous system. NgR1 was identified as serving as a high affinity binding protein for the three classical myelin-associated inhibitors (MAIs) Nogo-A, myelin-associated glycoprotein (MAG) and oligodendrocyte myelin glycoprotein (OMgp), which limit axon regeneration and sprouting in the injured brain. Recent studies suggest that NgR signaling may also play an essential role in the intact adult CNS in restricting axonal and synaptic plasticity and are involved in neurodegenerative diseases, particularly in Alzheimer's disease pathology through modulation of β-secretase cleavage. Here, we outline the biochemical properties of NgRs and their functional roles in the intact and diseased CNS.

Two Monoclonal Antibodies Recognising aa 634-668 and aa 1026-1055 of NogoA Enhance Axon Extension and Branching in Cultured Neurons

“…Three areas are of particular interest. One such area is Nogo-66 (aa 1026–1091) in the C-terminal region of NogoA, which is reported to bind to the GPI-linked Nogo receptor/p75 complex on axons and induce growth cone collapse [19], [20]. Two other regions in the N-terminus have also been discovered to have bioactivity.…”

Genome-wide meta-analysis identifies new susceptibility loci for migraine

“…Notably, the protein encoded by MMP16 (MT-MMP2) cleaves LRP1 12 , encoded by a previously reported migraine gene 2 . In addition, MMP16 has recently been shown to be involved in basal NgR1 (Nogo-66 receptor) shedding in cortical neurons, thereby increasing axonal and synaptic plasticity 13 .…”

Polymorphism within a Neuronal Activity-Dependent Enhancer of <b><i>NgR1</i></b> Is Associated with Corpus Callosum Morphology in Humans

“…NgR1, a receptor for Nogo-A, represses synaptogenesis and axonal sprouting [43] and is downregulated by neuronal activity [39,44,45] . This NgR1-mediated mechanism is thought to be important for restricting synaptic plasticity and maintaining preformed neuronal wiring [5,39] .…”