Proteolipid Protein 1 (PLP1) Kits ELISA

Human Proteolipid Protein 1 (PLP1) interaction partners

1. Findings suggest that PLP1 and CNTN1 gene variations modulate specific aspects of callosal microstructure that are in line with their gene function.

2. three single nucleotide polymorphisms in PLP1 that were associated with interhemispheric integration via the corpus callosum in a previous study also are relevant for functional hemispheric asymmetries.

3. This study demonstrated that the plp and alpha-synuclein transgenic mouse model of multiple system atrophy showed the Progressive striatonigral degeneration.

4. Pelizaeus-Merzbacher disease (PMD) is an X-linked disorder caused by mutations in the PLP1 gene, which encodes the proteolipid protein of myelinating oligodendroglia.

5. Proteolipid protein 1 and contactin 1 gene variation modulates interhemispheric integration

6. Using whole exome sequencing, a novel pathogenic PLP1 missense mutation c.251C > A (p.Ala84Asp) was detected in a Moroccan family, allowing a diagnosis of Pelizaeus-Merzbacher Disease.

7. down-regulated in cord blood by prenatal smoking

8. Authors investigated the disease progression in mouse models carrying PLP1 point mutations previously found in patients displaying clinical features of multiple sclerosis. These mouse models show loss-of-function of PLP1 associated with neuroinflammation.

9. Review focusing on sequences in hPLP1 intron 1 DNA deemed important for hPLP1 gene activity as well as a couple of "human-specific" supplementary exons within the first intron which are utilized to generate novel splice variants, and the potential role that these sequences may play in PLP1-linked disorders.

10. it seems that the epitopes of some microorganisms mimicking PLP such as PLP58-74 might have a potential role in the initiation of Multiple Sclerosis.

11. Human induced pluripotent stem cells-derived oligodendrocytes from 12 individuals with Pelizaeus-Merzbacher and identified individual and shared defects in PLP1 mRNA expression and splicing, oligodendrocyte progenitor development, and oligodendrocyte morphology and capacity for myelination.

12. report a novel mutation of the PLP1 gene in two siblings with Pelizaeus-Merzbacher disease associated with a rare and protean neuroimaging finding of optic nerve enlargement

13. Identification and functional study of novel PLP1 mutations in Chinese patients with Pelizaeus-Merzbacher disease. We identified PLP1 mutations in seven male patients with PMD.

14. In major depressive disorder there was a significantly reduced expression of PLP1 mRNA.

15. Study investigated 17 unrelated Pelizaeus-Merzbacher disease subjects with copy number gains at the PLP1 locus including triplication and quadruplication of specific genomic intervals-16/17 were found to have a duplication-inverted triplication-duplication rearrangement product.

16. Myelin proteolipid protein is critical to regulating oligodendrocyte progenitor cell migration.

17. PLP1 splicing mutations may result in a wide variety of disease phenotypes through a combination of multiple molecular pathogenic mechanisms.

18. this study provides new insight into the genotype-phenotype correlations of patients with PLP1 splice-site mutations.

19. Insertion of an extra copy of Xq22.2 into 1p36 results in functional duplication of the PLP1 gene in a girl with classical Pelizaeus-Merzbacher disease.

20. Data strongly suggest that a secondary structure within intron 3 is important for controlling regulation of the PLP1 alternative splice and that patient mutations can cause Pelizaeus-Merzbacher disease by disrupting this structure.

Mouse (Murine) Proteolipid Protein 1 (PLP1) interaction partners

1. These results suggest that colitis promotes rapid enteric neurogenesis in adult mice and humans through differentiation of Sox2- and PLP1-expressing cells, which represent enteric glia and/or neural progenitors

2. This study demonstrated that Genetic dissection of oligodendroglial and neuronal Plp1 function in a novel mouse model of spastic paraplegia type 2.

3. The rumpshaker missense mutation in the Plp1 gene gives rise to subcortical myoclonus

4. axonal mitochondria, smooth endoplasmic reticulum, and microtubules were characterized in rodent optic nerves where PLP is replaced by the peripheral nerve myelin protein, P0.

5. The observations collectively support the idea that GST-pi(Nuc)/DM-20 mRNA-expressing cells are the progeny of NG2-positive OPCs rather than a novel type of oligodendrocyte-lineage progenitor cells and that DM-20 mRNA expression is dynamically regulated during differentiation of OPCs into oligodendrocytes.

6. In the absence of P0, thus, PLP also contributes to myelination by Schwann cells and to the preservation of peripheral axons

7. while PLP can co-exist with P0 in peripheral nervous system(PNS) myelin, PLP cannot replace P0 as the major structural protein of PNS myelin.

8. Both extracellular and intracellular epitopes of PLP contribute to the pathogenesis of MP4-induced experimental autoimmune encephalomyelitis already in the setting of intact myelin.

9. The insertion of native PLP into Olg mitochondria of animals with PLP1/Plp1 regulates extracellular pH and adenosine triphosphate.

10. This study shows for the first time that Plp-null mice exhibit severe early-onset thermal hyperalgesia that is not associated with changes in thermal allodynic behavior.

11. A novel mechanism sheds light on the immune regulation by which sulfatide-reactive type II natural killer (NK)T cells suppress inflammatory class II histocompatibility-restricted pathogenic CD4+ T cell responses in a T cell-mediated autoimmune disease.

12. that an early reactive glia response occurs following mutations in the PLP gene

13. Result suggest that plp1 plays a role either in the structural integrity of oligodendrocyte progenitor cell processes or in their response to extracellular cues that orient process outgrowth.

14. PLP significantly suppresses both models of experimental autoimmune encephalitis (EAE)even when there is some evidence of epitope spreading in the myelin oligodendrocyte (MOG)38-50-induced EAE model.

15. PLP contributes to the high cholesterol content of myelin by association and co-transport in the central nervous system.

16. Olig2/Plp-positive progenitor cells give rise to Bergmann glia in the cerebellum.

17. PLP1 mutants inhibit Golgi apparatus to endoplasmic reticulum trafficking and have a role in pathogenesis of Pelizaeus-Merzbacher disease

18. The results presented here suggest that the antisilencer/enhancer is largely dispensable for the developmental regulation of Plp1 gene expression in vivo.

19. Our data indicate that miR-20a, a component of the cluster that controls oligodendrocyte cell number, regulates myelin proteolipid protein gene expression

20. PLP gene expression is evident in both neuronal and oligodendroglial phenotypes in developing neostriatum.