Introduction of GPM6B
Neuronal membrane glycoprotein M6-b (GPM6B) is a protein that in humans is encoded by the GPM6B gene. GPM6B gene expression may be regulated by MITF in melanocytic cells. Pseudogenes of this gene are located on chromosomes Y and 22. The neuronal membrane glycoprotein M6-b belongs to the proteolipid protein family, the members of which are expressed in most brain regions. They are considered to be involved in cellular housekeeping functions such as cell-to-cell communication and membrane trafficking. Neuronal membrane glycoprotein M6-b may also be involved in osteoblast differentiation. Alternate splicing leads to multiple transcript variants.
|Basic Information of GPM6B|
|Protein Name||Neuronal membrane glycoprotein M6-b|
|Organism||Homo sapiens (Human)|
Function of GPM6B Membrane Protein
Neuronal membrane glycoprotein M6-b is a novel component of the nodal Schwann cell microvilli. M6B is a four-transmembrane protein belonging to the proteolipid protein family which mediates intercellular contact and regulates membrane growth, composition, and targeting. In the CNS, M6B is expressed in neurons, oligodendrocytes, and astrocytes. M6B has been shown to cooperate with its paralogs proteolipid protein (PLP) and neuronal membrane glycoprotein M6A in regulating membrane growth of oligodendrocytes and neurons, respectively. Outside the nervous system, M6B plays a role in osteoblast differentiation by regulating actin cytoskeleton, ECM remodeling, and cell adhesion. M6B may be involved in neural development and regulation of osteoblast function and bone formation. Diseases associated with GPM6B include Rett syndrome and hypomyelinating leukodystrophy.
Fig.1 Interacting proteins for GPM6B gene.
Application of GPM6B Membrane Protein in Literature
This article reveals that M6B is a Schwann cell microvilli component which preserves the structural integrity of peripheral nodes of Ranvier.
Authors in this group use Gpm6b null mutant mice to search for behavioral functions of Gpm6b. The results show that Gpm6b deficiency impairs sensorimotor gating and modulates the behavioral response to a serotonergic challenge.
The article indicates that GPM6B controls cytoskeleton and matrix vesicle release and can be used as a novel regulator of osteoblast function and bone formation.
The article reveals that GPM6A and GPM6B may act as novel oncogenes in the development of human lymphoid leukemia-associated oncogenes.
This article reports that copy number changes in GPM6B and intragenic duplications of PLP1 are very unlikely to be involved in the etiology of UHL.
GPM6B Preparation Options
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