Mouse ULBP1, also known as RAET1I and NKG2DL1, is a member of the ULBP/RAET1 gene family. ULBP1 plays an important role in immune responses, especially in cancer and infectious diseases, and is well-known to bind to NKG2D together with at least ULBP 2 and 3. These proteins are distantly related to major histocompatibility class I (MHC I) molecules, possessing the alpha 1 and alpha 2 Ig-like domains, but lacking the alpha 3 domain. Unlike MHC Class I, they have no capacity to bind peptide or interact with beta2-microglobulin. It can activate multiple signaling pathways in primary NK cells, gamma delta T cells, and CD8+ alpha beta T cells, resulting in the production of cytokines and chemokines.ULBP1 is expressed in wide range of tissues including heart, brain, lung, liver, bone marrow and some tumor cells, T-cells, B-cells, As an unconventional member of the MHC class I family, ULBP1 is able to interact with soluble CMV glycoprotein UL16 in CMV infected cells. The interaction with UL16 blocked the interaction with the NKG2D receptor, and thus might escape the immune surveillance. Furthermore, UL16 also causes ULBP1 to be retained in the ER and cis-Golgi apparatus so that it does not reach the cell surface. The ULBP1 regulation may have implications for development of new therapeutic strategies against cancer cells.
NKG2-D type II integral membrane protein (NKG2D) is a type II transmembrane glycoprotein which belongs to the CD94/NKG2 family. NKG2D is expressed on natural killer (NK) cells, CD8+ alpha-beta and gamma-delta T-cells. As an activating and costimulatory receptor, it involved in immunosurveillance upon binding to various cellular stress-inducible ligands displayed at the surface of autologous tumor cells and virus-infected cells. It provides both stimulatory and costimulatory innate immune responses on activated killer (NK) cells, leading to cytotoxic activity. It stimulates perforin-mediated elimination of ligand-expressing tumor cells. Signaling involves calcium influx, culminating in the expression of TNF-alpha. NKG2D participates in NK cell-mediated bone marrow graft rejection and survival of NK cells. It Binds to ligands belonging to various subfamilies of MHC class I-related glycoproteins including MICA, MICB, RAET1E, RAET1G, ULBP1, ULBP2, ULBP3 (ULBP2>ULBP1>ULBP3) and ULBP4.
Plays a stimulatory role on natural killer (NK) cell cytotoxicity.
Noggin is a secreted homodimeric glycoprotein that is an antagonist of bone morphogenetic proteins (BMPs). Mouse Noggin cDNA encodes a 232 amino acid (aa) residue precursor protein with 19 aa residue putative signal peptide that is cleaved to generate the 213 aa residue mature protein which is secreted as a homodimeric glycoprotein. Secreted Noggin probably remains close to the cell surface due to its binding of heparin-containing proteoglycans. Noggin binds some BMPs such as BMP4 with high affinity and others such as BMP7 with lower affinity. It antagonizes BMP bioactivities by blocking epitopes on BMPs that are needed for binding to both type I and type II receptors. Noggin is expressed in defined areas of the adult central nervous system and peripheral tissues such as lung, skeletal muscle and skin. During culture of human embryonic stem cells (hESC) or neural stem cells under certain conditions, addition of Noggin to antagonize BMP activity may allow stem cells to proliferate while maintaining their undifferentiated state, or alternatively, to differentiate into dopaminergic neurons.
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.
Protein NOV homolog, also known as Nephroblastoma-overexpressed gene protein homolog, NOV, and CCN3, is a putative ligand for integrin receptors, is tightly associated with the extracellular matrix, and mediates diverse cellular functions, including cell adhesion and proliferation. CCN3 has been shown to negatively regulate growth althoμgh it promotes migration in a cell type-specific manner. This secreted protein belongs to the CCN family, and its expression was observed in a broad variety of tissues from the early stage of development, and altered expression of CCN3 has been observed in a variety of tumors, including hepatocellular carcinomas, Wilm's tumors, Ewing's sarcomas, gliomas, rhabdomyosarcomas, and adrenocortical carcinomas. Mature CCN3 protein has five distinct modules and truncated protein variants with altered function are found in many cancers. CCN3 acts throμgh the core stem cell signaling pathways including Notch and Bone Morphogenic Protein, connecting CCN3 with the modulation of self-renewal and maturation of some cell lineages including hematopoietic, osteogenic, and chondrogenic. CCN3 may affect the extracellular environment of the niche for hematopoietic stem cells. CCN3 has emerged as a key player in stem cell regulation, hematopoiesis, and a crucial component within the bone marrow microenvironment.
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