Proteolipid Proteins (PLPs)

Designed for biological research and industrial applications, not intended for individual clinical or medical purposes.
CAT# Product Name M.W Molecular Formula Inquiry
P14001 [Ala144]-PLP (139-151) A144-PLP(139-151) 1406.6
P14002 [Gln144]-PLP (139-151), Q144-PLP(139-151) 1463.7
P14003 [Leu144, Arg147]-PLP (139-151), [L144, R147-PLP(139-151)] 1467.7
P14004 [Leu144]-PLP (139-151), L144-PLP(139-151) 1448.7
P14006 PLP (139-151) 1537.8
P14007 PLP (178-191) 1583.8
P14008 PLP (190-209) 2030.4
P14009 PLP (48-70) 2820.1
P14010 PLP (56-70) 1887.1
P14011 PLP (57-70) 1772.0

Introduction

Proteolipid Proteins (PLPs) is the most abundant protein in the central nervous system (CNS) myelin, accounting for about 50% of the central nervous system myelin protein, is a hydrophobic intact membrane protein. The amino acid sequence of PLPs is highly conserved in mammals, human and mouse PLPs are identical and exhibit greater than 99% homology to PLPs from dogs and cattle. Not only PLPs are highly homologous, but also they contain sequences similar to the channel forming regions of the nicotinic acetylcholine receptor and the glutamate receptor at the transmembrane region and the cysteine position. PLPs is synthesized in the myelin sheath by oligodendrocytes on the membrane-bound polyribosome as a mature protein, and the half-life of PLPs in myelin is about 90 days. PLPs plays an important role in the neurotransmission function of lipid metabolism in the brain.

Mechanism of action

A number of studies have shown that PLPs has multiple functions in myelin. PLPs can promote multi-functional membrane adhesion and myelination compaction, the formation of the mid-myelin line, oligodendrocyte maturation, involvement in the early stages of oligodendrocyte/axon interaction and encapsulation, maintenance of axons Survival. Lack of PLPs will shorten the length of the internode of Nodes of Ranvier, degeneration of the axonal line, and greatly reduce the number of mature oligodendrocytes, which will seriously affect the nerve function. In addition, the lack of PLPs results in a myelinating disease that causes severe CNS myelin, a significant reduction in white matter, an ultrastructural abnormality in the formation of a small amount of myelin, and premature apoptotic myelin deposition of oligodendrocytes at that time.

Application of Proteolipid Proteins

PLPs is an important component of the central nervous system, so it is important in some neurological diseases (such as Pelizaeus-Merzbacher disease, PMD). It can prevent white matter damage during aging, prevent cognitive decline, and improve the quality of life of the elderly. In addition, because PLPs synthetic expression is directly related to the normal conduction function of nerve fibers, it can alleviate cerebral concussion.

References

  1. Kitagawa, K., Sinoway, M. P., Yang, C., Gould, R. M., & Colman, D. R. (1993). A proteolipid protein gene family: expression in sharks and rays and possible evolution from an ancestral gene encoding a pore-forming polypeptide. Neuron, 11(3), 433-448.
  2. Campagnoni, A. T., & Skoff, R. P. (2001). The pathobiology of myelin mutants reveal novel biological functions of the MBP and PLP genes. Brain Pathology, 11(1), 74-91.