Reticulon 4 receptor (RTN4R), also known as Nogo-66 Receptor (NgR), is a glycosylphosphoinositol (GPI)-anchored protein that belongs to the Nogo recptor family including three members. Mouse RTN4R cDNA contains 10 LRP (Leucine-rich) repeats. RTN4R is expressed predominantly in neurons and their axons in the central nervous systems (CNS). As a receptor for myelin-derived proteins Nogo, myelin-associated glycoprotein (MAG), and myelin oligodendrocyte glycoprotein (OMG), RTN4R mediates axonal growth inhibition and may play a role in regulating axonal regeneration and plasticity in the adult CNS. It has been shown that RTN4R performs its inhibitory actions by interacting with the p75 neurotrophin receptor (p75NTR), a TNFRSF member also known for modulating the activities of the Trk family and for inducing apoptosis in neurons and oligodendrocytes. RTN4R may be proposed as a potential drug target for treatment of various neurological conditions such as spinal cord injury, CNS lesions, peripheral nerve injury, stroke and Alzheimer's disease (AD). Additionally, RTN4R may play a role in regulating the function of the gap junctions.
Nogo Receptor (NgR) is a glycosylphosphoinositol (GPI)-anchored protein that belongs to the Nogo recptor family. Human NgR is predominantly expressed in neurons and their axons in the central nervous systems. As a receptor for myelin-derived proteins Nogo; myelin-associated glycoprotein (MAG) and myelin oligodendrocyte glycoprotein (OMG); NgR mediates axonal growth inhibition and may play a role in regulating axonal regeneration and plasticity in the adult central nervous system. NgR may be proposed as a potential drug target for treatment of various neurological conditions. Additionally; NgR may play a role in regulating the function of gap junctions.
Nucleolar protein 3 is encoded by NOL3 gene. Multiple transcript variants encoding different isoforms have been found for this gene. So far; Nucleolar protein 3 has show to have two Isoforms. Isoform 1 may be involved in RNA splicing. Isoform 2 functions as an apoptosis repressor that blocks multiple modes of cell death. It inhibits extrinsic apoptotic pathways through two different ways. Firstly; it by interacting with FAS and FADD upon FAS activation blocking death-inducing signaling complex (DISC) assembly. Secondly by interacting with CASP8 in a mitochondria localization- and phosphorylation-dependent manner; limiting the amount of soluble CASP8 available for DISC-mediated activation. It has been shown to down-regulate the enzyme activities of caspase 2; caspase 8 and tumor protein p53.
Nucleolar Protein 3 is encoded by NOL3 gene; multiple transcript variants encoding different isoforms have been found for this gene. So far; Nucleolar protein 3 has show to have two Isoforms. Isoform 1 may be involved in RNA splicing.Isoform 2 may inhibit apoptosis.It has been shown to down-regulate the enzyme activities of caspase 2; caspase 8 and tumor protein p53.
Notch-2 is a 300 kDa type I transmembrane glycoprotein that is one of four human Notch homologues involved in developmental processes. Functions as a receptor for membrane-bound ligands Jagged-1 (JAG1), Jagged-2 (JAG2) and Delta-1 (DLL1) to regulate cell-fate determination. Human Notch-2 ECD (aa 26-530) shows 93%, 93%, 96% and 96% aa identity with the corresponding regions of mouse, rat, canine, and bovine Notch-2, respectively. Hajdu Cheney Syndrome (HCS) is a rare disease associated with mutations of NOTCH2 that lead to the translation of a truncated, presumably stable, NOTCH2 protein. NOTCH2 is down-regulated in colon cancer, and reduced expression is associated with a less differentiated, more aggressive phenotype, and reduced overall survival. NOTCH2 has also been shown to have pro-apoptotic and growth suppressive effects in thyroid carcinoma, and carcinoid tumors. NOTCH2 acts as an oncogene that promotes bladder cancer growth and metastasis through EMT, cell-cycle progression, and maintenance of stemness.
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